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Статті в журналах з теми "CELL CYCLE DEREGULATION"

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Автор: Grafiati

Опубліковано: 11 вересня 2023

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1

Sánchez-Beato, Margarita, Abel Sánchez-Aguilera, and Miguel A. Piris. "Cell cycle deregulation in B-cell lymphomas." Blood 101, no. 4 (February 15, 2003): 1220–35. http://dx.doi.org/10.1182/blood-2002-07-2009.

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Disruption of the physiologic balance between cell proliferation and death is a universal feature of all cancers. In general terms, human B-cell lymphomas can be subdivided into 2 main groups, low- and high-growth fraction lymphomas, according to the mechanisms through which this imbalance is achieved. Most types of low-growth fraction lymphomas are initiated by molecular events resulting in the inhibition of apoptosis, such as translocations affecting BCL2, in follicular lymphoma, or BCL10 and API2/MLT1, in mucosa-associated lymphoid tissue (MALT) lymphomas. This results in cell accumulation as a consequence of prolonged cell survival. In contrast, high-growth fraction lymphomas are characterized by an enhanced proliferative activity, as a result of the deregulation of oncogenes with cell cycle regulatory functions, such asBCL6, in large B-cell lymphoma, or c-myc, in Burkitt lymphoma. Low- and high-growth fraction lymphomas are both able to accumulate other alterations in cell cycle regulation, most frequently involving tumor suppressor genes such asp16INK4a, p53, andp27KIP1. As a consequence, these tumors behave as highly aggressive lymphomas. The simultaneous inactivation of several of these regulators confers increased aggressivity and proliferative advantage to tumoral cells. In this review we discuss our current knowledge of the alterations in each of these pathways, with special emphasis on the deregulation of cell cycle progression, in an attempt to integrate the available information within a global model that describes the contribution of these molecular changes to the genesis and progression of B-cell lymphomas.

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2

Savona, Michael, and Moshe Talpaz. "Cell-cycle deregulation in progressive CML." Nature Reviews Cancer 8, no. 7 (July 2008): 563. http://dx.doi.org/10.1038/nrc2368-c2.

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3

Kowalewski, Ashley A., R. Lor Randall, and Stephen L. Lessnick. "Cell Cycle Deregulation in Ewing's Sarcoma Pathogenesis." Sarcoma 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/598704.

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Ewing's sarcoma is a highly aggressive pediatric tumor of bone that usually contains the characteristic chromosomal translocation t(11;22)(q24;q12). This translocation encodes the oncogenic fusion protein EWS/FLI, which acts as an aberrant transcription factor to deregulate target genes necessary for oncogenesis. One key feature of oncogenic transformation is dysregulation of cell cycle control. It is therefore likely that EWS/FLI and other cooperating mutations in Ewing's sarcoma modulate the cell cycle to facilitate tumorigenesis. This paper will summarize current published data associated with deregulation of the cell cycle in Ewing's sarcoma and highlight important questions that remain to be answered.

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4

El-Deiry, Wafik S. "Akt takes centre stage in cell-cycle deregulation." Nature Cell Biology 3, no. 3 (March 2001): E71—E73. http://dx.doi.org/10.1038/35060148.

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5

Nacusi, Lucas P., and Robert J. Sheaff. "Deregulation of Cell Cycle Machinery in Pancreatic Cancer." Pancreatology 7, no. 4 (September 2007): 373–77. http://dx.doi.org/10.1159/000107398.

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6

Barlin, J., M. Leitao, L. Qin, M. Bisogna, N. Olvera, K. Shih, M. Hensley, G. Schwartz, J. Boyd, and D. Levine. "Uterine leiomyosarcomas are driven by cell cycle deregulation." Gynecologic Oncology 125 (March 2012): S135. http://dx.doi.org/10.1016/j.ygyno.2011.12.329.

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7

Clurman, Bruce E., James M. Roberts, and Mark Groudine. "Deregulation of cell cycle control in hematologic malignancies." Current Opinion in Hematology 3, no. 4 (1996): 315–20. http://dx.doi.org/10.1097/00062752-199603040-00011.

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8

Jackson, Kimberly M., Marisela DeLeon, C. Reynold Verret, and Wayne B. Harris. "Dibenzoylmethane induces cell cycle deregulation in human prostate cancer cells." Cancer Letters 178, no. 2 (April 2002): 161–65. http://dx.doi.org/10.1016/s0304-3835(01)00844-8.

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9

Azzam, Edouard I., Hatsumi Nagasawa, Yongjia Yu, Chuan-Yuan Li, and John B. Little. "Cell Cycle Deregulation and Xeroderma Pigmentosum Group C Cell Transformation." Journal of Investigative Dermatology 119, no. 6 (December 2002): 1350–54. http://dx.doi.org/10.1046/j.1523-1747.2002.19628.x.

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10

Shao, Zonghong, Jun Shi, Hong Liu, Juan Sun, Hairong Jia, Jie Bai, Guangsheng He, et al. "Aberrant Cell Cycle and Expression Profiles of Cell Cycle Regulatory Genes in Myelodysplastic Syndrome." Blood 106, no. 11 (November 16, 2005): 4897. http://dx.doi.org/10.1182/blood.v106.11.4897.4897.

