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Journal articles on the topic 'Paraptosi'

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Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Raimondi, Michela, Fabrizio Fontana, Monica Marzagalli, Matteo Audano, Giangiacomo Beretta, Patrizia Procacci, Patrizia Sartori, Nico Mitro, and Patrizia Limonta. "Ca2+ overload- and ROS-associated mitochondrial dysfunction contributes to δ-tocotrienol-mediated paraptosis in melanoma cells." Apoptosis 26, no. 5-6 (April 3, 2021): 277–92. http://dx.doi.org/10.1007/s10495-021-01668-y.

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Abstract Melanoma is an aggressive tumor with still poor therapy outcomes. δ-tocotrienol (δ-TT) is a vitamin E derivative displaying potent anti-cancer properties. Previously, we demonstrated that δ-TT triggers apoptosis in human melanoma cells. Here, we investigated whether it might also activate paraptosis, a non-canonical programmed cell death. In accordance with the main paraptotic features, δ-TT was shown to promote cytoplasmic vacuolization, associated with endoplasmic reticulum/mitochondrial dilation and protein synthesis, as well as MAPK activation in A375 and BLM cell lines. Moreover, treated cells exhibited a significant reduced expression of OXPHOS complex I and a marked decrease in oxygen consumption and mitochondrial membrane potential, culminating in decreased ATP synthesis and AMPK phosphorylation. This mitochondrial dysfunction resulted in ROS overproduction, found to be responsible for paraptosis induction. Additionally, δ-TT caused Ca2+ homeostasis disruption, with endoplasmic reticulum-derived ions accumulating in mitochondria and activating the paraptotic signaling. Interestingly, by using both IP3R and VDAC inhibitors, a close cause-effect relationship between mitochondrial Ca2+ overload and ROS generation was evidenced. Collectively, these results provide novel insights into δ-TT anti-melanoma activity, highlighting its ability to induce mitochondrial dysfunction-mediated paraptosis. Graphic Abstract δ-tocotrienol induces paraptotic cell death in human melanoma cells, causing endoplasmic reticulum dilation and mitochondrial swelling. These alterations induce an impairment of mitochondrial function, ROS production and calcium overload.

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2

Balachandran, Chandrasekar, Kenta Yokoi, Kana Naito, Jebiti Haribabu, Yuichi Tamura, Masakazu Umezawa, Koji Tsuchiya, Toshitada Yoshihara, Seiji Tobita, and Shin Aoki. "Cyclometalated Iridium(III) Complex–Cationic Peptide Hybrids Trigger Paraptosis in Cancer Cells via an Intracellular Ca2+ Overload from the Endoplasmic Reticulum and a Decrease in Mitochondrial Membrane Potential." Molecules 26, no. 22 (November 21, 2021): 7028. http://dx.doi.org/10.3390/molecules26227028.

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In our previous paper, we reported that amphiphilic Ir complex–peptide hybrids (IPHs) containing basic peptides such as KK(K)GG (K: lysine, G: glycine) (e.g., ASb-2) exhibited potent anticancer activity against Jurkat cells, with the dead cells showing a strong green emission. Our initial mechanistic studies of this cell death suggest that IPHs would bind to the calcium (Ca2+)–calmodulin (CaM) complex and induce an overload of intracellular Ca2+, resulting in the induction of non-apoptotic programmed cell death. In this work, we conduct a detailed mechanistic study of cell death induced by ASb-2, a typical example of IPHs, and describe how ASb-2 induces paraptotic programmed cell death in a manner similar to that of celastrol, a naturally occurring triterpenoid that is known to function as a paraptosis inducer in cancer cells. It is suggested that ASb-2 (50 µM) induces ER stress and decreases the mitochondrial membrane potential (ΔΨm), thus triggering intracellular signaling pathways and resulting in cytoplasmic vacuolization in Jurkat cells (which is a typical phenomenon of paraptosis), while the change in ΔΨm values is negligibly induced by celastrol and curcumin. Other experimental data imply that both ASb-2 and celastrol induce paraptotic cell death in Jurkat cells, but this induction occurs via different signaling pathways.

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3

Lee, A. Reum, Min Ji Seo, Jin Kim, Dong Min Lee, In Young Kim, Mi Jin Yoon, Hur Hoon, and Kyeong Sook Choi. "Lercanidipine Synergistically Enhances Bortezomib Cytotoxicity in Cancer Cells via Enhanced Endoplasmic Reticulum Stress and Mitochondrial Ca2+ Overload." International Journal of Molecular Sciences 20, no. 24 (December 4, 2019): 6112. http://dx.doi.org/10.3390/ijms20246112.

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The proteasome inhibitor (PI), bortezomib (Btz), is effective in treating multiple myeloma and mantle cell lymphoma, but not solid tumors. In this study, we show for the first time that lercanidipine (Ler), an antihypertensive drug, enhances the cytotoxicity of various PIs, including Btz, carfilzomib, and ixazomib, in many solid tumor cell lines by inducing paraptosis, which is accompanied by severe vacuolation derived from the endoplasmic reticulum (ER) and mitochondria. We found that Ler potentiates Btz-mediated ER stress and ER dilation, possibly due to misfolded protein accumulation, in MDA-MB 435S cells. In addition, the combination of Btz and Ler triggers mitochondrial Ca2+ overload, critically contributing to mitochondrial dilation and subsequent paraptotic events, including mitochondrial membrane potential loss and ER dilation. Taken together, our results suggest that a combined regimen of PI and Ler may effectively kill cancer cells via structural and functional perturbations of the ER and mitochondria.

