Статті в журналах: "Autophagy, breast cancer, IKBKE"

1

Zhao, Zhen, Yuanke Li, Hao Liu, Akshay Jain, Pratikkumar Vinodchandra Patel, and Kun Cheng. "Co-delivery of IKBKE siRNA and cabazitaxel by hybrid nanocomplex inhibits invasiveness and growth of triple-negative breast cancer." Science Advances 6, no. 29 (July 2020): eabb0616. http://dx.doi.org/10.1126/sciadv.abb0616.

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IKBKE is an oncogene in triple-negative breast cancer (TNBC), and we demonstrate that IKBKE small interfering RNA (siRNA) inhibits the proliferation, migration, and invasion of TNBC cells. Despite the recent success of siRNA therapeutics targeting to the liver, there still remains a great challenge to deliver siRNAs to solid tumors. Here, we report a hybrid nanocomplex to co-deliver the IKBKE siRNA and cabazitaxel to TNBC to achieve an optimal antitumor effect. The nanocomplex is modified with hyaluronic acid to target CD44 on TNBC cells. The nanocomplex shows higher cellular uptake and better tumor penetration of the encapsulated cargos. The nanocomplex also exhibits high tumor accumulation and antitumor activity in an orthotopic TNBC mouse model. Encapsulation of cabazitaxel in the nanocomplex enhances the activity of the IKBKE siRNA. The hybrid nanocomplex provides a novel and versatile platform for combination therapies using siRNAs and chemotherapy.

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2

Boehm, Jesse S., Jean J. Zhao, Jun Yao, So Young Kim, Ron Firestein, Ian F. Dunn, Sarah K. Sjostrom, et al. "Integrative Genomic Approaches Identify IKBKE as a Breast Cancer Oncogene." Cell 129, no. 6 (June 2007): 1065–79. http://dx.doi.org/10.1016/j.cell.2007.03.052.

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3

Barbie, Thanh U., Gabriela Alexe, Amir R. Aref, Shunqiang Li, Zehua Zhu, Xiuli Zhang, Yu Imamura, et al. "Targeting an IKBKE cytokine network impairs triple-negative breast cancer growth." Journal of Clinical Investigation 124, no. 12 (November 3, 2014): 5411–23. http://dx.doi.org/10.1172/jci75661.

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4

Maycotte, Paola. "Targeting autophagy in breast cancer." World Journal of Clinical Oncology 5, no. 3 (2014): 224. http://dx.doi.org/10.5306/wjco.v5.i3.224.

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5

Cocco, Stefania, Alessandra Leone, Michela Piezzo, Roberta Caputo, Vincenzo Di Lauro, Francesca Di Rella, Giuseppina Fusco, et al. "Targeting Autophagy in Breast Cancer." International Journal of Molecular Sciences 21, no. 21 (October 22, 2020): 7836. http://dx.doi.org/10.3390/ijms21217836.

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Breast cancer is a heterogeneous disease consisting of different biological subtypes, with differences in terms of incidence, response to diverse treatments, risk of disease progression, and sites of metastases. In the last years, several molecular targets have emerged and new drugs, targeting PI3K/Akt/mTOR and cyclinD/CDK/pRb pathways and tumor microenvironment have been integrated into clinical practice. However, it is clear now that breast cancer is able to develop resistance to these drugs and the identification of the underlying molecular mechanisms is paramount to drive further drug development. Autophagy is a highly conserved homeostatic process that can be activated in response to antineoplastic agents as a cytoprotective mechanism. Inhibition of autophagy could enhance tumor cell death by diverse anti-cancer therapies, representing an attractive approach to control mechanisms of drug resistance. In this manuscript, we present a review of autophagy focusing on its interplay with targeted drugs used for breast cancer treatment.

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6

Ostendorf, Benjamin N., and Sohail F. Tavazoie. "Autophagy Suppresses Breast Cancer Metastasis." Developmental Cell 52, no. 5 (March 2020): 542–44. http://dx.doi.org/10.1016/j.devcel.2020.02.005.

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7

Qiao, Jianghua, Yibing Chen, Yanjun Mi, Huan Jin, Lina Wang, Ting Huang, Haolong Li, et al. "Macrophages confer resistance to BET inhibition in triple-negative breast cancer by upregulating IKBKE." Biochemical Pharmacology 180 (October 2020): 114126. http://dx.doi.org/10.1016/j.bcp.2020.114126.

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8

Liu, Caigang, Lisha Sun, Jie Yang, Tong Liu, Yongliang Yang, Se-Min Kim, Xunyan Ou, et al. "FSIP1 regulates autophagy in breast cancer." Proceedings of the National Academy of Sciences 115, no. 51 (December 3, 2018): 13075–80. http://dx.doi.org/10.1073/pnas.1809681115.

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Fibrous sheath interacting protein 1 (FSIP1) is a cancer antigen expressed in the majority of breast cancer tissues and is associated with poor prognosis. However, the role of FSIP1 in the progression and drug sensitivity of triple-negative breast cancer (TNBC) has not been explored. Here, we show that FSIP1 deficiency by shRNA-mediated knockdown or CRISPR-Cas9–mediated knockout significantly inhibits the proliferation and invasion of TNBC cells and impairs chemotherapy-induced growth inhibition in vivo. Computational modeling predicted that FSIP1 binds to ULK1, and this was established by coimmunoprecipitation. FSIP1 deficiency promoted autophagy, enhanced AMP-activated protein kinase (AMPK) signaling, and decreased mechanistic target of rapamycin (mTOR) and Wnt/β-catenin activity. In contrast, knockdown of AMPK or inhibition of autophagy restored the sensitivity to chemotherapy drugs in TNBC cells. Our findings uncover a role of FSIP1 as well as mechanisms underlying FSIP1 action in drug sensitivity and may, therefore, aid in design of TNBC therapies.

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9

Karantza, Vassiliki, and Eileen White. "Role of Autophagy in Breast Cancer." Autophagy 3, no. 6 (November 26, 2007): 610–13. http://dx.doi.org/10.4161/auto.4867.

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10

Cook, Katherine L., Ayesha N. Shajahan, and Robert Clarke. "Autophagy and endocrine resistance in breast cancer." Expert Review of Anticancer Therapy 11, no. 8 (August 2011): 1283–94. http://dx.doi.org/10.1586/era.11.111.

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11

Ulasov, Ilya V., Anton V. Borovjagin, Peter Timashev, Massimo Cristofanili, and Danny R. Welch. "KISS1 in breast cancer progression and autophagy." Cancer and Metastasis Reviews 38, no. 3 (September 2019): 493–506. http://dx.doi.org/10.1007/s10555-019-09814-4.

