Potential Role of CCND1 G870A Genotype as a Predictor for Urothelial Carcinoma Susceptibility and Muscle-Invasiveness in Taiwan

Lin, Hui; Ke, Hung‐Lung; Hsiao, Kuang Hung; Tsai, Chia Wen; Wu, Wen‐Jeng; Bau, Da Tian; Chang, Lin

doi:10.4077/cjp.2011.amm123

Cited by 13 publications

(8 citation statements)

References 30 publications

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“…It can promote G0/G1 to S phase transition, accelerate cell cycle, and consequently promote cell growth. Abnormal expression of CCND1 has been reported in a variety of human tumors, including breast cancer [18,19], bladder cancer [20,21], colon cancer [22,23], and glioma also included [24,25]. Growing evidence demonstrated that CCND1 is a potential therapeutic target in cancer [26,27].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-383 inhibits anchorage-independent growth and induces cell cycle arrest of glioma cells by targeting CCND1

Zhou

Zeng

Tian

et al. 2014

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 99%

MicroRNA-383 inhibits anchorage-independent growth and induces cell cycle arrest of glioma cells by targeting CCND1

Zhou

Zeng

Tian

et al. 2014

Biochemical and Biophysical Research Communications

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“…Overexpression of cyclin D1 appeared to play an important role in the early stage of urothelial tumorigenesis and correlated with early recurrence in superficial bladder cancers [22]. Moreover, the polymorphism within the cyclin D1 gene was associated with risk and clinicopathologic characteristics of urinary bladder cancer [23,24]. Therefore, inhibition of cyclin D1 seems to be an effective molecular target for the treatment of bladder cancer.…”

Section: Discussionmentioning

confidence: 99%

The Antidiabetic Drug Metformin Inhibits the Proliferation of Bladder Cancer Cells in Vitro and in Vivo

Zhang

Guo

Zhang

et al. 2013

IJMS

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Recent studies suggest that metformin, a widely used antidiabetic agent, may reduce cancer risk and improve prognosis of certain malignancies. However, the mechanisms for the anti-cancer effects of metformin remain uncertain. In this study, we investigated the effects of metformin on human bladder cancer cells and the underlying mechanisms. Metformin significantly inhibited the proliferation and colony formation of 5637 and T24 cells in vitro; specifically, metformin induced an apparent cell cycle arrest in G0/G1 phases, accompanied by a strong decrease of cyclin D1, cyclin-dependent kinase 4 (CDK4), E2F1 and an increase of p21waf-1. Further experiments revealed that metformin activated AMP-activated protein kinase (AMPK) and suppressed mammalian target of rapamycin (mTOR), the central regulator of protein synthesis and cell growth. Moreover, daily treatment of metformin led to a substantial inhibition of tumor growth in a xenograft model with concomitant decrease in the expression of proliferating cell nuclear antigen (PCNA), cyclin D1 and p-mTOR. The in vitro and in vivo results demonstrate that metformin efficiently suppresses the proliferation of bladder cancer cells and suggest that metformin may be a potential therapeutic agent for the treatment of bladder cancer.

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“…Subsequently, we noticed that, compared with cyclin G1-GFP-transfected CHO cells, exogenous cyclin G1 protein expression was weak in cyclin G1-GFP transfected ECCs, and was undetectable in KLE cells. Previous researches on human endometrial carcinoma mostly have focussed on cyclins that are positively regulating cell cycle, such as cyclin A, cyclin D and cyclin E (3,11,22). Here, we report for the first time that cyclin G1 exerts negative control in proliferation of human ECCs.…”

Section: Discussionmentioning

confidence: 74%

Effects of Expression of Exogenous Cyclin G1 on Proliferation of Human Endometrial Carcinoma Cells

Liu

Gao²,

Yu³

et al. 2013

Chin. J. Physiol.

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Cyclin G1 is the only cyclin that has either positive or negative effects on cell growth. Our previous study found decreased expression of cyclin G1 in human endometrial carcinoma tissues compared with normal endometrial tissues. The study aimed to evaluate cyclin G1 expression and its effect on proliferation of human endometrial carcinoma cells (ECCs). Cyclin G1-GFP (green fluorescence protein) plasmid was constructed and transfected into various differentiated human ECCs, including Ishikawa, HEC-1-B and KLE cells, and proliferation of the transfected cells was determined by the CCK-8 method. Exogenous cyclin G1 mRNA and protein were measured by RT-PCR and Western blot, respectively, and GFP signal was monitored by fluorescence microscopy. Chinese hamster ovary (CHO) cells were transfected with the same constructs as a cell control. Cyclin G1-GFP-transfected Ishikawa cells were further treated with MG132, an inhibitor of proteasome, to analyze if low expression of cyclin G1 is related to its abnormal degradation in ECCs. Ectopic expression of exogenous cyclin G1 was found to significantly suppress the proliferation of Ishikawa and HEC-1-B cells but not KLE cells. Compared with cyclin G1-transfected CHO cells, exogenous cyclin G1 protein expression was low in Ishikawa and HEC-1-B cells, and was undetectable in KLE cells. However, all ECC lines and CHO cells expressed similar levels of exogenous cyclin G1 and GFP mRNA. MG132 treatment increased cyclin G1 protein expression in cyclin G1-GFP-transfected Ishikawa cells. This is the first study to present evidence to suggest that cyclin G1 exerts negative control on proliferation of ECCs. Exogenous cyclin G1 shows different protein expression levels in ECCs with different malignancies, and cyclin G1 protein is highly unstable and is rapidly degraded in ECCs.

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Potential Role of CCND1 G870A Genotype as a Predictor for Urothelial Carcinoma Susceptibility and Muscle-Invasiveness in Taiwan

Cited by 13 publications

References 30 publications

MicroRNA-383 inhibits anchorage-independent growth and induces cell cycle arrest of glioma cells by targeting CCND1

MicroRNA-383 inhibits anchorage-independent growth and induces cell cycle arrest of glioma cells by targeting CCND1

The Antidiabetic Drug Metformin Inhibits the Proliferation of Bladder Cancer Cells in Vitro and in Vivo

Effects of Expression of Exogenous Cyclin G1 on Proliferation of Human Endometrial Carcinoma Cells

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