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4

Qian, Xi-Feng, Jia-Hao Zhang, Yue-Xue Mai, Xin Yin, Yu-Bin Zheng, Zi-Yuan Yu, Guo-Dong Zhu, and Xu-Guang Guo. "A Novel Insight into Paraptosis-Related Classification and Signature in Lower-Grade Gliomas." International Journal of Genomics 2022 (November 14, 2022): 1–32. http://dx.doi.org/10.1155/2022/6465760.

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Lower-grade gliomas (LGG) are the most common intracranial malignancies that readily evolve to high-grade gliomas and increase drug resistance. Paraptosis is defined as a nonapoptotic form of programmed cell death, which is gradually focused on patients with gliomas to develop treatment options. However, the specific role of paraptosis in LGG and its correlation is still vague. In this study, we first establish the novel paraptosis-based prognostic model for LGG patients. The relevant data of LGG patients were acquired from The Cancer Genome Atlas database, and we found that LGG patients could be divided into three different clusters based on paraptosis via consensus cluster analysis. Through least absolute shrinkage and selection operator regression analysis and multivariate Cox regression analysis, 10-paraptosis-related gene (PRG) signatures (CDK4, TNK2, DSTYK, CDKN3, CCR4, CASP9, HSPA5, RGR, LPAR1, and PDCD6IP) were identified to separate LGG patients into high- and low-risk subgroups successfully. The Kaplan–Meier analysis and time-dependent receiver-operating characteristic showed that the performances of predicting overall survival (OS) were dramatically high. The parallel results were reappeared and verified by using the Chinese Glioma Genome Atlas and Gene Expression Omnibus databases. Independent prognostic analysis and nomogram construction implied that risk scores could be considered the independent factor to predict OS. Enrichment analysis indicated that immune-related biological processes were generally enriched, and different immune statuses were highly infiltrated in high-risk group. We also confirmed the potential relationship of 10-PRG signatures and drug sensitivity of Food and Drug Administration–approved drugs. In summary, our findings provide a novel knowledge of paraptosis status and crucial direction to further explore the role of PRG signatures in LGG.

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5

Nguyen, Phuong Linh, Chang Hoon Lee, Heesoon Lee, and Jungsook Cho. "Induction of Paraptotic Cell Death in Breast Cancer Cells by a Novel Pyrazolo[3,4-h]quinoline Derivative through ROS Production and Endoplasmic Reticulum Stress." Antioxidants 11, no. 1 (January 5, 2022): 117. http://dx.doi.org/10.3390/antiox11010117.

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Chemotherapy has been a standard intervention for a variety of cancers to impede tumor growth, mainly by inducing apoptosis. However, development of resistance to this regimen has led to a growing interest and demand for drugs targeting alternative cell death modes, such as paraptosis. Here, we designed and synthesized a novel derivative of a pyrazolo[3,4-h]quinoline scaffold (YRL1091), evaluated its cytotoxic effect, and elucidated the underlying molecular mechanisms of cell death in MDA-MB-231 and MCF-7 breast cancer (BC) cells. We found that YRL1091 induced cytotoxicity in these cells with numerous cytoplasmic vacuoles, one of the distinct characteristics of paraptosis. YRL1091-treated BC cells displayed several other distinguishing features of paraptosis, excluding autophagy or apoptosis. Briefly, YRL1091-induced cell death was associated with upregulation of microtubule-associated protein 1 light chain 3B, downregulation of multifunctional adapter protein Alix, and activation of extracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase. Furthermore, the production of reactive oxygen species (ROS) and newly synthesized proteins were also observed, subsequently causing ubiquitinated protein accumulation and endoplasmic reticulum (ER) stress. Collectively, these results indicate that YRL1091 induces paraptosis in BC cells through ROS generation and ER stress. Therefore, YRL1091 can serve as a potential candidate for the development of a novel anticancer drug triggering paraptosis, which may provide benefit for the treatment of cancers resistant to conventional chemotherapy.

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6

Liu, Xiaoli, Yan Gu, Yaoyao Bian, Danhong Cai, Yu Li, Ye Zhao, Zhaofeng Zhang, Mei Xue, and Liang Zhang. "Honokiol induces paraptosis-like cell death of acute promyelocytic leukemia via mTOR & MAPK signaling pathways activation." Apoptosis 26, no. 3-4 (February 7, 2021): 195–208. http://dx.doi.org/10.1007/s10495-020-01655-9.