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12

Gu, Yunyan, Pengfei Li, Fuduan Peng, Mengmeng Zhang, Yuanyuan Zhang, Haihai Liang, Wenyuan Zhao, et al. "Autophagy-related prognostic signature for breast cancer." Molecular Carcinogenesis 55, no. 3 (January 25, 2015): 292–99. http://dx.doi.org/10.1002/mc.22278.

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13

Finnegan, Ryan M., Ahmed M. Elshazly, Patricia V. Schoenlein, and David A. Gewirtz. "Therapeutic Potential for Targeting Autophagy in ER+ Breast Cancer." Cancers 14, no. 17 (September 1, 2022): 4289. http://dx.doi.org/10.3390/cancers14174289.

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While endocrine therapy remains the mainstay of treatment for ER-positive, HER2-negative breast cancer, tumor progression and disease recurrence limit the utility of current standards of care. While existing therapies may allow for a prolonged progression-free survival, however, the growth-arrested (essentially dormant) state of residual tumor cells is not permanent and is frequently a precursor to disease relapse. Tumor cells that escape dormancy and regain proliferative capacity also tend to acquire resistance to further therapies. The cellular process of autophagy has been implicated in the adaptation, survival, and reactivation of dormant cells. Autophagy is a cellular stress mechanism induced to maintain cellular homeostasis. Tumor cells often undergo therapy-induced autophagy which, in most contexts, is cytoprotective in function; however, depending on how the autophagy is regulated, it can also be non-protective, cytostatic, or cytotoxic. In this review, we explore the literature on the relationship(s) between endocrine therapies and autophagy. Moreover, we address the different functional roles of autophagy in response to these treatments, exploring the possibility of targeting autophagy as an adjuvant therapeutic modality together with endocrine therapies.

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14

Kim, Hye Min, and Ja Seung Koo. "The Role of Autophagy in Breast Cancer Metastasis." Biomedicines 11, no. 2 (February 18, 2023): 618. http://dx.doi.org/10.3390/biomedicines11020618.

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Patient morbidity and mortality is significantly increased in metastatic breast cancer. The metastasis process of breast cancer is very complicated and is delicately controlled by various factors. Autophagy is one of the important regulatory factors affecting metastasis in breast cancer by engaging in cell mobility, metabolic adaptation, tumor dormancy, and cancer stem cells. Here, we discuss the effects of autophagy on metastasis in breast cancer and assess the potential use of autophagy modulators for metastasis treatment.

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15

Zarzynska, Joanna Magdalena. "The Importance of Autophagy Regulation in Breast Cancer Development and Treatment." BioMed Research International 2014 (2014): 1–9. http://dx.doi.org/10.1155/2014/710345.

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Breast cancer (BC) is a potentially life-threatening malignant tumor that still causes high mortality among women. One of the mechanisms through which cancer development could be controlled is autophagy. This process exerts different effects during the stages of cancer initiation and progression due to the occurring superimposition of signaling pathways of autophagy and carcinogenesis. Chronic inhibition of autophagy or autophagy deficiency promotes cancer, due to instability of the genome and defective cell growth and as a result of cell stress. However, increased induction of autophagy can become a mechanism which allows tumor cells to survive the conditions of hypoxia, acidosis, or chemotherapy. Therefore, in the development of cancer, autophagy is regarded as a double-edged sword. Determination of the molecular mechanisms underlying autophagy regulation and its role in tumorigenesis is an essential component of modern anticancer strategies. Results of scientific studies show that inhibition of autophagy may enhance the effectiveness of currently used anticancer drugs and other therapies (like radiotherapy). However, in some cases, the promotion of autophagy can induce death and, hence, elimination of the cancer cells and reduction of tumor size. This review summarizes the current knowledge on autophagy regulation in BC and up-to-date anticancer strategies correlated with autophagy.

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16

Berardi, Damian E., Paola B. Campodónico, Maria Ines Díaz Bessone, Alejandro J. Urtreger, and Laura B. Todaro. "Autophagy: Friend or Foe in Breast Cancer Development, Progression, and Treatment." International Journal of Breast Cancer 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/595092.

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Autophagy is a catabolic process responsible for the degradation and recycling of long-lived proteins and organelles by lysosomes. This degradative pathway sustains cell survival during nutrient deprivation, but in some circumstances, autophagy leads to cell death. Thereby, autophagy can serve as tumor suppressor, as the reduction in autophagic capacity causes malignant transformation and spontaneous tumors. On the other hand, this process also functions as a protective cell-survival mechanism against environmental stress causing resistance to antineoplastic therapies. Although autophagy inhibition, combined with anticancer agents, could be therapeutically beneficial in some cases, autophagy induction by itself could lead to cell death in some apoptosis-resistant cancers, indicating that autophagy induction may also be used as a therapy. This paper summarizes the most important findings described in the literature about autophagy and also discusses the importance of this process in clinical settings.

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17

Vega-Rubín-de-Celis, Silvia, Zhongju Zou, Álvaro F. Fernández, Bo Ci, Min Kim, Guanghua Xiao, Yang Xie, and Beth Levine. "Increased autophagy blocks HER2-mediated breast tumorigenesis." Proceedings of the National Academy of Sciences 115, no. 16 (April 2, 2018): 4176–81. http://dx.doi.org/10.1073/pnas.1717800115.

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Allelic loss of the autophagy gene, beclin 1/BECN1, increases the risk of patients developing aggressive, including human epidermal growth factor receptor 2 (HER2)-positive, breast cancers; however, it is not known whether autophagy induction may be beneficial in preventing HER2-positive breast tumor growth. We explored the regulation of autophagy in breast cancer cells by HER2 in vitro and the effects of genetic and pharmacological strategies to increase autophagy on HER2-driven breast cancer growth in vivo. Our findings demonstrate that HER2 interacts with Beclin 1 in breast cancer cells and inhibits autophagy. Mice with increased basal autophagy due to a genetically engineered mutation in Becn1 are protected from HER2-driven mammary tumorigenesis, and HER2 fails to inhibit autophagy in primary cells derived from these mice. Moreover, treatment of mice with HER2-positive human breast cancer xenografts with the Tat-Beclin 1 autophagy-inducing peptide inhibits tumor growth as effectively as a clinically used HER2 tyrosine kinase inhibitor (TKI). This inhibition of tumor growth is associated with a robust induction of autophagy, a disruption of HER2/Beclin 1 binding, and a transcriptional signature in the tumors distinct from that observed with HER2 TKI treatment. Taken together, these findings indicate that the HER2-mediated inhibition of Beclin 1 and autophagy likely contributes to HER2-mediated tumorigenesis and that strategies to block HER2/Beclin 1 binding and/or increase autophagy may represent a new therapeutic approach for HER2-positive breast cancers.