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Abstract Deregulation of the cell cycle machinery, especially G1/S phase deregulation, is known to contribute to the uncontrolled cell proliferation and malignant transformation in haematological malignances. However, little is known about the aberrant bone marrow cell cycle and its molecular mechanisms in myelodysplastic syndromes (MDS). In this study, we conducted the cell cycle analysis of bone marrow mononuclear cells (BMMC) before and after exposure to haematopoietic growth factors (HGFs) cocktail, in combination with the analysis of the expression of Ki-67 antigen in BMMC and CD34+ cells in twenty-seven MDS patients. In addition, we examined the expression profiles of cell cycle regulatory genes. We found that MDS patients had higher percentage of BMMC in G0/G1 phase and lower ratio of cells in S+G2/M, and higher proportion of CD34+ Ki-67+ cells. After exposure to HGFs cocktail in vitro, high proportion of G0/G1 phase cells decreased significantly in MDS. All types of four cyclins (cyclin D2, D3, E, and A1) were at higher level had high amount of mRNA transcripts in MDS, together with higher activation of CDK2, CDK6, and RB genes. Furthermore, we also demonstrated higher activation of p21 and p27 genes. These results demonstrated that G1 arrest occurred in MDS Ki-67+ hematopoietic cells. High activation of cyclins, CDKs, and RB genes are the molecular bases of large proportion of Ki-67+ proliferate BMMC population. High activation of p21 and p27 genes in MDS blocked hematopoietic cells entry into the following cell cycle.

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11

Buttitta, Laura A., Alexia J. Katzaroff, and Bruce A. Edgar. "A robust cell cycle control mechanism limits E2F-induced proliferation of terminally differentiated cells in vivo." Journal of Cell Biology 189, no. 6 (June 14, 2010): 981–96. http://dx.doi.org/10.1083/jcb.200910006.

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Terminally differentiated cells in Drosophila melanogaster wings and eyes are largely resistant to proliferation upon deregulation of either E2F or cyclin E (CycE), but exogenous expression of both factors together can bypass cell cycle exit. In this study, we show this is the result of cooperation of cell cycle control mechanisms that limit E2F-CycE positive feedback and prevent cycling after terminal differentiation. Aberrant CycE activity after differentiation leads to the degradation of E2F activator complexes, which increases the proportion of CycE-resistant E2F repressor complexes, resulting in stable E2F target gene repression. If E2F-dependent repression is lost after differentiation, high anaphase-promoting complex/cyclosome (APC/C) activity degrades key E2F targets to limit cell cycle reentry. Providing both CycE and E2F activities bypasses exit by simultaneously inhibiting the APC/C and inducing a group of E2F target genes essential for cell cycle reentry after differentiation. These mechanisms are essential for proper development, as evading them leads to tissue outgrowths composed of dividing but terminally differentiated cells.

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12

Jacobsen, Kivin, Anja Groth, and Berthe M. Willumsen. "Ras-inducible immortalized fibroblasts: focus formation without cell cycle deregulation." Oncogene 21, no. 19 (May 2002): 3058–67. http://dx.doi.org/10.1038/sj.onc.1205423.

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13

Mishra, Rajakishore. "Cell cycle-regulatory cyclins and their deregulation in oral cancer." Oral Oncology 49, no. 6 (June 2013): 475–81. http://dx.doi.org/10.1016/j.oraloncology.2013.01.008.

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14

Panwar, Hariom, Gorantla V. Raghuram, Deepika Jain, Alok K. Ahirwar, Saba Khan, Subodh K. Jain, Neelam Pathak, Smita Banerjee, Kewal K. Maudar, and Pradyumna K. Mishra. "Cell cycle deregulation by methyl isocyanate: Implications in liver carcinogenesis." Environmental Toxicology 29, no. 3 (January 5, 2012): 284–97. http://dx.doi.org/10.1002/tox.21757.

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15

Chan, Edward, and Anjaruwee S. Nimnual. "Deregulation of the cell cycle by breast tumor kinase (Brk)." International Journal of Cancer 127, no. 11 (February 16, 2010): 2723–31. http://dx.doi.org/10.1002/ijc.25263.

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16

Wu, Lingtao, Ping Chen, Chung H. Shum, Cheng Chen, Lora W. Barsky, Kenneth I. Weinberg, Ambrose Jong, and Timothy J. Triche. "MAT1-Modulated CAK Activity Regulates Cell Cycle G1 Exit." Molecular and Cellular Biology 21, no. 1 (January 1, 2001): 260–70. http://dx.doi.org/10.1128/mcb.21.1.260-270.2001.

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ABSTRACT The cyclin-dependent kinase (CDK)-activating kinase (CAK) is involved in cell cycle control, transcription, and DNA repair (E. A. Nigg, Curr. Opin. Cell. Biol. 8:312–317, 1996). However, the mechanisms of how CAK is integrated into these signaling pathways remain unknown. We previously demonstrated that abrogation of MAT1 (ménage à trois 1), an assembly factor and targeting subunit of CAK, induces G1 arrest (L. Wu, P. Chen, J. J. Hwang, L. W. Barsky, K. I. Weinberg, A. Jong, and V. A. Starnes, J. Biol. Chem. 274:5564–5572, 1999). This result led us to investigate how deregulation of CAK by MAT1 abrogation affects the cell cycle G1 exit, a process that is regulated most closely by phosphorylation of retinoblastoma tumor suppressor protein (pRb). Using mammalian cellular models that undergo G1arrest evoked by antisense MAT1 abrogation, we found that deregulation of CAK inhibits pRb phosphorylation and cyclin E expression, CAK phosphorylation of pRb is MAT1 dose dependent but cyclin D1/CDK4 independent, and MAT1 interacts with pRb. These results suggest that CAK is involved in the regulation of cell cycle G1 exit while MAT1-modulated CAK formation and CAK phosphorylation of pRb may determine the cell cycle specificity of CAK in G1progression.