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AbstractAcute promyelocytic leukemia (APL) is a blood system disease caused by the accumulation of a large number of immature blood cells in bone marrow. Although the introduction of all-trans retinoic acid (ATRA) and arsenic has reached a high level of complete remission rate and 5-year disease-free survival rate, the occurrence of various adverse reactions still severely affects the quality of life of patients. As a natural product, honokiol (HNK) has the advantages of low toxicity and high efficiency, and it is a potential drug for the treatment of cancer. Since cancer cells can escape apoptotic cell death through multiple adaptive mechanisms, HNK, a drug that induces cancer cell death in a nonapoptotic way, has attracted much interest. We found that HNK reduced the viability of human APL cell line (NB4 cells) by inducing paraptosis-like cell death. The process was accompanied by excessive reactive oxygen species (ROS), mitochondrial damage, endoplasmic reticulum stress, and increased microtubule-associated protein 1 light chain 3 (LC3) processing. The inactivation of proteasome activity was the main cause of misfolded and unfolded protein accumulation in endoplasmic reticulum, such as LC3II/I and p62. This phenomenon could be alleviated by adding cycloheximide (CHX), a protein synthesis inhibitor. We found that mTOR signaling pathway participated in paraptosis-like cell death induced by HNK in an autophagy-independent process. Moreover, the mitogen-activated protein kinase (MAPK) signaling pathway induced paraptosis of NB4 cells by promoting endoplasmic reticulum stress. In summary, these findings indicate that paraptosis may be a new way to treat APL, and provide novel insights into the potential mechanism of paraptosis-like cell death.

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7

Lee, Hong-Jae, Dong-Min Lee, Min-Ji Seo, Ho-Chul Kang, Seok-Kyu Kwon, and Kyeong-Sook Choi. "PSMD14 Targeting Triggers Paraptosis in Breast Cancer Cells by Inducing Proteasome Inhibition and Ca2+ Imbalance." International Journal of Molecular Sciences 23, no. 5 (February 28, 2022): 2648. http://dx.doi.org/10.3390/ijms23052648.

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PSMD14, a subunit of the 19S regulatory particles of the 26S proteasome, was recently identified as a potential prognostic marker and therapeutic target in diverse human cancers. Here, we show that the silencing and pharmacological blockade of PSMD14 in MDA-MB 435S breast cancer cells induce paraptosis, a non-apoptotic cell death mode characterized by extensive vacuolation derived from the endoplasmic reticulum (ER) and mitochondria. The PSMD14 inhibitor, capzimin (CZM), inhibits proteasome activity but differs from the 20S proteasome subunit-inhibiting bortezomib (Bz) in that it does not induce aggresome formation or Nrf1 upregulation, which underlie Bz resistance in cancer cells. In addition to proteasome inhibition, the release of Ca2+ from the ER into the cytosol critically contributes to CZM-induced paraptosis. Induction of paraptosis by targeting PSMD14 may provide an attractive therapeutic strategy against cancer cells resistant to proteasome inhibitors or pro-apoptotic drugs.

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8

Wepsic, H. Terry, and Neil Hoa. "Paraptosis and tumor immunity." International Immunopharmacology 114 (January 2023): 109491. http://dx.doi.org/10.1016/j.intimp.2022.109491.

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9

Yang, Min Hee, In Jin Ha, Seok-Geun Lee, Junhee Lee, Jae-Young Um, Gautam Sethi, and Kwang Seok Ahn. "Brassinin Induces Apoptosis, Autophagy, and Paraptosis via MAPK Signaling Pathway Activation in Chronic Myelogenous Leukemia Cells." Biology 12, no. 2 (February 14, 2023): 307. http://dx.doi.org/10.3390/biology12020307.

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Brassinin (BSN), a potent phytoalexin found in cruciferous vegetables, has been found to exhibit diverse anti-neoplastic effects on different cancers. However, the impact of BSN on chronic myelogenous leukemia (CML) cells and the possible mode of its actions have not been described earlier. We investigated the anti-cytotoxic effects of BSN on the KBM5, KCL22, K562, and LAMA84 CML cells and its underlying mechanisms of action in inducing programmed cell death. We noted that BSN could induce apoptosis, autophagy, and paraptosis in CML cells. BSN induced PARP cleavage, subG1 peak increase, and early apoptosis. The potential action of BSN on autophagy activation was confirmed by an LC3 expression and acridine orange assay. In addition, BSN induced paraptosis through increasing the reactive oxygen species (ROS) production, mitochondria damage, and endoplasmic reticulum (ER) stress. Moreover, BSN promoted the activation of the MAPK signaling pathway, and pharmacological inhibitors of this signaling pathway could alleviate all three forms of cell death induced by BSN. Our data indicated that BSN could initiate the activation of apoptosis, autophagy, and paraptosis through modulating the MAPK signaling pathway.

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10

Tripathy, Suman Kumar, Umasankar De, Niranjan Dehury, Paltan Laha, Manas Kumar Panda, Hyung Sik Kim, and Srikanta Patra. "Cyclometallated iridium complexes inducing paraptotic cell death like natural products: synthesis, structure and mechanistic aspects." Dalton Transactions 45, no. 38 (2016): 15122–36. http://dx.doi.org/10.1039/c6dt00929h.

