Cyclin D1 Promotes Androgen-Dependent DNA Damage Repair in Prostate Cancer Cells

Casimiro, Mathew C.; Sante, Gabriele Di; Ju, Xiaoming; Li, Zhiping; Chen, Ke; Crosariol, Marco; Yaman, İsmail; Gormley, Michael; Meng, Hui; Lisanti, Michael P.; Pestell, Richard G.

doi:10.1158/0008-5472.can-15-0999

Cited by 38 publications

(43 citation statements)

References 54 publications

(55 reference statements)

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“…Cyclin D1, a transcription factor, is associated with cell proliferation via the promotion of the cell cycle from G1 to the S transition (22,23). Previous studies found that cyclin D1 is overexpressed and contributes to the androgen-dependent DNA damage repair in PCa cells (24). Although we had a lack of data from the trials to address the changes in the PCa cell cycle after SOX18 silencing, the decreased level of cyclin D1 expression caused by SOX18 silencing indicated that SOX18 may promote cell cycle transition from the G1 to the S phase via the regulation of the expression of cyclin D1 to accelerate the aggressiveness of PCa.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of SOX18 promotes prostate cancer progression via the regulation of TCF1, c-Myc, cyclin D1 and MMP-7

et al. 2016

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Sex determining region Y (SRY)-box 18 (SOX18) gene encodes transcription factors that have been recently confirmed to be overexpressed in various human types of cancer and maintain the malignant behavior of cancer cells. However, the role and its potential function in prostate cancer (PCa) has not been demonstrated and the mechanisms of SOX18 involved in tumor progression remain largely unclear. In the present study, the expression of SOX18 was analyzed in 98 PCa and 81 adjacent non-tumor tissues using immunohistochemistry. The data showed that SOX18 was overexpressed in 72 of 98 (73.5%) PCa tissues compared with that in 28 of 81 (34.6%) non-tumor tissues. In addition, the expression of SOX18 was related with the clinical features of patients with PCa. To explore the potential role of SOX18 in PCa cells, Cell Counting Kit-8 (CCK-8), migration, invasion and xenograft assays were performed. Our data showed that knockdown of SOX18 decreased the proliferation, migration and invasion of PCa cells in vitro, in addition to the tumor growth in vivo. Markedly, SOX18 knockdown caused the decreased expression of TCF1, c-Myc, cyclin D1 and MMP-7. In conclusion, SOX18 was overexpressed in PCa and may regulate the malignant capacity of cells via the upregulation of TCF1, c-Myc, cyclin D1 and MMP-7.

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Section: Discussionmentioning

confidence: 99%

Overexpression of SOX18 promotes prostate cancer progression via the regulation of TCF1, c-Myc, cyclin D1 and MMP-7

et al. 2016

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“…The pSM2 vector containing shRNA for cyclin D1 and control vector were used as described (16). The pCDNA3.1-3X-FLAG expression vector encoding human cyclin D1 wild type ( cyclin D1 WT ), human cyclin D1 kinase dead mutant ( cyclin D1 KE ) and control vector were used as described (17).…”

Section: Methodsmentioning

confidence: 99%

Cyclin D1 Restrains Oncogene-Induced Autophagy by Regulating the AMPK–LKB1 Signaling Axis

et al. 2017

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Autophagy activated after DNA damage or other stresses mitigates cellular damage by removing damaged proteins, lipids and organelles. Activation of the master metabolic kinase AMPK enhances autophagy. Here we report that cyclin D1 restrains autophagy by modulating the activation of AMPK. In cell models of human breast cancer or in a cyclinD1-deficient model, we observed a cyclin D1-mediated reduction in AMPK activation. Mechanistic investigations showed that Cyclin D1 inhibited mitochondrial function, promoted glycolysis and reduced activation of AMPK (pT172), possibly through a mechanism that involves cyclin D1-Cdk4/Cdk6 phosphorylation of LKB1. Our findings suggest how AMPK activation by cyclin D1 may couple cell proliferation to energy homeostasis.

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“…CCND1 overexpression is commonly observed in various types of human cancers, including HCC, and serves a critical role in the initiation of carcinogenesis (12). CCND1 is also involved in abnormal cell growth processes, angiogenesis and resistance to apoptosis, making it a potential therapeutic target for controlling tumor growth (13,14). However, the association of Hotair and CCND1 expression in HCC remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of Hotair suppresses proliferation and cell cycle progression in hepatocellular carcinoma cell by downregulating CCND1 expression

Zhou

Cheng

et al. 2017

Molecular Medicine Reports

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The long noncoding RNA, homeobox transcript antisense RNA (Hotair), has been demonstrated to have an important role in regulating various biological processes in various cancers, including hepatocellular carcinoma (HCC). However, the importance of Hotair in HCC proliferation and cell cycle progression remains to be elucidated. In the present study, knockdown of HOTAIR expression by RNA interference inhibited cell proliferation and induced G0/G1 cell cycle arrest in Huh7 hepatocellular carcinoma cells. In addition, the expression levels of CCND1 mRNA and its cyclin D1 protein product were reduced in Huh7 cells following knockdown of HOTAIR. Knockdown of HOTAIR reduced the expression of phosphorylated signal transducer and activator of transcription 3 (STAT3) and HOTAIR knockdown combined with STAT3 inhibition led to an additional decrease in cyclin D1 expression. The present study suggested that Hotair may have a critical role in the proliferation of HCC by regulating cell cycle, STAT3 activity and cyclin D1 expression. Therefore, Hotair may be a novel potential therapeutic target for HCC treatment.

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Cyclin D1 Promotes Androgen-Dependent DNA Damage Repair in Prostate Cancer Cells

Cited by 38 publications

References 54 publications

Overexpression of SOX18 promotes prostate cancer progression via the regulation of TCF1, c-Myc, cyclin D1 and MMP-7

Overexpression of SOX18 promotes prostate cancer progression via the regulation of TCF1, c-Myc, cyclin D1 and MMP-7

Cyclin D1 Restrains Oncogene-Induced Autophagy by Regulating the AMPK–LKB1 Signaling Axis

Knockdown of Hotair suppresses proliferation and cell cycle progression in hepatocellular carcinoma cell by downregulating CCND1 expression

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