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17

Lummus, Seth C., Andrew M. Donson, Katherine Gowan, Kenneth L. Jones, Rajeev Vibhakar, Nicholas K. Foreman, and B. K. Kleinschmidt-DeMasters. "p16Loss and E2F/cell cycle deregulation in infant posterior fossa ependymoma." Pediatric Blood & Cancer 64, no. 12 (May 26, 2017): e26656. http://dx.doi.org/10.1002/pbc.26656.

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18

Yoshida, Noriaki, Kennosuke Karube, Atae Utsunomiya, Kunihiro Tsukasaki, Yoshitaka Imaizumi, Naoya Taira, Naokuni Uike, et al. "Cell Cycle Deregulation Determines Acute Transformation In Chronic Type Adult T-Cell Leukemia/Lymphoma." Blood 122, no. 21 (November 15, 2013): 845. http://dx.doi.org/10.1182/blood.v122.21.845.845.

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Abstract Introduction Adult T-cell leukemia/lymphoma (ATL) is a human T-cell leukemia virus type-1-induced neoplasm with four clinical subtypes; acute, lymphoma, chronic and smoldering. Although chronic and smoldering subtypes are regarded as indolent ATL, about half of these cases progress to acute type ATL and subsequent death. Therefore, cases of indolent ATL also have poor prognosis and acute transformation is a predictive indicator for patients with indolent ATL. However, the molecular pathogenesis of acute transformation remains unknown. In the present study, oligo-array comparative genomic hybridization (CGH) and comprehensive gene-expression profiling (GEP) were applied to 27 and 35 cases of chronic and acute type ATL, respectively, in an effort to delineate the molecular pathogeneses of ATL, and especially the molecular mechanism of acute transformation. Materials and Methods All DNA and RNA used in this study were extracted from purified CD4-positive cells. Oligo-array CGH analyses and comprehensive GEP analyses were performed on 27 and 35 cases of chronic and acute type ATL, respectively. Subsequently, we established Tet-OFF ATL cell lines for functional analyses. Results Oligo-array CGH revealed that genomic loss of 9p21.3 was significantly characteristic of acute type ATL, but not chronic type ATL (p-value= 0.039). Although the minimal common deleted region of 9p21.3 contained MTAP, CDKN2A and CDKN2B, the expression level of only CDKN2A was reduced with genomic loss of 9p21.3 (Figure 1). Moreover, analysis of serial samples of a chronic type ATL patient showing acute transformation also revealed that reduction of CDKN2A expression by 9p21.3 loss was associated with acute transformation in this case. CDKN2A contains two known variants, INK4a and ARF. Re-expression of INK4a and ARF suppressed proliferation of Tet-OFF ATL cell lines, while the suppression efficiency of INK4a was stronger than that of ARF (Figure 2). In cell-cycle assays, the induction of INK4a and ARF decreased the proportion of S-phase cells. Additionally, re-expression of INK4a also increased the amount of apoptotic cells in induced cell lines, while re-expression of ARF did not have this effect. Since CDKN2A is a well-known cell cycle regulator, deregulation of the cell-cycle might be involved in acute transformation of chronic type ATL. In fact, deregulation of the cell-cycle pathway has been reported as a predictive indicator for the outcome in diffuse large B-cell lymphoma patients (Cancer Cell, 22:359-372). Therefore, we examined whether chronic ATL patients had alterations in cell-cycle related genes and found that chronic ATL patients could be divided into two groups. The group possessing alterations in these genes (referred to as “Cell cycle Alteration”) showed poorer prognosis compared with the group lacking such alterations (referred to as “Clean”) (p-value= 0.037) (Figure 3). Additionally, patients with such alterations tended to have earlier progression to acute type ATL. Conclusion These findings indicated that cell cycle-related genes play an important role in acute transformation and should serve as good prognostic markers for chronic type ATL. Disclosures: No relevant conflicts of interest to declare.

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19

Sterlacci, William, Michael Fiegl, and Alexandar Tzankov. "Prognostic and Predictive Value of Cell Cycle Deregulation in Non-Small-Cell Lung Cancer." Pathobiology 79, no. 4 (2012): 175–94. http://dx.doi.org/10.1159/000336462.

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20

Atkins, Derek John, Christian Gingert, Christina Justenhoven, Gerd Emil Schmahl, Marcellus Stephanus Bonato, Hiltrud Brauch та Stephan Störkel. "Concomitant deregulation of HIF1α and cell cycle proteins in VHL-mutated renal cell carcinomas". Virchows Archiv 447, № 3 (1 липня 2005): 634–42. http://dx.doi.org/10.1007/s00428-005-1262-y.

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21

Cerquetti, Lidia, Camilla Sampaoli, Donatella Amendola, Barbara Bucci, Laura Masuelli, Rodolfo Marchese, Silvia Misiti, et al. "Rosiglitazone induces autophagy in H295R and cell cycle deregulation in SW13 adrenocortical cancer cells." Experimental Cell Research 317, no. 10 (June 2011): 1397–410. http://dx.doi.org/10.1016/j.yexcr.2011.02.014.