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18

Marsh, Timothy, and Jayanta Debnath. "Autophagy suppresses breast cancer metastasis by degrading NBR1." Autophagy 16, no. 6 (April 14, 2020): 1164–65. http://dx.doi.org/10.1080/15548627.2020.1753001.

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19

Zhou, Jie, Wei Zhang, Bing Liang, Mathew C. Casimiro, Diana Whitaker-Menezes, Min Wang, Michael P. Lisanti, Susan Lanza-Jacoby, Richard G. Pestell та Chenguang Wang. "PPARγ activation induces autophagy in breast cancer cells". International Journal of Biochemistry & Cell Biology 41, № 11 (листопад 2009): 2334–42. http://dx.doi.org/10.1016/j.biocel.2009.06.007.

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20

Wang, Xuan, Yuanpeng Liu, Huan Qin, Guocui Qi, Xuehong Chen, Yi Lyu, and Yantao Han. "RIP1 Mediates Manzamine-A-Induced Secretory Autophagy in Breast Cancer." Marine Drugs 21, no. 3 (February 25, 2023): 151. http://dx.doi.org/10.3390/md21030151.

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Cancer-derived small extracellular vesicles (sEVs) serve as critical mediators of cell-to-cell communication. Manzamine A (MA), a unique marine-derived alkaloid with various bioactivities, exerts anticancer effects against several kinds of tumors, but it remains unclear whether it has the same activity against breast cancer. Here, we proved that MA inhibits MDA-MB-231 and MCF-7 cell proliferation, migration, and invasion in a time- and dose-dependent manner. In addition, MA promotes autophagosome formation but suppresses autophagosome degradation in breast cancer cells. Importantly, we also found that MA stimulates sEVs secretion and increases autophagy-related protein accumulation in secreted sEVs, further potentiated by autophagy inhibitor chloroquine (CQ). Mechanistically, MA decreases the expression level of RIP1, the key upstream regulator of the autophagic pathway, and reduces the acidity of lysosome. Overexpression of RIP1 activated AKT/mTOR signaling, thus attenuating MA-induced autophagy and the corresponding secretion of autophagy-associated sEVs. Collectively, these data suggested that MA is a potential inhibitor of autophagy by preventing autophagosome turnover, and RIP1 mediates MA-induced secretory autophagy, which may be efficacious for breast cancer treatment.

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21

McGrath, Michael K., McKenzie L. Hagan, Timmothy Summers, Jesse Wayson, Carol Joseph, Amanda C. Barrett, John T. Barrett, and Patricia V. Schoenlein. "Abstract 3006: Effects of JNK/Jun blockade on breast cancer cell autophagy are dependent on breast cancer subtype." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3006. http://dx.doi.org/10.1158/1538-7445.am2022-3006.

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Abstract Our long-term goal is to elucidate the role of JNK/Jun signaling in breast cancer cell autophagy induced by anti-estrogen treatment and/or chemotherapy in ERα expressing and TNBC cells, respectively. In this study, we analyzed the role of JNK/Jun signaling in regulating the high basal autophagy levels in TNBC. To do so, we utilized the highly metastatic murine 4T1 and the human MDA-MB-231 TNBC models. In addition, we performed autophagic flux assays after treating breast cancer cells with JNK-IN8, a non-reversible small molecule JNK1/2 inhibitor. Treatments were performed for various times in the presence and absence of chloroquine (CQ) to allow analysis of steady state levels of atg8 (LC3-II) and sequestosome-1 (p62). These LC3-II and p62 proteins are involved in autophagosome formation and function, and are catabolized during autolysosomal turnover. To impair this process, CQ is a lysosomotropic agent that raises the pH of the lysosome and blocks such turnover. We also determined the effect of JNK-IN-8 on 4T1 and MDA-MB-231 cell number (proliferation). These studies determined that JNK-IN8 was an effective inhibitor of autophagic flux in the TNBC cells when used at concentrations that effectively blocked cJun phosphorylation, the downstream readout of JNK-IN8 efficacy used for our experiments. Blockade of autophagic flux by JNK-1/2 inhibition in TNBC was in stark contrast to results obtained with JNK-IN-8 treatment of ERα expressing MCF-7 and T47-D breast cancer cells, in which JNK-IN-8 induced a robust autophagy response with elevations in the steady state levels and flux of LC3-II and p62. Induction of autophagy by JNK-IN-8 in ERα expressing breast cancer cells occurred concomitantly with a substantial reduction in cell proliferation but minimal induction of apoptosis. Overall, these pre-clinical in vitro studies support the following conclusions: (1) JNK1/2 targeting in TNBC effectively blocks autophagic flux and may be particularly effective when used in combination with chemotherapies that induce pro-survival autophagy which is a current focus of our studies; and (2) JNK1/2 targeting in ERα expressing breast cancers has the potential to mediate a pro-survival autophagic activity in response to endocrine therapy or chemotherapy and should be cautiously approached. Ongoing studies are aimed at understanding the underlying mechanisms of the differential effects of JNK/Jun signaling on autophagy in TNBC versus ERα expressing breast cancer. Such an understanding should provide important information to aid in the ongoing interest in utilizing JNK1/2 as a molecular target for improved treatment of TNBC. Citation Format: Michael K. McGrath, McKenzie L. Hagan, Timmothy Summers, Jesse Wayson, Carol Joseph, Amanda C. Barrett, John T. Barrett, Patricia V. Schoenlein. Effects of JNK/Jun blockade on breast cancer cell autophagy are dependent on breast cancer subtype [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3006.

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22

Basu, Alakananda. "Regulation of Autophagy by Protein Kinase C-ε in Breast Cancer Cells". International Journal of Molecular Sciences 21, № 12 (15 червня 2020): 4247. http://dx.doi.org/10.3390/ijms21124247.

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Protein kinase C-ε (PKCε), an anti-apoptotic protein, plays critical roles in breast cancer development and progression. Although autophagy is an important survival mechanism, it is not known if PKCε regulates autophagy in breast cancer cells. We have shown that silencing of PKCε by siRNA inhibited basal and starvation-induced autophagy in T47D breast cancer cells as determined by the decrease in LC3-II, increase in p62, and decrease in autophagy puncta both in the presence and absence of bafilomycin A1. The mechanistic target of rapamycin (mTOR) associates with Raptor or Rictor to form complex-1 (mTORC1) or complex-2 (mTORC2), respectively. Knockdown of PKCε attenuated an increase in autophagy caused by the depletion of Raptor and Rictor. Overexpression of PKCε in MCF-7 cells caused activation of mTORC1 and an increase in LC3-I, LC3-II, and p62. The mTORC1 inhibitor rapamycin abolished the increase in LC3-I and p62. Knockdown of mTOR and Rictor or starvation enhanced autophagy in PKCε overexpressing cells. While overexpression of PKCε in MCF-7 cells inhibited apoptosis, it induced autophagy in response to tumor necrosis factor-α. However, inhibition of autophagy by Atg5 knockdown restored apoptosis in PKCε-overexpressing cells. Thus, PKCε promotes breast cancer cell survival not only by inhibiting apoptosis but also by inducing autophagy.