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11

Li, Cai, Kwok-Wa Ip, Wai-Lun Man, Dan Song, Ming-Liang He, Shek-Man Yiu, Tai-Chu Lau, and Guangyu Zhu. "Cytotoxic (salen)ruthenium(iii) anticancer complexes exhibit different modes of cell death directed by axial ligands." Chemical Science 8, no. 10 (2017): 6865–70. http://dx.doi.org/10.1039/c7sc02205k.

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12

Ye, Rui-Rong, Cai-Ping Tan, Yan-Nan Lin, Liang-Nian Ji, and Zong-Wan Mao. "A phosphorescent rhenium(i) histone deacetylase inhibitor: mitochondrial targeting and paraptosis induction." Chemical Communications 51, no. 39 (2015): 8353–56. http://dx.doi.org/10.1039/c5cc02354h.

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A phosphorescent rhenium(i) tricarbonyl polypyridine complex with mitochondria-specific localization, HDAC inhibitory activity and paraptosis-inducing capability has been explored as a multifunctional agent.

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13

Solovieva, Marina, Yuri Shatalin, Irina Odinokova, Olga Krestinina, Yulia Baburina, Yana Lomovskaya, Anton Pankratov, et al. "Disulfiram Oxy-Derivatives Suppress Protein Retrotranslocation across the ER Membrane to the Cytosol and Initiate Paraptosis-like Cell Death." Membranes 12, no. 9 (August 29, 2022): 845. http://dx.doi.org/10.3390/membranes12090845.

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Disulfiram (DSF) and its derivatives were here investigated as antineoplastic agents, and their important feature is the ability to influence the UPS. We have recently shown that hydroxocobalamin catalyzes the aerobic oxidation of diethyldithiocarbamate to form disulfiram and its oxy-derivatives (DSFoxy; i.e., sulfones and sulfoxides), which induce cytoplasm vacuolization and paraptosis-like cancer cell death. We used LC-MS/MS and bioinformatics analysis to determine the key points in these processes. DSFoxy was found to induce an increase in the number of ubiquitinated proteins, including oxidized ones, and a decrease in the monomeric ubiquitin. Enhanced ubiquitination was revealed for proteins involved in the response to exogenous stress, regulation of apoptosis, autophagy, DNA damage/repair, transcription and translation, folding and ubiquitination, retrograde transport, the MAPK cascade, and some other functions. The results obtained indicate that DSF oxy-derivatives enhance the oxidation and ubiquitination of many proteins regulating proteostasis (including E3 ligases and deubiquitinases), which leads to inhibition of protein retrotranslocation across the ER membrane into the cytosol and accumulation of misfolded proteins in the ER followed by ER swelling and initiates paraptosis-like cell death. Our results provide new insight into the role of protein ubiquitination/deubiquitination in regulating protein retrotranslocation across the ER membrane into the cytosol and paraptosis-like cell death.

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14

Zhu, Dongrong, Chen Chen, Yuanzheng Xia, Ling-Yi Kong, and Jianguang Luo. "A Purified Resin Glycoside Fraction from Pharbitidis Semen Induces Paraptosis by Activating Chloride Intracellular Channel-1 in Human Colon Cancer Cells." Integrative Cancer Therapies 18 (January 2019): 153473541882212. http://dx.doi.org/10.1177/1534735418822120.

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Pharbitidis Semen has worldwide recognition in traditional medicine for the treatment of several illnesses apart from its purgative properties, and it is also reported to show anticancer effect. However, limited pharmacological studies are available on the extract or resin glycosides fraction of Pharbitidis Semen. The purpose of this study was to determine the mechanism of the colon cancer cell cytotoxic effect of a purified resin glycoside fraction from Pharbitidis Semen (RFP). Our results showed that the RFP-induced cell death was mediated by the caspase-independent and autophagy-protective paraptosis, a type of cell death that is characterized by the accumulation of cytoplasmic vacuoles and mitochondria swelling. RFP significantly stimulated endoplasmic reticulum stress, inhibited proteasome-dependent degradation, and activated the MAPK signaling pathway in human colon cancer cell lines. Furthermore, we found that RFP activated chloride intracellular channel-1 (CLIC1) and increased the intracellular Cl− concentration. Blockage of CLIC1 by DIDS (disodium 4,4′-diisothiocyanato-2,2′-stilbenedisulfonate hydrate) attenuated cell death, cytoplasmic vacuolization, and endoplasmic reticulum stress, suggesting that CLIC1 acts as a critical early signal in RFP-induced paraptosis. In conclusion, results obtained indicated that the cytotoxic effect of RFP in colon cancer cells was the outcome of paraptosis mediated by activation of CLIC1.

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15

Hu, Lelin, Hao Wang, Yong Zhao, and Junjie Wang. "125I Seeds Radiation Induces Paraptosis-Like Cell Death via PI3K/AKT Signaling Pathway in HCT116 Cells." BioMed Research International 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/8145495.