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22

Holthuis, J., TA Owen, AJ van Wijnen, KL Wright, A. Ramsey-Ewing, MB Kennedy, R. Carter, et al. "Tumor cells exhibit deregulation of the cell cycle histone gene promoter factor HiNF-D." Science 247, no. 4949 (March 23, 1990): 1454–57. http://dx.doi.org/10.1126/science.247.4949.1454.

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23

Holthuis, J., T. Owen, A. van Wijnen, K. Wright, A. Ramsey-Ewing, M. Kennedy, R. Carter, et al. "Tumor cells exhibit deregulation of the cell cycle histone gene promoter factor HiNF-D." Science 247, no. 4949 (March 23, 1990): 1454–57. http://dx.doi.org/10.1126/science.2321007.

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24

Donson, Andrew, Seth Lummus, Rajeev Vibhakar, Nicholas Foreman, and BK Kleinshmidt-DeMasters. "EPND-11. P16 LOSS AND E2F/CELL CYCLE DEREGULATION IN INFANT EPENDYMOMA." Neuro-Oncology 19, suppl_4 (May 31, 2017): iv17. http://dx.doi.org/10.1093/neuonc/nox083.069.

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25

Valois, Caroline R. A., and Ricardo B. Azevedo. "Cell-cycle deregulation induced by three different root canal sealers in vitro." Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology 106, no. 5 (November 2008): 763–67. http://dx.doi.org/10.1016/j.tripleo.2008.06.016.

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26

Florimond, A., P. Chouteau, N. Defer, A. Gaudin, H. Lerat, and J. M. Pawlotsky. "282 CELL CYCLE DEREGULATION BY HCV PROTEIN EXPRESSION, A POTENTIAL HEPATOCARCINOGENIC TRIGGER." Journal of Hepatology 58 (April 2013): S119—S120. http://dx.doi.org/10.1016/s0168-8278(13)60284-6.

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27

Diccianni, Mitchell B., Motoko Omura-Minamisawa, Ayse Batova, T. Le, Louis Bridgeman, and Alice L. Yu. "Frequent deregulation ofp16 and thep16/G1 cell cycle-regulatory pathway in neuroblastoma." International Journal of Cancer 80, no. 1 (January 5, 1999): 145–54. http://dx.doi.org/10.1002/(sici)1097-0215(19990105)80:1<145::aid-ijc26>3.0.co;2-g.

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28

de Almeida Engler, Janice, and Godelieve Gheysen. "Nematode-Induced Endoreduplication in Plant Host Cells: Why and How?" Molecular Plant-Microbe Interactions® 26, no. 1 (January 2013): 17–24. http://dx.doi.org/10.1094/mpmi-05-12-0128-cr.

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Plant-parasitic root-knot and cyst nematodes have acquired the ability to induce remarkable changes in host cells during the formation of feeding sites. Root-knot nematodes induce several multinucleate giant cells inside a gall whereas cyst nematodes provoke the formation of a multinucleate syncytium. Both strategies impinge on the deregulation of the cell cycle, involving a major role for endoreduplication. This review will first describe the current knowledge on the control of normal and aberrant cell cycles. Thereafter, we will focus on the role of both cell-cycle routes in the transformation process of root cells into large and highly differentiated feeding sites as induced by the phytoparasitic root-knot and cyst nematodes.

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29

Pérez-Peña, Javier, Elena Díaz-Rodríguez, Eduardo Sanz, and Atanasio Pandiella. "Central Role of Cell Cycle Regulation in the Antitumoral Action of Ocoxin." Nutrients 11, no. 5 (May 14, 2019): 1068. http://dx.doi.org/10.3390/nu11051068.

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Nutritional supplements which include natural antitumoral compounds could represent safe and efficient additives for cancer patients. One such nutritional supplement, Ocoxin Oral solution (OOS), is a composite formulation that contains several antioxidants and exhibits antitumoral properties in several in vitro and in vivo tumor conditions. Here, we performed a functional genomic analysis to uncover the mechanism of the antitumoral action of OOS. Using in vivo models of acute myelogenous leukemia (AML, HEL cells, representative of a liquid tumor) and small-cell lung cancer (GLC-8, representative of a solid tumor), we showed that OOS treatment altered the transcriptome of xenografted tumors created by subcutaneously implanting these cells. Functional transcriptomic studies pointed to a cell cycle deregulation after OOS treatment. The main pathway responsible for this deregulation was the E2F–TFDP route, which was affected at different points. The alterations ultimately led to a decrease in pathway activation. Moreover, when OOS-deregulated genes in the AML context were analyzed in patient samples, a clear correlation with their levels and prognosis was observed. Together, these data led us to suggest that the antitumoral effect of OOS is due to blockade of cell cycle progression mainly caused by the action of OOS on the E2F–TFDP pathway.

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30

Quereda, Victor, and Marcos Malumbres. "Cell cycle control of pituitary development and disease." Journal of Molecular Endocrinology 42, no. 2 (November 5, 2008): 75–86. http://dx.doi.org/10.1677/jme-08-0146.