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23

Niklaus, Nicolas J., Igor Tokarchuk, Mara Zbinden, Anna M. Schläfli, Paola Maycotte, and Mario P. Tschan. "The Multifaceted Functions of Autophagy in Breast Cancer Development and Treatment." Cells 10, no. 6 (June 9, 2021): 1447. http://dx.doi.org/10.3390/cells10061447.

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Macroautophagy (herein referred to as autophagy) is a complex catabolic process characterized by the formation of double-membrane vesicles called autophagosomes. During this process, autophagosomes engulf and deliver their intracellular content to lysosomes, where they are degraded by hydrolytic enzymes. Thereby, autophagy provides energy and building blocks to maintain cellular homeostasis and represents a dynamic recycling mechanism. Importantly, the clearance of damaged organelles and aggregated molecules by autophagy in normal cells contributes to cancer prevention. Therefore, the dysfunction of autophagy has a major impact on the cell fate and can contribute to tumorigenesis. Breast cancer is the most common cancer in women and has the highest mortality rate among all cancers in women worldwide. Breast cancer patients often have a good short-term prognosis, but long-term survivors often experience aggressive recurrence. This phenomenon might be explained by the high heterogeneity of breast cancer tumors rendering mammary tumors difficult to target. This review focuses on the mechanisms of autophagy during breast carcinogenesis and sheds light on the role of autophagy in the traits of aggressive breast cancer cells such as migration, invasion, and therapeutic resistance.

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24

Chen, Yongqiang, Ruobing Wang, Shujun Huang, Elizabeth S. Henson, Jayce Bi, and Spencer B. Gibson. "Erb-b2 Receptor Tyrosine Kinase 2 (ERBB2) Promotes ATG12-Dependent Autophagy Contributing to Treatment Resistance of Breast Cancer Cells." Cancers 13, no. 5 (March 2, 2021): 1038. http://dx.doi.org/10.3390/cancers13051038.

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The epidermal growth factor receptor (EGFR) family member erb-b2 receptor tyrosine kinase 2 (ERBB2) is overexpressed in many types of cancers leading to (radio- and chemotherapy) treatment resistance, whereas the underlying mechanisms are still unclear. Autophagy is known to contribute to cancer treatment resistance. In this study, we demonstrate that ERBB2 increases the expression of different autophagy genes including ATG12 (autophagy-related 12) and promotes ATG12-dependent autophagy. We clarify that lapatinib, a dual inhibitor for EGFR and ERBB2, promoted autophagy in cells expressing only EGFR but inhibited autophagy in cells expressing only ERBB2. Furthermore, breast cancer database analysis of 35 genes in the canonical autophagy pathway shows that the upregulation of ATG12 and MAP1LC3B is associated with a low relapse-free survival probability of patients with ERBB2-positive breast tumors following treatments. Downregulation of ERBB2 or ATG12 increased cell death induced by chemotherapy drugs in ERBB2-positive breast cancer cells, whereas upregulation of ERBB2 or ATG12 decreased the cell death in ERBB2-negative breast cancer cells. Finally, ERBB2 antibody treatment led to reduced expression of ATG12 and autophagy inhibition increasing drug or starvation-induced cell death in ERBB2-positive breast cancer cells. Taken together, this study provides a novel approach for the treatment of ERBB2-positive breast cancer by targeting ATG12-dependent autophagy.

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25

Chen, Shuyi, Yabiao Gao, Ping Zhu, Xue Wang, Linzi Zeng, Youping Jin, Xiuling Zhi, Huanjun Yang, and Ping Zhou. "Anti-cancer Drug Anlotinib Promotes Autophagy and Apoptosis in Breast Cancer." Frontiers in Bioscience-Landmark 27, no. 4 (April 7, 2022): 125. http://dx.doi.org/10.31083/j.fbl2704125.

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26

Aqbi, Hussein F., Timothy Smith, Savannah Butler, Michael Idowu, Kyle K. Payne, and Masoud H. Manjili. "Autophagy-deficient breast cancer shows early escape from dormancy and recurrence following chemotherapy." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 122.23. http://dx.doi.org/10.4049/jimmunol.200.supp.122.23.

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Abstract Breast cancer patients who respond to cancer therapies often end up with a distant recurrence of the disease. It is not clear why people with the same type of breast cancer respond to treatments differently, some escape from dormancy and relapse earlier than others. In addition, some tumor clones respond to immunotherapy while others do not. Here, we investigated the role of autophagy in expediting or delaying recurrence of neu overexpressing mammary carcinoma (MMC) following adriamycin (ADR) chemotherapy, and in affecting response to immunotherapy. We took two strategies, including a transient blockade of autophagy with chloroquine (CQ) which transiently blocks fusion of autophagosome and lysosome, and a stable knockdown of autophagy, which inhibits the formation of autophagosome in MMC. We found that while CQ prolonged tumor dormancy, a stable knockdown of autophagy resulted in early escape from dormancy and recurrence. Interestingly, MMC with a stable knockdown of autophagy contained an increased frequency of ADR-induced polyploidy cells which rendered MMC resistant to immunotherapy. On the other hand, a transient blockade of autophagy did not affect the sensitivity of MMC to immunotherapy. Our observations suggest that while chemotherapy-induced autophagy may facilitate tumor relapse, cell intrinsic autophagy delays tumor relapse by inhibiting the formation of polyploidy tumor cells. Our findings are consistent with other reports showing that autophagy-deficient cells contain polyploid nuclei because of increased levels of reactive oxygen species. Our results also suggest that responsiveness of breast cancer patients to neoadjuvant therapies might be determined by tumor intrinsic autophagy.

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27

Park, Jong Hoon, Jee Won Park, Yesol Kim, Jaehee Jun, and Yejin Ahn. "Abstract 5826: Autophagy regulates cancer stem cell properties in triple negative breast cancer via miR-181a-mediated regulation of ATG5/ATG2B." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5826. http://dx.doi.org/10.1158/1538-7445.am2022-5826.

