Deregulation of cell cycle and related microRNA expression induced by vinyl chloride monomer in hepatocytes of rats

2021 ◽  
pp. 074823372110155
Author(s):  
Weizhe Pan ◽  
Shengnan Yu ◽  
Jin Jia ◽  
Junyang Hu ◽  
Liang Jie ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Vinyl Chloride ◽  
Male Rats ◽  
Cell Cycle Distribution ◽  
Vinyl Chloride Monomer ◽  
Dynamic Changes ◽  
Cell Cycle Deregulation ◽  
Change Dynamic ◽  
Related Proteins

Vinyl chloride (VC) is a confirmed human carcinogen associated with hepatocellular carcinoma and angiosarcoma. However, the role of microRNAs (miRNAs) in liver cell cycle changes under VC exposure remains unclear, which prevents research on the mechanism of VC-induced carcinogenesis. In this study, male rats were injected intraperitoneally with VC (0, 5, 25, and 125 mg/kg body weight) for 6, 8, and 12 weeks. Cell cycle analysis of liver cells, miRNA-222, miRNA-199a, miRNA-195, and miRNA-125b expression in the liver and serum, and target protein expression were performed at different time points. The results showed a higher percentage of hepatocytes in the G1/G0 and S phases at the end of 6 and 12 weeks of VC exposure, respectively. MiRNA-222 expression decreased initially and then increased, whereas miRNA-199a, miRNA-195, and miRNA-125b expression increased initially and then decreased, which corresponded with changes in cell cycle distribution and related target proteins expression (p27, cyclinA, cyclinD1, and CDK6). The corresponding expression levels of miRNAs in serum did not change. Dynamic changes in miR-222, miR-199a, miR-195, and miR-125b induced by VC can lead to cell cycle deregulation by affecting cell cycle-related proteins, and these miRNAs can serve as early biomarkers for malignant transformation caused by VC.

Plk3 phosphorylates topoisomerase IIα at Thr1342, a site that is not recognized by Plk1

2008 ◽  
Vol 411 (1) ◽  
pp. 27-32 ◽  
Author(s):  
Masato Iida ◽  
Masao Matsuda ◽  
Hideya Komatani
Keyword(s):  
Cell Cycle ◽  
Kinase Assay ◽  
Cell Cycle Distribution ◽  
Physical Interaction ◽  
Topoisomerase Iiα ◽  
In Vitro Kinase Assay ◽  
A Site ◽  
Cycle Regulation

The Plk (polo-like kinase) family is involved in cell-cycle machinery. Despite the possible overlapping involvement of Plk1 and Plk3 in cell-cycle distribution, the precise role of each Plk might be different. To investigate mechanisms that may differentiate their physiological roles, we compared the substrate specificities of Plk1 and Plk3 using synthetic peptides. Among these substrate peptides, topoisomerase IIα EKT1342DDE-containing synthetic peptide was strongly phosphorylated by Plk3 but not by Plk1. By modulating the topoisomerase IIα peptide, we identified residues at positions +1, +2 and +4 as determinants of differential substrate recognition between Plk1 and Plk3. Acidic residues at positions +2 and +4 appear to be a positive determinant for Plk3 but not Plk1. Variation at position +1 appears to be tolerated by Plk3, while a hydrophobic residue at +1 is critical for Plk1 activity. The direct phosphorylation of Thr1342 of topoisomerase IIα by Plk3 was demonstrated with an in vitro kinase assay, and overexpression of Plk3 induced the phosphorylation of Thr1342 in cellular topoisomerase IIα. Furthermore, the physical interaction between Plk3 and topoisomerase IIα was also demonstrated in cells in addition to phosphorylation. These data suggest that topoisomerase IIα is a novel physiological substrate for Plk3 and that Plk1 and Plk3 play different roles in cell-cycle regulation.

CD147 Promote Proliferation in Prostate Cancer Cell

2014 ◽  
Vol 912-914 ◽  
pp. 1915-1918
Author(s):  
Qing Fang ◽  
Fang Fang ◽  
Yu Lian Liu ◽  
Wen Ping Li ◽  
Li Guo Wang
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Prostate Cancer Cell ◽  
Cell Cycle Distribution ◽  
Cell Cycle Protein ◽  
Phase Arrest ◽  
Cd147 Expression ◽  
Potential Therapeutic Application

CD147 is expressed on the cell surface of most tumor cells, which results in cancer cells proliferation, invasion, metastasis and angiogenes. Our previous study indicated that CD147 could promote invasion andmetastasis of prostate cancer. However the role of CD147 on cell proliferation has not to be explored inprostate cancer. In this study, the effects of CD147 on cell proliferation of hormone-independent prostatecancer (LNCaP-AI) was investigated. In the present study, cell cycle distribution was investigated by flowcytometry and cell cycle protein were analysis by wester blot. The results demonstrated that knock-donwn CD147 expression induced G0/G1 phase arrest, and expression of cyclin D1 has potential suppressed with western blot analysis. The results suggest that CD147 could inhibit cell prolifearion and as potential therapeutic application in treatment of proste cancer.

Principles of K-Ras effector organization and the role of oncogenic K-Ras in cancer initiation through G1 cell cycle deregulation

2015 ◽  
Vol 12 (6) ◽  
pp. 669-682 ◽  
Author(s):  
Ruth Nussinov ◽  
Chung-Jung Tsai ◽  
Serena Muratcioglu ◽  
Hyunbum Jang ◽  
Attila Gursoy ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cancer Initiation ◽  
Cell Cycle Deregulation

The role of respiration in vinyl chloride monomer excretion in rats

1980 ◽  
Vol 5 (3-4) ◽  
pp. 213-217
Author(s):  
Ettore Zuccato ◽  
Franca Marcucci ◽  
Emilio Mussini
Keyword(s):  
Vinyl Chloride ◽  
Vinyl Chloride Monomer

scholarly journals P53-dependent suppression of the human calcyclin gene (S100A6): the role of Sp1 and of NFkappaB.