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The pituitary gland regulates diverse physiological functions, including growth, metabolism, reproduction, stress response, and ageing. Early genetic models in the mouse taught us that the pituitary is highly sensitive to genetic alteration of specific cell cycle regulators such as the retinoblastoma protein (pRB) or the cell cycle inhibitor p27Kip1. The molecular analysis of human pituitary neoplasias has now corroborated that cell cycle deregulation is significantly implicated in pituitary tumorigenesis. In particular, proteins involved in cyclin-dependent kinase regulation or the pRB pathway are altered in nearly all human pituitary tumors. Additional cell cycle regulators such as PTTG1/securin may have critical roles in promoting genomic instability in pituitary neoplasias. Recent experimental data suggest that these cell cycle regulators may have significant implications in the biology of putative progenitor cells and pituitary homeostasis. Understanding how cell cycle regulation controls pituitary biology may provide us with new therapeutic approaches against pituitary diseases.

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31

Falzano, Loredana, Perla Filippini, Sara Travaglione, Alessandro Giamboi Miraglia, Alessia Fabbri, and Carla Fiorentini. "Escherichia coli Cytotoxic Necrotizing Factor 1 Blocks Cell Cycle G2/M Transition in Uroepithelial Cells." Infection and Immunity 74, no. 7 (July 2006): 3765–72. http://dx.doi.org/10.1128/iai.01413-05.

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ABSTRACT Evidence is accumulating that a growing number of bacterial toxins act by modulating the eukaryotic cell cycle machinery. In this context, we provide evidence that a protein toxin named cytotoxic necrotizing factor 1 (CNF1) from uropathogenic Escherichia coli is able to block cell cycle G2/M transition in the uroepithelial cell line T24. CNF1 permanently activates the small GTP-binding proteins of the Rho family that, beside controlling the actin cytoskeleton organization, also play a pivotal role in a large number of other cellular processes, including cell cycle regulation. The results reported here show that CNF1 is able to induce the accumulation of cells in the G2/M phase by sequestering cyclin B1 in the cytoplasm and down-regulating its expression. The possible role played by the Rho GTPases in the toxin-induced cell cycle deregulation has been investigated and discussed. The activity of CNF1 on cell cycle progression can offer a novel view of E. coli pathogenicity.

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32

Shaikh, Jahara, Kavitkumar Patel, and Tabassum Khan. "Advances in Pyrazole Based Scaffold as Cyclin-dependent Kinase 2 Inhibitors for the Treatment of Cancer." Mini-Reviews in Medicinal Chemistry 22, no. 8 (May 2022): 1211–29. http://dx.doi.org/10.2174/1389557521666211027104957.

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: The transformation of a normal cell into a tumor cell is one of the initial steps in cell cycle deregulation. The cell cycle is regulated by cyclin-dependent kinases (CDKs) that belong to the protein kinase family. CDK2 is an enchanting target for specific genotype tumors since cyclin E is selective for CDK2 and the deregulation of specific cancer types. Thus, CDKs inhibitor, specifically CDK2/cyclin A-E, has the potential to be a valid cancer target as per the currently undergoing clinical trials. Most of the pyrazole scaffolds have shown selectivity and potency for CDK2 inhibitors. This review aims at examining pyrazole and pyrazole fused with other heterocyclic rings for antiproliferative activity. Based on the invitro and molecular docking studies, the most potent analogues for CDK2 inhibition are exhibited by IC50 value. Moreover, the review emphasizes the various lead analogs of pyrazole hybrids which can be very potent and selective for anti-cancer drugs.

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33

Brito, J. L. R., B. Walker, M. Jenner, N. J. Dickens, N. J. M. Brown, F. M. Ross, A. Avramidou, et al. "MMSET deregulation affects cell cycle progression and adhesion regulons in t(4;14) myeloma plasma cells." Haematologica 94, no. 1 (January 1, 2009): 78–86. http://dx.doi.org/10.3324/haematol.13426.

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34

Santucci, Maria Alessandra, Laura Mercatali, Gianluca Brusa, Laura Pattacini, Enza Barbieri, and Paolo Perocco. "Cell-cycle deregulation in BALB/c 3T3 cells transformed by 1,2-dibromoethane and folpet pesticides." Environmental and Molecular Mutagenesis 41, no. 5 (2003): 315–21. http://dx.doi.org/10.1002/em.10162.

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35

Terasawa, Katsuhiko, Satoru Sagae, Tomoyuki Takeda, Shinichi Ishioka, Kanji Kobayashi, and Ryuichi Kudo. "Telomerase activity in malignant ovarian tumors with deregulation of cell cycle regulatory proteins." Cancer Letters 142, no. 2 (August 1999): 207–17. http://dx.doi.org/10.1016/s0304-3835(99)00170-6.

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36

Yeh, Hung-Wei, Mei-Chi Chang, Chun-Pin Lin, Wan-Yu Tseng, Hsiao-Hua Chang, Tong-Mei Wang, Yi-Jane Chen, et al. "Comparative cytotoxicity of five current dentin bonding agents: Role of cell cycle deregulation." Acta Biomaterialia 5, no. 9 (November 2009): 3404–10. http://dx.doi.org/10.1016/j.actbio.2009.05.036.

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37

Vermeulen, Katrien, Dirk R. Van Bockstaele, and Zwi N. Berneman. "The cell cycle: a review of regulation, deregulation and therapeutic targets in cancer." Cell Proliferation 36, no. 3 (June 2003): 131–49. http://dx.doi.org/10.1046/j.1365-2184.2003.00266.x.

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38

Kumar, Pankaj, Masanao Murakami, Rajeev Kaul, Abhik Saha, Qiliang Cai, and Erle S. Robertson. "Deregulation of the cell cycle machinery by Epstein–Barr virus nuclear antigen 3C." Future Virology 4, no. 1 (January 2009): 79–91. http://dx.doi.org/10.2217/17460794.4.1.79.