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125I seeds brachytherapy implantation has been extensively performed in unresectable and rerecurrent rectal carcinoma. Many studies on the cancer-killing activity of125I seeds radiation mainly focused on its ability to trigger apoptosis, which is the most well-known and dominant type of cell death induced by radiation. However our results showed some unique morphological features such as cell swelling, cytoplasmic vacuolation, and plasma membrane integrity, which is obviously different to apoptosis. In this study, clonogenic proliferation was carried out to assay survival fraction. Transmission electron microscopy was used to analyze ultrastructural and evaluate morphologic feature of HCT116 cells after exposure to125I seeds radiation. Immunofluorescence analysis was used to detect the origin of cytoplasmic vacuoles. Flow cytometry analysis was employed to detect the size and granularity of HCT116 cells. Western blot was performed to measure the protein level of AIP1, caspase-3, AKT, p-Akt (Thr308), p-Akt (Ser473), andβ-actin. We found that125I seeds radiation activated PI3K/AKT signaling pathway and could trigger paraptosis-like cell death. Moreover, inhibitor of PI3K/AKT signaling pathway could inhibit paraptosis-like cell death induced by125I seeds radiation. Our data suggest that125I seeds radiation can induce paraptosis-like cell death via PI3K/AKT signaling pathway.

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16

Cini, Melchior, Huw Williams, Mike W. Fay, Mark S. Searle, Simon Woodward, and Tracey D. Bradshaw. "Enantiopure titanocene complexes – direct evidence for paraptosis in cancer cells." Metallomics 8, no. 3 (2016): 286–97. http://dx.doi.org/10.1039/c5mt00297d.

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17

Kessel, David. "Photodynamic therapy: apoptosis, paraptosis and beyond." Apoptosis 25, no. 9-10 (September 4, 2020): 611–15. http://dx.doi.org/10.1007/s10495-020-01634-0.

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18

Peega, Tebogo, Rachael N. Magwaza, Leonie Harmse, and Izak A. Kotzé. "Synthesis and evaluation of the anticancer activity of [Pt(diimine)(N,N-dibutyl-N′-acylthiourea)]+ complexes." Dalton Transactions 50, no. 34 (2021): 11742–62. http://dx.doi.org/10.1039/d1dt01385h.

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A series of platinum(ii) diimine acylthiourea complexes are reported with potent in vitro activity against two lung cancer cell lines (A549 and H1975) and a colorectal cancer cell line (HT-29) by inducing cell death by both apoptosis and paraptosis.

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19

Kessel, David. "Paraptosis and Photodynamic Therapy: A Progress Report." Photochemistry and Photobiology 96, no. 5 (April 23, 2020): 1096–100. http://dx.doi.org/10.1111/php.13242.

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20

Korsnes, Mónica Suárez, Arild Espenes, Dyveke Lem Hetland, and Lene C. Hermansen. "Paraptosis-like cell death induced by yessotoxin." Toxicology in Vitro 25, no. 8 (December 2011): 1764–70. http://dx.doi.org/10.1016/j.tiv.2011.09.005.

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21

QUAN, YING-YAO, CHAOYANG WANG, XIAO-PING WANG, and TONG-SHENG CHEN. "TAXOL INDUCES CELL DEATH WITH CYTOPLASM VACUOLIZATION IN PARAPTOSIS-LIKE BUT NOT ONCOSIS FASHION IN ASTC-a-1 CELLS." Journal of Innovative Optical Health Sciences 06, no. 04 (October 2013): 1350046. http://dx.doi.org/10.1142/s1793545813500466.

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Recently, we found that high concentration of taxol (70 μM) induced cell death with cytoplasm vacuolization, the typical characteristic of both paraptosis and oncosis, in human lung carcinoma (ASTC-a-1) cells. This report was designed to further determine the form of taxol-induced cell death with cytoplasm vacuolization. It is generally considered that the cytoplasm vacuolization in oncosis due to the swelling of endoplasmic reticulum (ER), mitochondria, lysosomes and nuclei occurs after the loss of mitochondrial membrane potential (ΔΨm). However, flow cytometry (FCM) analysis showed that taxol-induced cytoplasm vacuolization preceded the loss of ΔΨm. Moreover, taxol treatment did not induce the collapse of microtubule, the typical characteristic of oncosis. These data demonstrated that taxol-induced cell death with cytoplasm vacuolization is not oncosis. FCM analysis by Annexin V-FITC/PI apoptosis detection kit further demonstrated that taxol-induced cell death with cytoplasm vacuolization is not apoptosis. In conclusion, in combination with our recent in vitro and in vivo data, this report further demonstrates that high concentration of taxol induces cell death with cytoplasm vacuolization in paraptosis-like but not oncosis fashion.

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22

He, Liang, Kang-Nan Wang, Yue Zheng, Jian-Jun Cao, Ming-Fang Zhang, Cai-Ping Tan, Liang-Nian Ji, and Zong-Wan Mao. "Cyclometalated iridium(iii) complexes induce mitochondria-derived paraptotic cell death and inhibit tumor growthin vivo." Dalton Transactions 47, no. 20 (2018): 6942–53. http://dx.doi.org/10.1039/c8dt00783g.

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23

Kessel, David, and John J. Reiners. "Photodynamic therapy: autophagy and mitophagy, apoptosis and paraptosis." Autophagy 16, no. 11 (June 25, 2020): 2098–101. http://dx.doi.org/10.1080/15548627.2020.1783823.