2008 ◽  
Vol 55 (3) ◽  
pp. 559-570 ◽  
Author(s):  
Weronika Króliczak ◽  
Maciej Pietrzak ◽  
Monika Puzianowska-Kuznicka
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Control ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Wild Type ◽  
Lower Efficiency ◽  
Wild Type P53 ◽  
Cell Cycle Deregulation ◽  
Cancer Tissues

Calcyclin (S100A6) is believed to participate in cell cycle control. It was, however, unclear if its expression depends on p53, a key regulator of apoptosis and cell cycle. We therefore performed transcription regulation assays in HeLa cells and found that wild type p53 suppressed the S100A6 promoter up to 12-fold in a dose-dependent manner. In contrast, the well-characterized V143A, R175H, R249S, and L344A p53 mutants cloned from human cancers suppressed this promoter with a 6 to 9-fold lower efficiency. All the sites mediating the p53-dependent suppression were contained in the -167 to +134 fragment of the S100A6 promoter. Separate overexpression of either Sp1 or of NFkappaB only partially counteracted the p53 inhibitory effect on the S100A6 promoter, while simultaneous overexpression of both these transactivators resulted in a complete abolishment of the p53 inhibitory effect on this promoter. Sp1 and NFkappaB binding to the probes resembling their putative binding sites present in the S100A6 promoter was decreased in the presence of wild type p53. We propose that the suppression of S100A6 is yet another mechanism by which p53 inhibits proliferation. Insufficient suppression of this gene by p53 mutants could well be responsible for calcyclin overexpression and cell cycle deregulation observed in cancer tissues.

scholarly journals The Role of Non-Coding RNAs in Controlling Cell Cycle Related Proteins in Cancer Cells

2020 ◽  
Vol 10 ◽  
Author(s):  
Soudeh Ghafouri-Fard ◽  
Hamed Shoorei ◽  
Farhad Tondro Anamag ◽  
Mohammad Taheri
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Cyclin Dependent Kinases ◽  
Human Disorders ◽  
Non Coding Rnas ◽  
Regulation Of Cell Cycle ◽  
Related Proteins ◽  
Regulate Cell Cycle Progression

Cell cycle is regulated by a number of proteins namely cyclin-dependent kinases (CDKs) and their associated cyclins which bind with and activate CDKs in a phase specific manner. Additionally, several transcription factors (TFs) such as E2F and p53 and numerous signaling pathways regulate cell cycle progression. Recent studies have accentuated the role of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in the regulation of cell cycle. Both lncRNAs and miRNAs interact with TFs participating in the regulation of cell cycle transition. Dysregulation of cell cycle regulatory miRNAs and lncRNAs results in human disorders particularly cancers. Understanding the role of lncRNAs, miRNAs, and TFs in the regulation of cell cycle would pave the way for design of anticancer therapies which intervene with the cell cycle progression. In the current review, we describe the role of lncRNAs and miRNAs in the regulation of cell cycle and their association with human malignancies.

scholarly journals CircNFIX promotes progression of glioma through regulating miR-378e/RPN2 axis

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Chenyu Ding ◽  
Zanyi Wu ◽  
Honghai You ◽  
Hongliang Ge ◽  
Shufa Zheng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Xenograft Model ◽  
Circular Rna ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Cycle Distribution ◽  
Glioma Progression

Abstract Background Circular RNA nuclear factor I X (circNFIX) has been reported to play an important role in glioma progression. However, the mechanism by which circNFIX participates in glioma progression remains poorly understood. Methods GERIA online were used to analyze the abnormally expressed genes in glioma tissues. The expression levels of circNFIX, microRNA (miR)-378e and Ribophorin-II (RPN2) were measured by quantitative real-time polymerase chain reaction or western blot. Cell cycle distribution, apoptosis, glycolysis, migration and invasion were determined by flow cytometry, special kit and trans-well assays, respectively. The target association between miR-378e and circNFIX or RPN2 was confirmed by luciferase reporter assay, RNA immunoprecipitation and pull-down. Xenograft model was established to investigate the role of circNFIX in vivo. Results The expression of circNFIX was enhanced in glioma tissues and cells compared with matched controls and high expression of circNFIX indicated poor outcomes of patients. Knockdown of circNFIX led to arrest of cell cycle, inhibition of glycolysis, migration and invasion and promotion of apoptosis in glioma cells. circNFIX was a sponge of miR-378e. miR-378e overexpression suppressed cell cycle process, glycolysis, migration and invasion but promoted apoptosis. miR-378e silence abated the suppressive role of circNFIX knockdown in glioma progression. RPN2 as a target of miR-378e was positively regulated via circNFIX by competitively sponging miR-378e. Silencing circNFIX decreased glioma xenograft tumor growth by regulating miR-378e/RPN2 axis. Conclusion Knockdown of circNFIX inhibits progression of glioma in vitro and in vivo by increasing miR-378e and decreasing RPN2, providing a novel mechanism for understanding the pathogenesis of glioma.

Comparative cytotoxicity of five current dentin bonding agents: Role of cell cycle deregulation

2009 ◽  
Vol 5 (9) ◽  
pp. 3404-3410 ◽  
Author(s):  
Hung-Wei Yeh ◽  
Mei-Chi Chang ◽  
Chun-Pin Lin ◽  
Wan-Yu Tseng ◽  
Hsiao-Hua Chang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bonding Agents ◽  
Dentin Bonding ◽  
Dentin Bonding Agents ◽  
Cell Cycle Deregulation
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