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39

Reed, Susanna Ekholm, Charles H. Spruck, Olle Sangfelt, Frank van Drogen, Elisabeth Mueller-Holzner, Martin Widschwendter, Anders Zetterberg, and Steven I. Reed. "Mutation of hCDC4 Leads to Cell Cycle Deregulation of Cyclin E in Cancer." Cancer Research 64, no. 3 (February 1, 2004): 795–800. http://dx.doi.org/10.1158/0008-5472.can-03-3417.

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40

De Meyer, T., ITGW Bijsmans, KK Van de Vijver, S. Bekaert, J. Oosting, W. Van Criekinge, M. van Engeland, and NLG Sieben. "E2Fs mediate a fundamental cell-cycle deregulation in high-grade serous ovarian carcinomas." Journal of Pathology 217, no. 1 (January 2009): 14–20. http://dx.doi.org/10.1002/path.2452.

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41

Tschanter, Petra, Nicole Baeumer, Lisa Lohmeyer, Frank Berkenfeld, Lara Tickenbrock, Sven Diederichs, Martin Stehling, et al. "Loss of the Cell Cycle Regulator p26INCA1 Induces Exhaustion of Leukemic Stem Cells." Blood 116, no. 21 (November 19, 2010): 96. http://dx.doi.org/10.1182/blood.v116.21.96.96.

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Abstract Abstract 96 Acute myeloid leukemia is a clonal disease characterized by a malignant proliferation and accumulation of myeloid progenitor cells. Current therapeutic strategies are often not able to eradicate the leukemic cells. Malignancy is associated with deregulation of cell cycle check- points and the deregulation of checkpoints is associated with altered stem cell properties. A better understanding of malignant stem cells and their cell cycle regulation might help to develop new therapies. Recently, we identified p26INCA1 as a novel cell cycle regulator. GST pulldown assays revealed binding of INCA1 predominantly to CDK2- specific Cyclins and we demonstrated an inhibitory effect of INCA1 on CDK2/ CyclinA complexes in kinase activity assays. The loss of INCA1 and its inhibitory effect on the cell cycle regulation led to an increased cell cycling and consequently to an enlarged stem cell pool in vivo. Upon cytotoxic stress, the loss of Inca1 enhanced cell cycling and bone marrow exhaustion. To analyze a potential role of INCA1 in leukemogenesis we retrovirally transduced wildtype and Inca1−/− bone marrow cells with AML1-ETO9a (A1E9a) and transplanted these cells into wildtype recipients. Most of the wildtype cell- transplanted recipients died due to AML. In contrast, only one of the Inca1−/− cell- transplanted mice developed AML. Engraftment was higher upon transplantion of Inca1−/− cells but engraftment was not sustained. To consider the repopulation capacity of the leukemic cells we performed transplantation of primary leukemic cells into secondary recipients. A1E9a induced leukemia in Inca1 wildtype cells was transplantable and lethal. However Inca1−/− leukemic cells were severely impaired in leukemia development in secondary recipients. Colony forming units and replating capacity were significantly reduced in A1E9a Inca1−/− bone marrow cells although these cells showed increased CDK2 activity. Exhaustion of leukemic cells in the absence of Inca1 was confirmed by cloning efficiency assays. Further analyses were performed with c-myc induced leukemias. Interestingly, Inca1 deletion precluded the development of leukemias in secondary recipients. Taken together, these findings identify an important role for p26INCA1 in the maintenance of leukemia and potentially the self-renewal capacity of leukemic stem cells. Disclosures: No relevant conflicts of interest to declare.

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42

Piezzo, Michela, Stefania Cocco, Roberta Caputo, Daniela Cianniello, Germira Di Gioia, Vincenzo Di Lauro, Giuseppina Fusco, et al. "Targeting Cell Cycle in Breast Cancer: CDK4/6 Inhibitors." International Journal of Molecular Sciences 21, no. 18 (September 4, 2020): 6479. http://dx.doi.org/10.3390/ijms21186479.

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Deregulation of cell cycle, via cyclin D/CDK/pRb pathway, is frequently observed in breast cancer lending support to the development of drugs targeting the cell cycle control machinery, like the inhibitors of the cycline-dependent kinases (CDK) 4 and 6. Up to now, three CDK4/6 inhibitors have been approved by FDA for the treatment of hormone receptor-positive (HR+), HER2-negative metastatic breast cancer. These agents have been effective in improving the clinical outcomes, but the development of intrinsic or acquired resistance can limit the efficacy of these treatments. Clinical and translational research is now focused on investigation of the mechanism of sensitivity/resistance to CDK4/6 inhibition and novel therapeutic strategies aimed to improve clinical outcomes. This review summarizes the available knowledge regarding CDK4/6 inhibitor, the discovery of new biomarkers of response, and the biological rationale for new combination strategies of treatment.

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43

Mukherji, Atish, Vaibhao C. Janbandhu, and Vijay Kumar. "HBx-dependent cell cycle deregulation involves interaction with cyclin E/A–cdk2 complex and destabilization of p27Kip1." Biochemical Journal 401, no. 1 (December 11, 2006): 247–56. http://dx.doi.org/10.1042/bj20061091.