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24

Ma, Mengjiao, Xiaoyi Luan, Hao Zheng, Xiaoning Wang, Shuqi Wang, Tao Shen, and Dongmei Ren. "A Mulberry Diels-Alder-Type Adduct, Kuwanon M, Triggers Apoptosis and Paraptosis of Lung Cancer Cells through Inducing Endoplasmic Reticulum Stress." International Journal of Molecular Sciences 24, no. 2 (January 5, 2023): 1015. http://dx.doi.org/10.3390/ijms24021015.

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The mulberry tree (Morus alba) has been cultivated in China for thousands of years. Mulberry Diels-Alder-type adducts (MDAAs) are characteristic constituents of the genus Morus. The unique structure and diverse bioactivities of MDAAs have attracted the attention of researchers. Kuwanon M (KWM) is an MDAA isolated from the root bark of Morus alba. This research reports the growth inhibitory effects of KWM on human lung cancer cells and its possible mechanism. In A549 and NCI-H292 cells, KWM treatment induced suppression of cell proliferation and migration. The appearance of chromatin condensation, phosphatidyl serine exposure and caspase cleavage indicated the arising of apoptosis. The loss of mitochondrial membrane potential (MMP), release of cytochrome c and dysregulation of Bax/Bcl-2 demonstrated that the KWM-induced apoptosis was through the mitochondrial pathway. Paraptosis was simultaneously detected under KWM treatment, as evidenced by the exhibition of cytoplasmic vacuolation, down-regulation of Alix and up-regulation of endoplasmic reticulum (ER) stress-related proteins. Mechanistically, ER stress induced activation of unfolded protein response (UPR) pathways and activation of the MAPK (JNK and ERK) pathway, all of which were critical for KWM-induced apoptosis and paraptosis. These findings suggested the possibility that KWM might be considered as a potential lung cancer therapeutic agent.

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25

Akogullari, Damla, Elgin Turkoz Uluer, and H. Seda Vatansever. "Investigation of the Relation between Follicular Atresia and Granulosa Cells in Terms of Cell Death Mechanisms in Premature Ovarian Failure Model." Proceedings 2, no. 25 (December 6, 2018): 1529. http://dx.doi.org/10.3390/proceedings2251529.

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Premature Ovarian Failure; is characterized by the dysfunction or early depletion of ovarian reserves due to follicular loss in the ovary in women under age of 40. POF is the important cause of infertility and its etiology is still not clearly understood. Investigation of cell death mechanisms (CDM) that play a role in the follicular atresia (FA) triggered by excessive loss of granulosa cells (GCs) that provide metabolic support for oocyte and follicle development in the ovary will help to understand POF etiology. It was known that apoptosis and autophagy play a role in FA. Recent studies have shown that paraptosis, associated with endoplasmic reticulum stress (ERS), also exist in FA. POF model was established in C57BL/6 female mice by CTX and it was confirmed by increased follicle stimulating hormone (FSH), luteal hormone (LH) and decreased estradiol (E2) blood levels and follicle count. According to the results of the immunohistochemistry (IHC) cell death markers were significantly more expressed than control (C) and sham (S) groups in the POF model. In addition, more apoptotic cells were observed in the POF group compared to C and S in the TUNEL analysis. In consequence of this study apoptosis and autophagy as well as paraptosis play a role in the FA leading to POF, will help to develop new treatment protocols.

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26

Torres-Ramírez, Nayeli, María L. Escobar, Gerardo H. Vázquez-Nin, Rosario Ortiz, and Olga M. Echeverría. "Paraptosis-like cell death in Wistar rat granulosa cells." Development, Growth & Differentiation 58, no. 8 (September 29, 2016): 651–63. http://dx.doi.org/10.1111/dgd.12322.

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27

Lee, Dongjoo, In Young Kim, Sharmistha Saha, and Kyeong Sook Choi. "Paraptosis in the anti-cancer arsenal of natural products." Pharmacology & Therapeutics 162 (June 2016): 120–33. http://dx.doi.org/10.1016/j.pharmthera.2016.01.003.

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28

Tian, Wei, Junying Li, Zhengying Su, Fu Lan, Zhaoquan Li, Dandan Liang, Chunmiao Wang, Danrong Li, and Huaxin Hou. "Novel Anthraquinone Compounds Induce Cancer Cell Death through Paraptosis." ACS Medicinal Chemistry Letters 10, no. 5 (March 25, 2019): 732–36. http://dx.doi.org/10.1021/acsmedchemlett.8b00624.

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29

Garrido-Armas, Monika, Juan Carlos Corona, Maria Luisa Escobar, Leda Torres, Francisco Ordóñez-Romero, Abrahan Hernández-Hernández, and Francisco Arenas-Huertero. "Paraptosis in human glioblastoma cell line induced by curcumin." Toxicology in Vitro 51 (September 2018): 63–73. http://dx.doi.org/10.1016/j.tiv.2018.04.014.

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30

JIA, DONG-PEI, SONG WANG, BAO-CHAO ZHANG, and FANG FANG. "Paraptosis triggers mitochondrial pathway-mediated apoptosis in Alzheimer's disease." Experimental and Therapeutic Medicine 10, no. 2 (May 29, 2015): 804–8. http://dx.doi.org/10.3892/etm.2015.2531.