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Abstract Autophagy has a dual role in the maintenance of cancer stem cells (CSCs), but the precise relationship between autophagy and cancer stemness requires further investigation. In this study, it was found that luminal and triple-negative breast cancer require distinct therapeutic approaches because of their different expressions of autophagy flux. We identified that autophagy flux was inhibited in triple-negative breast cancer (TNBC) CSCs. Moreover, miRNA-181a (miR-181a) is upregulated both in TNBC CSCs and patients. ATG5 and ATG2B participate in the early formation of autophagosomes and were revealed as targets of miR-181a. Inhibition of miR-181a expression led to attenuation of TNBC cancer stemness and an increase in autophagy flux. Furthermore, treatment with curcumin led to attenuation of cancer stemness in TNBC CSCs; the expression of ATG5 and ATG2B was enhanced and there was an increase of autophagy flux. These results indicated that ATG5 and ATG2B are involved in the suppression of cancer stemness in TNBC. In summary, autophagy inhibits cancer stemness through the miR-181a-regulated mechanism in TNBC. Promoting tumor-suppressive autophagy using curcumin may be a potential method for the treatment of TNBC. Citation Format: Jong Hoon Park, Jee Won Park, Yesol Kim, Jaehee Jun, Yejin Ahn. Autophagy regulates cancer stem cell properties in triple negative breast cancer via miR-181a-mediated regulation of ATG5/ATG2B [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5826.

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28

Giannopoulos, Spyridon, Cansu Cimen Bozkus, Eleni Zografos, Aikaterini Athanasiou, Ann Marie Bongiovanni, Georgios Doulaveris, Chris N. Bakoyiannis, et al. "Targeting Both Autophagy and Immunotherapy in Breast Cancer Treatment." Metabolites 12, no. 10 (October 12, 2022): 966. http://dx.doi.org/10.3390/metabo12100966.

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Анотація:

As clinical efforts towards breast-conserving therapy and prolonging survival of those with metastatic breast cancer increase, innovative approaches with the use of biologics are on the rise. Two areas of current focus are cancer immunotherapy and autophagy, both of which have been well-studied independently but have recently been shown to have intertwining roles in cancer. An increased understanding of their interactions could provide new insights that result in novel diagnostic, prognostic, and therapeutic strategies. In this breast cancer-focused review, we explore the interactions between autophagy and two clinically relevant immune checkpoint pathways; the programmed cell death-1 receptor with its ligand (PD-L1)/PD-1 and the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4)/CD80 and CD86 (B7-1 and B7-2). Furthermore, we discuss emerging preclinical and clinical data supporting targeting both immunotherapy and autophagy pathway manipulation as a promising approach in the treatment of breast cancer.

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29

Han, Xinwei, Jinggang Mo, Yingmei Yang, Yichao Wang, and Hongsheng Lu. "Crucial Roles of LncRNAs-Mediated Autophagy in Breast Cancer." International Journal of Medical Sciences 19, no. 6 (2022): 1082–92. http://dx.doi.org/10.7150/ijms.72621.

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30

Wang, Kui, Wei Gao, Qianhui Dou, Haining Chen, Qifu Li, Edouard C. Nice, and Canhua Huang. "Ivermectin induces PAK1-mediated cytostatic autophagy in breast cancer." Autophagy 12, no. 12 (November 1, 2016): 2498–99. http://dx.doi.org/10.1080/15548627.2016.1231494.

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31

Suman, S., T. P. Das, R. Reddy, A. M. Nyakeriga, J. E. Luevano, D. Konwar, P. Pahari, and C. Damodaran. "The pro-apoptotic role of autophagy in breast cancer." British Journal of Cancer 111, no. 2 (June 19, 2014): 309–17. http://dx.doi.org/10.1038/bjc.2014.203.

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32

Guo, Wei, Yu Wang, Zhu Wang, Yan‐Ping Wang, and Hong Zheng. "Inhibiting autophagy increases epirubicin's cytotoxicity in breast cancer cells." Cancer Science 107, no. 11 (November 2016): 1610–21. http://dx.doi.org/10.1111/cas.13059.

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33

Pooladanda, Venkatesh, Soumya Bandi, Sandhya Rani Mondi, Krishna Mohan Gottumukkala, and Chandraiah Godugu. "Nimbolide epigenetically regulates autophagy and apoptosis in breast cancer." Toxicology in Vitro 51 (September 2018): 114–28. http://dx.doi.org/10.1016/j.tiv.2018.05.010.

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34

Brunelli, Elisa, Giulia Pinton, Paolo Bellini, Alberto Minassi, Giovanni Appendino, and Laura Moro. "Flavonoid-induced autophagy in hormone sensitive breast cancer cells." Fitoterapia 80, no. 6 (September 2009): 327–32. http://dx.doi.org/10.1016/j.fitote.2009.04.002.

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35

吕, 敏. "Application of Targeted Autophagy in Triple Negative Breast Cancer." Advances in Clinical Medicine 13, no. 01 (2023): 62–67. http://dx.doi.org/10.12677/acm.2023.131010.

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36

Cotzomi-Ortega, Israel, Arely Rosas-Cruz, Dalia Ramírez-Ramírez, Julio Reyes-Leyva, Miriam Rodriguez-Sosa, Patricia Aguilar-Alonso, and Paola Maycotte. "Autophagy Inhibition Induces the Secretion of Macrophage Migration Inhibitory Factor (MIF) with Autocrine and Paracrine Effects on the Promotion of Malignancy in Breast Cancer." Biology 9, no. 1 (January 18, 2020): 20. http://dx.doi.org/10.3390/biology9010020.

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Анотація:

Breast cancer is the main cause of cancer-related death in women in the world. Because autophagy is a known survival pathway for cancer cells, its inhibition is currently being explored in clinical trials for treating several types of malignancies. In breast cancer, autophagy has been shown to be necessary for the survival of cancer cells from the triple negative subtype (TNBC), which has the worst prognosis among breast cancers and currently has limited therapeutic options. Autophagy has also been involved in the regulation of protein secretion and, of importance for this work, the inhibition of autophagy is known to promote the secretion of proinflammatory cytokines from distinct cell types. We found that the inhibition of autophagy in TNBC cell lines induced the secretion of the macrophage migration inhibitory factor (MIF), a pro-tumorigenic cytokine involved in breast cancer invasion and immunomodulation. MIF secretion was dependent on an increase in reactive oxygen species (ROS) induced by the inhibition of autophagy. Importantly, MIF secreted from autophagy-deficient cells increased the migration of cells not treated with autophagy inhibitors, indicating that autophagy inhibition in cancer cells promoted malignancy in neighboring cells through the release of secreted factors, and that a combinatorial approach should be evaluated for cancer therapy.

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37

Zhou, Xunian, Grace Gar-Lee Yue, Stephen Kwok-Wing Tsui, Jianxin Pu, Kwok-Pui Fung, and Clara Bik-San Lau. "Elaborating the Role of Natural Products on the Regulation of Autophagy and their Potentials in Breast Cancer Therapy." Current Cancer Drug Targets 18, no. 3 (February 19, 2018): 239–55. http://dx.doi.org/10.2174/1568009617666170330124819.