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The HBx (X protein of hepatitis B virus) is a promiscuous transactivator implicated to play a key role in hepatocellular carcinoma. However, HBx-regulated molecular events leading to deregulation of cell cycle or establishment of a permissive environment for hepatocarcinogenesis are not fully understood. Our cell culture-based studies suggested that HBx had a profound effect on cell cycle progression even in the absence of serum. HBx presence led to an early and sustained level of cyclin–cdk2 complex during the cell cycle combined with increased protein kinase activity of cdk2 heralding an early proliferative signal. The increased cdk2 activity also led to an early proteasomal degradation of p27Kip1 that could be reversed by HBx-specific RNA interference and blocked by a chemical inhibitor of cdk2 or the T187A mutant of p27. Further, our co-immunoprecipitation and in vitro binding studies with recombinant proteins suggested a direct interaction between HBx and the cyclin E/A–cdk2 complex. Interference with different signalling cascades known to be activated by HBx suggested a constitutive requirement of Src kinases for the association of HBx with these complexes. Notably, the HBx mutant that did not interact with cyclin E/A failed to destabilize p27Kip1 or deregulate the cell cycle. Thus HBx appears to deregulate the cell cycle by interacting with the key cell cycle regulators independent of its well-established role in transactivation.

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44

Rocca, Andrea, Alessio Schirone, Roberta Maltoni, Sara Bravaccini, Lorenzo Cecconetto, Alberto Farolfi, Giuseppe Bronte, and Daniele Andreis. "Progress with palbociclib in breast cancer: latest evidence and clinical considerations." Therapeutic Advances in Medical Oncology 9, no. 2 (November 21, 2016): 83–105. http://dx.doi.org/10.1177/1758834016677961.

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Deregulation of the cell cycle is a hallmark of cancer, and research on cell cycle control has allowed identification of potential targets for anticancer treatment. Palbociclib is a selective inhibitor of the cyclin-dependent kinases 4 and 6 (CDK4/6), which are involved, with their coregulatory partners cyclin D, in the G1-S transition. Inhibition of this step halts cell cycle progression in cells in which the involved pathway, including the retinoblastoma protein (Rb) and the E2F family of transcription factors, is functioning, although having been deregulated. Among breast cancers, those with functioning cyclin D-CDK4/6-Rb-E2F are mainly hormone-receptor (HR) positive, with some HER2-positive and rare triple-negative cases. Deregulation results from genetic or otherwise occurring hyperactivation of molecules subtending cell cycle progression, or inactivation of cell cycle inhibitors. Based on results of randomized clinical trials, palbociclib was granted accelerated approval by the US Food and Drug Administration (FDA) for use in combination with letrozole as initial endocrine-based therapy for metastatic disease in postmenopausal women with HR-positive, HER2-negative breast cancer, and was approved for use in combination with fulvestrant in women with HR-positive, HER2-negative advanced breast cancer with disease progression following endocrine therapy. This review provides an update of the available knowledge on the cell cycle and its regulation, on the alterations in cyclin D-CDK4/6-Rb-E2F axis in breast cancer and their roles in endocrine resistance, on the preclinical activity of CDK4/6 inhibitors in breast cancer, both as monotherapy and as partners of combinatorial synergic treatments, and on the clinical development of palbociclib in breast cancer.

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45

Atsaves, Vassilis, Lazaros Lekakis, Elias Drakos, Vasiliki Leventaki, Mehran Ghaderi, George E. Baltatzis, Dimitris Chioureas, et al. "The oncogenic JUNB/CD30 axis contributes to cell cycle deregulation in ALK+ anaplastic large cell lymphoma." British Journal of Haematology 167, no. 4 (August 22, 2014): 514–23. http://dx.doi.org/10.1111/bjh.13079.

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46

Zhao, Wenqing, and James L. Manley. "Deregulation of Poly(A) Polymerase Interferes with Cell Growth." Molecular and Cellular Biology 18, no. 9 (September 1, 1998): 5010–20. http://dx.doi.org/10.1128/mcb.18.9.5010.

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ABSTRACT Vertebrate poly(A) polymerase (PAP) contains a catalytic domain and a C-terminal Ser-Thr-rich regulatory region. Consensus and nonconsensus cyclin-dependent kinase (cdk) sites are conserved in the Ser-Thr-rich region in vertebrate PAPs. PAP is phosphorylated by cdc2-cyclin B on these sites in vitro and in vivo and is inactivated by hyperphosphorylation in M-phase cells, when cdc2-cyclin B is active. In the experiments described here, we undertook a genetic approach in chicken DT40 cells to study the function of PAP phosphorylation. We found that PAP is highly conserved in chicken and is essential in DT40 cells. While cells could tolerate reduced levels of PAP, even modest overexpression of either wild-type PAP or a mutant PAP with two consensus cdk sites mutated (cdk− PAP) was highly deleterious and at a minimum resulted in reduced growth rates. Importantly, cells that expressed cdk− PAP had a significantly lower growth rate than did cells that expressed similar levels of wild-type PAP, which was reflected in increased accumulation of cells in the G0-G1 phase of the cell cycle. We propose that the lower growth rate is due to the failure of hyperphosphorylation and thus M-phase inactivation of cdk−PAP.

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47

Lodewijckx, Inge, and Jan Cools. "Deregulation of the Interleukin-7 Signaling Pathway in Lymphoid Malignancies." Pharmaceuticals 14, no. 5 (May 8, 2021): 443. http://dx.doi.org/10.3390/ph14050443.