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Wang, Yujia, Xiang Wen, Nan Zhang, Lian Wang, Dan Hao, Xian Jiang, and Gu He. "Small-molecule compounds target paraptosis to improve cancer therapy." Biomedicine & Pharmacotherapy 118 (October 2019): 109203. http://dx.doi.org/10.1016/j.biopha.2019.109203.

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32

Kessel, David. "Pathways to Paraptosis After ER Photodamage in OVCAR ‐5 Cells." Photochemistry and Photobiology 95, no. 5 (April 29, 2019): 1239–42. http://dx.doi.org/10.1111/php.13103.

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33

Petrillo, Sara, Deborah Chiabrando, Tullio Genova, Veronica Fiorito, Giada Ingoglia, Francesca Vinchi, Federico Mussano, et al. "Heme accumulation in endothelial cells impairs angiogenesis by triggering paraptosis." Cell Death & Differentiation 25, no. 3 (December 11, 2017): 573–88. http://dx.doi.org/10.1038/s41418-017-0001-7.

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34

Wang, Lin, Justin H. Gundelach, and Richard J. Bram. "Cycloheximide promotes paraptosis induced by inhibition of cyclophilins in glioblastoma multiforme." Cell Death & Disease 8, no. 5 (May 2017): e2807-e2807. http://dx.doi.org/10.1038/cddis.2017.217.

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35

Cini, Melchior, Huw Williams, Mike W. Fay, Mark S. Searle, Simon Woodward, and Tracey D. Bradshaw. "Correction: Enantiopure titanocene complexes – direct evidence for paraptosis in cancer cells." Metallomics 8, no. 2 (2016): 260. http://dx.doi.org/10.1039/c6mt90005d.

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Sperandio, S., K. Poksay, I. de Belle, M. J. Lafuente, B. Liu, J. Nasir, and D. E. Bredesen. "Paraptosis: mediation by MAP kinases and inhibition by AIP-1/Alix." Cell Death & Differentiation 11, no. 10 (June 11, 2004): 1066–75. http://dx.doi.org/10.1038/sj.cdd.4401465.

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Sun, Qingrui, Tongsheng Chen, Xiaoping Wang, and Xunbin Wei. "Taxol induces paraptosis independent of both protein synthesis and MAPK pathway." Journal of Cellular Physiology 222, no. 2 (February 2010): 421–32. http://dx.doi.org/10.1002/jcp.21982.

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Zheng, Rongrong, Linping Zhao, Xiayun Chen, Lingshan Liu, Yibin Liu, Xiantong Chen, Chang Wang, Xiyong Yu, Hong Cheng, and Shiying Li. "Metal-coordinated nanomedicine for combined tumor therapy by inducing paraptosis and apoptosis." Journal of Controlled Release 336 (August 2021): 159–68. http://dx.doi.org/10.1016/j.jconrel.2021.06.021.

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Kessel, David. "Apoptosis, Paraptosis and Autophagy: Death and Survival Pathways Associated with Photodynamic Therapy." Photochemistry and Photobiology 95, no. 1 (July 17, 2018): 119–25. http://dx.doi.org/10.1111/php.12952.

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40

Samadder, Pranati, Robert Bittman, Hoe-Sup Byun, and Gilbert Arthur. "A glycosylated antitumor ether lipid kills cells via paraptosis-like cell death." Biochemistry and Cell Biology 87, no. 2 (April 2009): 401–14. http://dx.doi.org/10.1139/o08-147.

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Abstract:

Glycosylated antitumor ether lipids (GAELs) have superior anticancer properties relative to the alkyllysophospholipid class, but there have been no studies of the mechanisms of these compounds. The prototype GAEL, 1-O-hexadecyl-2-O-methyl-3-O-(2′-amino-2′-deoxy-β-d-glucopyranosyl)-sn-glycerol (Gln), effectively killed mouse embryonic fibroblasts (MEFs) lacking key molecules involved in caspase-dependent apoptosis, and cell death was not prevented by caspase inhibitors. Gln did not cause a loss of mitochondrial membrane potential, even in rounded-up dying cells. Gln stimulated the appearance and accumulation of LC3-II, a protein marker for autophagy, in a variety of cells, including wild-type MEFs, but not in MEFs lacking ATG5, a key protein required for autophagy. Gln induced LC3 puncta formation in Chinese hamster ovary cells stably expressing a LC3–green fluorescent protein fusion protein. Thus, Gln appears to induce autophagy. Autophagy was mTOR-independent and was not inhibited by 3-methyladenine or wortmannin. Although Gln is toxic, cellular ability to undergo autophagy was not essential for its toxicity. Furthermore, the GAEL analog 2-deoxy-C-Glc induced LC3 puncta formation but did not kill the cells. Gln, but not 2-deoxy-C-Glc, caused the accumulation of cytoplasmic acidic vacuoles in the cells. Our data suggest that GAELs may activate autophagy; however, GAELs do not kill cells by apoptosis or autophagy but rather by a paraptosis-like cell death mechanism.