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Autophagy is an intracellular lysosomal/vacuolar degradation system, in which the inner cytoplasmic cell membrane is degraded by the lysosomal hydrolases, followed by the resulting products released back into the cytosol. It is involved in many physiological processes which are crucial for cell growth and survival. However, disturbance in the autophagic process is often associated with a variety of human diseases, such as cancer. Breast cancer is one of the most malignant tumors characterized by the imbalanced cell proliferation, apoptosis as well as disordered autophagy regulation. The alterations of autophagy related genes or protein levels in breast cancer cells also suggested a potential implication of autophagy in breast cancer development and progression. Many natural products had been reported as potential anti-cancer agents or being considered as direct or indirect sources of new chemotherapy adjuvants to enhance the efficacy or to ameliorate the side effects through the modulation of autophagy. Investigation of the underlying mechanism of these compounds could be crucial for the development of new therapeutic or chemopreventive options for breast cancer treatment. In this review, a summary of those natural products that can regulate autophagy in breast cancer is presented and the potential value of such autophagy modulators on the development of anti-cancer drugs is also discussed.

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38

Wang, Yuntao, Wei Yue, Haiyan Lang, Xiaoqing Ding, Xinyi Chen, and Haiyan Chen. "Resuming Sensitivity of Tamoxifen-Resistant Breast Cancer Cells to Tamoxifen by Tetrandrine." Integrative Cancer Therapies 20 (January 2021): 153473542199682. http://dx.doi.org/10.1177/1534735421996822.

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Background: Tamoxifen is one of the medicines for adjuvant endocrine therapy of hormone-dependent breast cancer. However, development of resistance to tamoxifen occurs inevitably during treatment. This study aimed to determine whether sensitivity of tamoxifen-resistant breast cancer cells (TAM-R) could be reinstated by tetrandrine (Tet). Methods: All experiments were conducted in TAM-R cells derived from the MCF-7 breast cancer cell line by long-term tamoxifen exposure. Cell growth, apoptosis, and autophagy were end-points that evaluated the effect of Tet (0.9 μg/ml, 1.8 μg/ml, and 3.75 μg/ml) alone or in combination with TAM (1 μM). Cell apoptosis was determined by an ELISA assay and autophagy was determined by fluorescent staining using the Enzo autophagy detection kit. Immunoblotting was used to evaluate markers for apoptosis, autophagy, and related signal pathway molecules. Results: Growth of TAM-R cells was significantly inhibited by Tet. Combination of Tet with tamoxifen induced a greater inhibition on cell growth than tamoxifen alone, which was predominantly due to enhancement of pro-apoptotic effect of TAM by Tet. Autophagy was significantly inhibited in TAM-R cells treated with Tet plus TAM as shown by increased autophagosomes and the levels of LC3-II and p62. At 0.9 μg/ml, Tet increased the levels of both apoptosis and autophagy markers. Among them increase in p53 levels was more dramatic. Conclusions: Tet as a monotherapy inhibits TAM-R cells. Tet potentiates the pro-apoptotic effect of TAM via inhibition of autophagy.

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39

Zou, Peng, Longhua Liu, Louise D. Zheng, Kyle K. Payne, Masoud H. Manjili, Michael O. Idowu, Jinfeng Zhang, Eva M. Schmelz, and Zhiyong Cheng. "Coordinated Upregulation of Mitochondrial Biogenesis and Autophagy in Breast Cancer Cells: The Role of Dynamin Related Protein-1 and Implication for Breast Cancer Treatment." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/4085727.

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Overactive mitochondrial fission was shown to promote cell transformation and tumor growth. It remains elusive how mitochondrial quality is regulated in such conditions. Here, we show that upregulation of mitochondrial fission protein, dynamin related protein-1 (Drp1), was accompanied with increased mitochondrial biogenesis markers (PGC1α, NRF1, and Tfam) in breast cancer cells. However, mitochondrial number was reduced, which was associated with lower mitochondrial oxidative capacity in breast cancer cells. This contrast might be owing to enhanced mitochondrial turnover through autophagy, because an increased population of autophagic vacuoles engulfing mitochondria was observed in the cancer cells. Consistently, BNIP3 (a mitochondrial autophagy marker) and autophagic flux were significantly upregulated, indicative of augmented mitochondrial autophagy (mitophagy). The upregulation of Drp1 and BNIP3 was also observed in vivo (human breast carcinomas). Importantly, inhibition of Drp1 significantly suppressed mitochondrial autophagy, metabolic reprogramming, and cancer cell viability. Together, this study reveals coordinated increase of mitochondrial biogenesis and mitophagy in which Drp1 plays a central role regulating breast cancer cell metabolism and survival. Given the emerging evidence of PGC1αcontributing to tumor growth, it will be of critical importance to target both mitochondrial biogenesis and mitophagy for effective cancer therapeutics.

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40

Seyrek, Kamil, Fabian Wohlfromm, Johannes Espe, and Inna N. Lavrik. "The cross-talk of autophagy and apoptosis in breast carcinoma: implications for novel therapies?" Biochemical Journal 479, no. 14 (July 29, 2022): 1581–608. http://dx.doi.org/10.1042/bcj20210676.

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Breast cancer is still the most common cancer in women worldwide. Resistance to drugs and recurrence of the disease are two leading causes of failure in treatment. For a more efficient treatment of patients, the development of novel therapeutic regimes is needed. Recent studies indicate that modulation of autophagy in concert with apoptosis induction may provide a promising novel strategy in breast cancer treatment. Apoptosis and autophagy are two tightly regulated distinct cellular processes. To maintain tissue homeostasis abnormal cells are disposed largely by means of apoptosis. Autophagy, however, contributes to tissue homeostasis and cell fitness by scavenging of damaged organelles, lipids, proteins, and DNA. Defects in autophagy promote tumorigenesis, whereas upon tumor formation rapidly proliferating cancer cells may rely on autophagy to survive. Given that evasion of apoptosis is one of the characteristic hallmarks of cancer cells, inhibiting autophagy and promoting apoptosis can negatively influence cancer cell survival and increase cell death. Hence, combination of antiautophagic agents with the enhancement of apoptosis may restore apoptosis and provide a therapeutic advantage against breast cancer. In this review, we discuss the cross-talk of autophagy and apoptosis and the diverse facets of autophagy in breast cancer cells leading to novel models for more effective therapeutic strategies.

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41

Wang, Yi-Xuan, Yi-Yuan Jin, Jie Wang, Zi-Cheng Zhao, Ke-Wen Xue, He Xiong, Hui-Lian Che, Yun-Jun Ge, and Guo-Sheng Wu. "Icaritin Derivative IC2 Induces Cytoprotective Autophagy of Breast Cancer Cells via SCD1 Inhibition." Molecules 28, no. 3 (January 22, 2023): 1109. http://dx.doi.org/10.3390/molecules28031109.