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The cytokine interleukin-7 (IL-7) and its receptor are critical for lymphoid cell development. The loss of IL-7 signaling causes severe combined immunodeficiency, whereas gain-of-function alterations in the pathway contribute to malignant transformation of lymphocytes. Binding of IL-7 to the IL-7 receptor results in the activation of the JAK-STAT, PI3K-AKT and Ras-MAPK pathways, each contributing to survival, cell cycle progression, proliferation and differentiation. Here, we discuss the role of deregulated IL-7 signaling in lymphoid malignancies of B- and T-cell origin. Especially in T-cell leukemia, more specifically in T-cell acute lymphoblastic leukemia and T-cell prolymphocytic leukemia, a high frequency of mutations in components of the IL-7 signaling pathway are found, including alterations in IL7R, IL2RG, JAK1, JAK3, STAT5B, PTPN2, PTPRC and DNM2 genes.

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48

Fedele, Monica, Giovanna Maria Pierantoni, Maria Teresa Berlingieri, Sabrina Battista, Gustavo Baldassarre, Nikhil Munshi, Monica Dentice, et al. "Retraction: Overexpression of Proteins HMGA1 Induces Cell Cycle Deregulation and Apoptosis in Normal Rat Thyroid Cells." Cancer Research 78, no. 24 (December 13, 2018): 6910. http://dx.doi.org/10.1158/0008-5472.can-18-3460.

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49

Jonuleit, Tarja, Heiko van der Kuip, Cornelius Miething, Heike Michels, Michael Hallek, Justus Duyster, and Walter E. Aulitzky. "Bcr-Abl kinase down-regulates cyclin-dependent kinase inhibitor p27 in human and murine cell lines." Blood 96, no. 5 (September 1, 2000): 1933–39. http://dx.doi.org/10.1182/blood.v96.5.1933.

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Abstract Chronic myeloid leukemia (CML) is a malignant stem cell disease characterized by an expansion of myeloid progenitor cells expressing the constitutively activated Bcr-Abl kinase. This oncogenic event causes a deregulation of apoptosis and cell cycle progression. Although the molecular mechanisms protecting from apoptosis in CML cells are well characterized, the cell cycle regulatory event is poorly understood. An inhibitor of the cyclin-dependent kinases, p27, plays a central role in the regulation of growth factor dependent proliferation of hematopoietic cells. Therefore, we have analyzed the influence of Bcr-Abl in the regulation of p27 expression in various hematopoietic cell systems. An active Bcr-Abl kinase causes down-regulation of p27 expression in murine Ba/F3 cells and human M07 cells. Bcr-Abl blocks up-regulation of p27 after growth factor withdrawal and serum reduction. In addition, p27 induction by transforming growth factor-beta (TGF-β) is completely blocked in Bcr-Abl positive M07/p210 cells. This deregulation is directly mediated by the activity of the Bcr-Abl kinase. A Bcr-Abl kinase inhibitor completely abolishes p27 down-regulation by Bcr-Abl in both Ba/F3 cells transfected either with a constitutively active Bcr-Abl or with a temperature sensitive mutant. The down-regulation of p27 by Bcr-Abl depends on proteasomal degradation and can be blocked by lactacystin. Overexpression of wild-type p27 partially antagonizes Bcr-Abl–induced proliferation in Ba/F3 cells. We conclude that Bcr-Abl promotes cell cycle progression and activation of cyclin-dependent kinases by interfering with the regulation of the cell cycle inhibitory protein p27.

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50

Jonuleit, Tarja, Heiko van der Kuip, Cornelius Miething, Heike Michels, Michael Hallek, Justus Duyster, and Walter E. Aulitzky. "Bcr-Abl kinase down-regulates cyclin-dependent kinase inhibitor p27 in human and murine cell lines." Blood 96, no. 5 (September 1, 2000): 1933–39. http://dx.doi.org/10.1182/blood.v96.5.1933.h8001933_1933_1939.

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Анотація:

Chronic myeloid leukemia (CML) is a malignant stem cell disease characterized by an expansion of myeloid progenitor cells expressing the constitutively activated Bcr-Abl kinase. This oncogenic event causes a deregulation of apoptosis and cell cycle progression. Although the molecular mechanisms protecting from apoptosis in CML cells are well characterized, the cell cycle regulatory event is poorly understood. An inhibitor of the cyclin-dependent kinases, p27, plays a central role in the regulation of growth factor dependent proliferation of hematopoietic cells. Therefore, we have analyzed the influence of Bcr-Abl in the regulation of p27 expression in various hematopoietic cell systems. An active Bcr-Abl kinase causes down-regulation of p27 expression in murine Ba/F3 cells and human M07 cells. Bcr-Abl blocks up-regulation of p27 after growth factor withdrawal and serum reduction. In addition, p27 induction by transforming growth factor-beta (TGF-β) is completely blocked in Bcr-Abl positive M07/p210 cells. This deregulation is directly mediated by the activity of the Bcr-Abl kinase. A Bcr-Abl kinase inhibitor completely abolishes p27 down-regulation by Bcr-Abl in both Ba/F3 cells transfected either with a constitutively active Bcr-Abl or with a temperature sensitive mutant. The down-regulation of p27 by Bcr-Abl depends on proteasomal degradation and can be blocked by lactacystin. Overexpression of wild-type p27 partially antagonizes Bcr-Abl–induced proliferation in Ba/F3 cells. We conclude that Bcr-Abl promotes cell cycle progression and activation of cyclin-dependent kinases by interfering with the regulation of the cell cycle inhibitory protein p27.

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