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Nedungadi, Divya, Anupama Binoy, Nanjan Pandurangan, Sanjay Pal, Bipin G. Nair, and Nandita Mishra. "6-Shogaol induces caspase-independent paraptosis in cancer cells via proteasomal inhibition." Experimental Cell Research 364, no. 2 (March 2018): 243–51. http://dx.doi.org/10.1016/j.yexcr.2018.02.018.

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Sugimori, Naomi, J. Luis Espinoza, Ly Quoc Trung, Akiyoshi Takami, Yukio Kondo, Dao Thi An, Motoko Sasaki, Tomohiko Wakayama, and Shinji Nakao. "Paraptosis Cell Death Induction by the Thiamine Analog Benfotiamine in Leukemia Cells." PLOS ONE 10, no. 4 (April 7, 2015): e0120709. http://dx.doi.org/10.1371/journal.pone.0120709.

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Zhou, Yongcun, Feiteng Huang, Ying Yang, Pingli Wang, Zhen Zhang, Yining Tang, Youqing Shen, and Kai Wang. "Paraptosis-Inducing Nanomedicine Overcomes Cancer Drug Resistance for a Potent Cancer Therapy." Small 14, no. 7 (January 19, 2018): 1702446. http://dx.doi.org/10.1002/smll.201702446.

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Verburg, Shayla Grace, Rebecca Margaret Lelievre, Michael James Westerveld, Jordon Marcus Inkol, Yi Lin Sun, and Samuel Tekeste Workenhe. "Viral-mediated activation and inhibition of programmed cell death." PLOS Pathogens 18, no. 8 (August 11, 2022): e1010718. http://dx.doi.org/10.1371/journal.ppat.1010718.

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Abstract:

Viruses are ubiquitous intracellular genetic parasites that heavily rely on the infected cell to complete their replication life cycle. This dependency on the host machinery forces viruses to modulate a variety of cellular processes including cell survival and cell death. Viruses are known to activate and block almost all types of programmed cell death (PCD) known so far. Modulating PCD in infected hosts has a variety of direct and indirect effects on viral pathogenesis and antiviral immunity. The mechanisms leading to apoptosis following virus infection is widely studied, but several modalities of PCD, including necroptosis, pyroptosis, ferroptosis, and paraptosis, are relatively understudied. In this review, we cover the mechanisms by which viruses activate and inhibit PCDs and suggest perspectives on how these affect viral pathogenesis and immunity.

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Monel, Blandine, Alex A. Compton, Timothée Bruel, Sonia Amraoui, Julien Burlaud‐Gaillard, Nicolas Roy, Florence Guivel‐Benhassine, et al. "Zika virus induces massive cytoplasmic vacuolization and paraptosis‐like death in infected cells." EMBO Journal 36, no. 12 (May 4, 2017): 1653–68. http://dx.doi.org/10.15252/embj.201695597.

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Zhang, Jing-Shu, Da-Ming Li, Yue Ma, Ning He, Qing Gu, Feng-Shan Wang, Shu-Qing Jiang, Bing-Qing Chen, and Jia-Ren Liu. "γ-Tocotrienol Induces Paraptosis-Like Cell Death in Human Colon Carcinoma SW620 Cells." PLoS ONE 8, no. 2 (February 28, 2013): e57779. http://dx.doi.org/10.1371/journal.pone.0057779.

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Zheng, Hongbo, Yiwen Dong, Lin Li, Bin Sun, Lei Liu, Huiqing Yuan, and Hongxiang Lou. "Novel Benzo[a]quinolizidine Analogs Induce Cancer Cell Death through Paraptosis and Apoptosis." Journal of Medicinal Chemistry 59, no. 10 (May 11, 2016): 5063–76. http://dx.doi.org/10.1021/acs.jmedchem.6b00484.

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Man, Shuli, Panpan Lv, Jingxia Cui, Furui Liu, Lei Peng, Long Ma, Changxiao Liu, and Wenyuan Gao. "Paris saponin II-induced paraptosis-associated cell death increased the sensitivity of cisplatin." Toxicology and Applied Pharmacology 406 (November 2020): 115206. http://dx.doi.org/10.1016/j.taap.2020.115206.

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Hoa, Neil, Michael P. Myers, Thomas G. Douglass, Jian Gang Zhang, Christina Delgado, Lara Driggers, Linda L. Callahan, et al. "Molecular Mechanisms of Paraptosis Induction: Implications for a Non-Genetically Modified Tumor Vaccine." PLoS ONE 4, no. 2 (February 27, 2009): e4631. http://dx.doi.org/10.1371/journal.pone.0004631.

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Park, Seok Soon, Dong Min Lee, Jun Hee Lim, Dongjoo Lee, Sang Jun Park, Hwan Myung Kim, Seonghyang Sohn, et al. "Pyrrolidine dithiocarbamate reverses Bcl-xL-mediated apoptotic resistance to doxorubicin by inducing paraptosis." Carcinogenesis 39, no. 3 (January 10, 2018): 458–70. http://dx.doi.org/10.1093/carcin/bgy003.

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