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Breast cancer is one of the most prevalent malignancies and the leading cause of cancer-associated mortality in China. Icaritin (ICT), a prenyl flavonoid derived from the Epimedium Genus, has been proven to inhibit the proliferation and stemness of breast cancer cells. Our previous study demonstrated that IC2, a derivative of ICT, could induce breast cancer cell apoptosis by Stearoyl-CoA desaturase 1 (SCD1) inhibition. The present study further investigated the mechanism of the inhibitory effects of IC2 on breast cancer cells in vitro and in vivo. Our results proved that IC2 could stimulate autophagy in breast cancer cells with the activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling and mitogen-activated protein kinase (MAPK) signaling. Combination treatment of the AMPK inhibitor decreased IC2-induced autophagy while it markedly enhanced IC2-induced apoptosis. In common with IC2-induced apoptosis, SCD1 overexpression or the addition of exogenous oleic acid (OA) could also alleviate IC2-induced autophagy. In vivo assays additionally demonstrated that IC2 treatment markedly inhibited tumor growth in a mouse breast cancer xenograft model. Overall, our study was the first to demonstrate that IC2 induced cytoprotective autophagy by SCD1 inhibition in breast cancer cells and that the autophagy inhibitor markedly enhanced the anticancer activity of IC2. Therefore, IC2 was a potential candidate compound in combination therapy for breast cancer.

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42

Zambrano, Joelle, and Elizabeth S. Yeh. "Autophagy and Apoptotic Crosstalk: Mechanism of Therapeutic Resistance in HER2-Positive Breast Cancer." Breast Cancer: Basic and Clinical Research 10 (January 2016): BCBCR.S32791. http://dx.doi.org/10.4137/bcbcr.s32791.

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While breast cancer patients benefit from the use of HER2 inhibitors, many fail therapy and become resistant to treatment, indicating a critical need to prevent treatment failure. A number of studies have emerged that highlight the catabolic process of autophagy in breast cancer as a mechanism of resistance to chemotherapy and targeted inhibitors. Furthermore, recent research has begun to dissect how autophagy signaling crosstalks with apoptotic signaling. Thus, a possible strategy in fighting resistance is to couple targeting of apoptotic and autophagy signaling pathways. In this review, we discuss how cellular response by autophagy circumvents cell death to promote resistance of breast cancers to HER2 inhibitors, as well as the potential avenues of therapeutic intervention.

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43

Zhang, Ailian, and Jincheng Li. "Crocetin shifts autophagic cell survival to death of breast cancer cells in chemotherapy." Tumor Biology 39, no. 3 (March 2017): 101042831769453. http://dx.doi.org/10.1177/1010428317694536.

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The chemotherapy with fluorouracil is not always effective, in which some breast cancer cells may survive the fluorouracil treatment through enhanced autophagy. Crocetin is the major constituent of saffron, a Chinese traditional herb, which has recently found to have multiple pharmacological effects, including anticancer. However, the effects of Crocetin on the outcome of fluorouracil therapy for breast cancer have not been studied. Here, we showed that fluorouracil treatment inhibited the growth of breast cancer cells, in either a Cell Counting Kit-8 assay or an MTT assay. Inhibition of autophagy further suppressed breast cancer cell growth, suggesting that the breast cancer cells increased autophagic cell survival during fluorouracil treatment. However, Crocetin significantly increased the suppressive effects of fluorouracil on breast cancer cell growth, without affecting either cell apoptosis or autophagy. Inhibition of autophagy at the presence of Crocetin partially abolished the suppressive effects on breast cancer cell growth, suggesting that Crocetin may increase autophagic cell death in fluorouracil-treated breast cancer cells. Furthermore, Crocetin decreased Beclin-1 levels but increased ATG1 levels in fluorouracil-treated breast cancer cells. Together, these data suggest that Crocetin may shift autophagic cell survival to autophagic cell death in fluorouracil-treated breast cancer cells, possibly through modulation of the expression of ATG1 and Beclin-1.

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44

Yu, Tzu-Jung, Jun-Ping Shiau, Jen-Yang Tang, Chia-Hung Yen, Ming-Feng Hou, Yuan-Bin Cheng, Chih-Wen Shu, and Hsueh-Wei Chang. "Physapruin A Induces Reactive Oxygen Species to Trigger Cytoprotective Autophagy of Breast Cancer Cells." Antioxidants 11, no. 7 (July 11, 2022): 1352. http://dx.doi.org/10.3390/antiox11071352.

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Physalis peruviana-derived physapruin A (PHA) is a potent compound that selectively generates reactive oxygen species (ROS) and induces cancer cell death. Autophagy, a cellular self-clearance pathway, can be induced by ROS and plays a dual role in cancer cell death. However, the role of autophagy in PHA-treated cancer cells is not understood. Our study initially showed that autophagy inhibitors such as bafilomycin A1 enhanced the cytotoxic effects of PHA in breast cancer cell lines, including MCF7 and MDA-MB-231. PHA treatment decreased the p62 protein level and increased LC3-II flux. PHA increased the fluorescence intensity of DAPGreen and DALGreen, which are used to reflect the formation of autophagosome/autolysosome and autolysosome, respectively. ROS scavenger N-acetylcysteine (NAC) decreased PHA-elevated autophagy activity, implying that PHA-induced ROS may be required for autophagy induction in breast cancer cells. Moreover, the autophagy inhibitor increased ROS levels and enhanced PHA-elevated ROS levels, while NAC scavenges the produced ROS resulting from PHA and autophagy inhibitor. In addition, the autophagy inhibitor elevated the PHA-induced proportion of annexin V/7-aminoactinmycin D and cleavage of caspase-3/8/9 and poly (ADP-ribose) polymerase. In contrast, NAC and apoptosis inhibitor Z-VAD-FMK blocked the proportion of annexin V/7-aminoactinmycin D and the activation of caspases. Taken together, PHA induced ROS to promote autophagy, which might play an antioxidant and anti-apoptotic role in breast cancer cells.

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45

Wang, Mengchuan, Jian Zhang, Yizhe Huang, Shufeng Ji, Guoli Shao, Shaobo Feng, Danxun Chen, Kankan Zhao, Zixiang Wang, and Aiguo Wu. "Cancer-Associated Fibroblasts Autophagy Enhances Progression of Triple-Negative Breast Cancer Cells." Medical Science Monitor 23 (August 12, 2017): 3904–12. http://dx.doi.org/10.12659/msm.902870.

