Mini review: Multifaceted role played by cyclin D1 in tumor behavior

J of Cellular Biochemistry

et al. 2019

Lung cancer (especially, non–small cell lung cancer [NSCLC]) is one of the most malignant cancers in the world. Hinesol is the major component of the essential oil of Atractylodes lancea (Thunb.) DC and possesses the most promising anticancer function. However, the effects and molecular mechanism of hinesol on antiproliferation in NSCLC cells has not been well understood. In this study, we found that hinesol effectively inhibited the A549 and NCI‐H1299 cells in a dose‐ and time‐dependent manner by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazoliumbromide assay. In addition, hinesol induced cell cycle arrest at G0/G1 phase and apoptosis assessed by flow cytometry in A549 cells. Furthermore, Western blot analysis showed that hinesol decreased phosphorylation of mitogen‐activated protein kinase, extracellular signal‐regulated kinase, IκBα, and p65 inhibited the expressions of Bcl‐2, cyclin D1 and upregulated the expression of Bax. Based on these results, hinesol might be a potential drug candidate of anti‐NSCLC for therapy.

Section: Discussionmentioning

confidence: 99%

“…Therefore, we specifically focused on proteins that regulate the cell cycle. Cyclin D1 exercises powerful control over the mechanisms that regulate the mitotic cell cycle, and overexpression of cyclin D1 is common in human cancers . In hinesol‐treated A549 cells, the expression of cyclin D1 decreased in a dose‐dependent manner.…”

Section: Discussionmentioning

confidence: 99%

The antitumor effect of hinesol, extract from Atractylodes lancea (Thunb.) DC. by proliferation, inhibition, and apoptosis induction via MEK/ERK and NF‐κB pathway in non–small cell lung cancer cell lines A549 and NCI‐H1299

Guo

J of Cellular Biochemistry

et al. 2019

“…Cyclin D1, belonging to the highly conserved cyclin family, forms an active complex with CDK4 or CDK6 to drive cell cycle transition from G1 to the S phase . Overexpression of cyclin D1 or hyperactivation of CDK4 directly result in dysregulation of cell cycle and cell proliferation .…”

Section: Discussionmentioning

confidence: 99%

“…Cyclin D1, belonging to the highly conserved cyclin family, forms an active complex with CDK4 or CDK6 to drive cell cycle transition from G1 to the S phase. 22,23 Overexpression of cyclin D1 or hyperactivation of CDK4 directly result in dysregulation of cell cycle and cell proliferation. 23,24 Our data show that CABYR-a/b knockdown leads to an increased ratio of cells in G0/G1 phase, suppression of cell proliferation, and downregulation of cyclin D1 and CDK4, suggesting that CABYR-a/b downregulation affects HCC cell proliferation by regulating cyclin D1 and CDK4 levels.…”

Section: Discussionmentioning

confidence: 99%

Upregulated calcium‐binding tyrosine phosphorylation‐regulated protein‐a/b regulates cell proliferation and apoptosis and predicts poor prognosis in hepatocellular carcinoma

Guo

J of Cellular Biochemistry

et al. 2019

Background Calcium‐binding tyrosine phosphorylation‐regulated protein (CABYR) is a group of isoforms produced by alternative splicing and is overexpressed in human malignancies including hepatocellular carcinoma (HCC). However, the prognostic value and biological functions of its major protein isoforms, named CABYR‐a/b (combined CABYR‐a and CABYR‐b), in HCC remain to be established. Methods CABYR‐a/b expression was detected in HCC tissues and cell lines by quantitative real‐time polymerase chain reaction and Western blot analysis. The correlation of CABYR‐a/b expression with clinical characteristics and its prognosis impact were determined by statistical analysis. Finally, the biological functions and molecular mechanism of CABYR‐a/b were also investigated using molecular biology approaches. Results The present research found that CABYR‐a/b was markedly elevated in HCC specimens and cell lines. Upregulated CABYR‐a/b level had positive association with tumor size and differentiation in patients. Moreover, cases with elevated CABYR‐a/b level had poorer overall survival (OS) and disease‐free survival (DFS) than those with reduced CABYR‐a/b level. Multivariate analysis and prognostic nomograms demonstrated that CABYR‐a/b overexpression was an independent predictive indicator for OS and DFS. The calibration curve for the odds of OS and DFS demonstrated that the prediction by nomograms was in excellent accordance with actual situation. CABYR‐a/b downregulation suppressed cell proliferation and induced G1‐phase arrest via decreasing cyclin D1 and cyclin dependent kinase 4, while promoted apoptosis by reducing B‐cell lymphoma 2 (Bcl‐2) and increasing Bcl‐2‐associated death promoter. Conclusion Our research indicates that CABYR‐a/b exerts an oncogenic effect on HCC development and may become a new prognostic indicator for patients with HCC.

“…Knockdown of DPP8 significantly promoted cervical cancer G1/G0 phase arrest, and the present study demonstrated that depletion of DPP8 caused G1 phase block by changing the expression of a G1/G0 phase‐related protein (cyclin D1), suggesting that DPP8 has important functions in the cell cycle of cervical cancer cells. When cyclin D1 is activated, the cell cycle is initiated . When cyclin D1 is inactivated, the process of the cell cycle may be suppressed.…”

Section: Discussionmentioning

confidence: 99%

Targeting dipeptidyl peptidase 8 genes inhibits proliferation, migration and invasion by inhibition of cyclin D1 and MMP2MMP9 signal pathway in cervical cancer

Chen

The Journal of Gene Medicine

et al. 2018