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46

Actis, Chiara, Giuliana Muzio, and Riccardo Autelli. "Autophagy Triggers Tamoxifen Resistance in Human Breast Cancer Cells by Preventing Drug-Induced Lysosomal Damage." Cancers 13, no. 6 (March 12, 2021): 1252. http://dx.doi.org/10.3390/cancers13061252.

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Endocrine resistance is a major complication during treatment of estrogen receptor-positive breast cancer. Although autophagy has recently gained increasing consideration among the causative factors, the link between autophagy and endocrine resistance remains elusive. Here, we investigate the autophagy-based mechanisms of tamoxifen resistance in MCF7 cells. Tamoxifen (Tam) triggers autophagy and affects the lysosomal compartment of MCF7 cells, such that activated autophagy supports disposal of tamoxifen-damaged lysosomes by lysophagy. MCF7 cells resistant to 5 µM tamoxifen (MCF7-TamR) have a higher autophagic flux and an enhanced resistance to Tam-induced lysosomal alterations compared to parental cells, which suggests a correlation between the two events. MCF7-TamR cells overexpress messenger RNAs (mRNAs) for metallothionein 2A and ferritin heavy chain, and they are re-sensitized to Tam by inhibition of autophagy. Overexpressing these proteins in parental MCF7 cells protects lysosomes from Tam-induced damage and preserves viability, while inhibiting autophagy abrogates lysosome protection. Consistently, we also demonstrate that other breast cancer cells that overexpress selected mRNAs encoding iron-binding proteins are less sensitive to Tam-induced lysosomal damage when autophagy is activated. Collectively, our data demonstrate that autophagy triggers Tam resistance in breast cancer cells by favoring the lysosomal relocation of overexpressed factors that restrain tamoxifen-induced lysosomal damage.

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47

Rotem-Dai, Noa, Amitha Muraleedharan, and Etta Livneh. "PKCeta Promotes Stress-Induced Autophagy and Senescence in Breast Cancer Cells, Presenting a Target for Therapy." Pharmaceutics 14, no. 8 (August 16, 2022): 1704. http://dx.doi.org/10.3390/pharmaceutics14081704.

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The emergence of chemoresistance in neoplastic cells is one of the major obstacles in cancer therapy. Autophagy was recently reported as one of the mechanisms that promote chemoresistance in cancer cells by protecting against apoptosis and driving senescence. Thus, understanding the role of autophagy and its underlying signaling pathways is crucial for the development of new therapeutic strategies to overcome chemoresistance. We have previously reported that PKCη is a stress-induced kinase that confers resistance in breast cancer cells against chemotherapy by inducing senescence. Here, we show that PKCη promotes autophagy induced by ER and oxidative stress and facilitates the transition from autophagy to senescence. We demonstrate that PKCη knockdown reduces both the autophagic flux and markers of senescence. Additionally, using autophagy inhibitors such as chloroquine and 3-methyladenine, we show that PKCη and autophagy are required for establishing senescence in MCF-7 in response to oxidative stress. Different drugs used in the clinic are known to induce autophagy and senescence in breast cancer cells. Our study proposes PKCη as a target for therapeutic intervention, acting in synergy with autophagy-inducing drugs to overcome resistance and enhance cell death in breast cancer.

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48

Bellanger, Dorine, Cléa Dziagwa, Cyrille Guimaraes, Michelle Pinault, Jean-François Dumas, and Lucie Brisson. "Adipocytes Promote Breast Cancer Cell Survival and Migration through Autophagy Activation." Cancers 13, no. 15 (August 3, 2021): 3917. http://dx.doi.org/10.3390/cancers13153917.

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White adipose tissue interacts closely with breast cancers through the secretion of soluble factors such as cytokines, growth factors or fatty acids. However, the molecular mechanisms of these interactions and their roles in cancer progression remain poorly understood. In this study, we investigated the role of fatty acids in the cooperation between adipocytes and breast cancer cells using a co-culture model. We report that adipocytes increase autophagy in breast cancer cells through the acidification of lysosomes, leading to cancer cell survival in nutrient-deprived conditions and to cancer cell migration. Mechanistically, the disturbance of membrane phospholipid composition with a decrease in arachidonic acid content is responsible for autophagy activation in breast cancer cells induced by adipocytes. Therefore, autophagy might be a central cellular mechanism of white adipose tissue interactions with cancer cells and thus participate in cancer progression.

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49

Chen, Guang, Xiao-Fei Ding, Hakim Bouamar, Kyle Pressley, and Lu-Zhe Sun. "Everolimus induces G1 cell cycle arrest through autophagy-mediated protein degradation of cyclin D1 in breast cancer cells." American Journal of Physiology-Cell Physiology 317, no. 2 (August 1, 2019): C244—C252. http://dx.doi.org/10.1152/ajpcell.00390.2018.

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Everolimus inhibits mammalian target of rapamycin complex 1 (mTORC1) and is known to cause induction of autophagy and G1 cell cycle arrest. However, it remains unknown whether everolimus-induced autophagy plays a critical role in its regulation of the cell cycle. We, for the first time, suggested that everolimus could stimulate autophagy-mediated cyclin D1 degradation in breast cancer cells. Everolimus-induced cyclin D1 degradation through the autophagy pathway was investigated in MCF-10DCIS.COM and MCF-7 cell lines upon autophagy inhibitor treatment using Western blot assay. Everolimus-stimulated autophagy and decrease in cyclin D1 were also tested in explant human breast tissue. Inhibiting mTORC1 with everolimus rapidly increased cyclin D1 degradation, whereas 3-methyladenine, chloroquine, and bafilomycin A1, the classic autophagy inhibitors, could attenuate everolimus-induced cyclin D1 degradation. Similarly, knockdown of autophagy-related 7 (Atg-7) also repressed everolimus-triggered cyclin D1 degradation. In addition, everolimus-induced autophagy occurred earlier than everolimus-induced G1 arrest, and blockade of autophagy attenuated everolimus-induced G1 arrest. We also found that everolimus stimulated autophagy and decreased cyclin D1 levels in explant human breast tissue. These data support the conclusion that the autophagy induced by everolimus in human mammary epithelial cells appears to cause cyclin D1 degradation resulting in G1 cell cycle arrest. Our findings contribute to our knowledge of the interplay between autophagy and cell cycle regulation mediated by mTORC1 signaling and cyclin D1 regulation.

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50

Maycotte, Paola, Christy M. Gearheart, Rebecca Barnard, Suraj Aryal, Jean M. Mulcahy Levy, Susan P. Fosmire, Ryan J. Hansen, et al. "STAT3-Mediated Autophagy Dependence Identifies Subtypes of Breast Cancer Where Autophagy Inhibition Can Be Efficacious." Cancer Research 74, no. 9 (March 3, 2014): 2579–90. http://dx.doi.org/10.1158/0008-5472.can-13-3470.

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