cvt-313 and Neoplasms

cvt-313 has been researched along with Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for cvt-313 and Neoplasms

Article	Year
CDK2 differentially controls normal cell senescence and cancer cell proliferation upon exposure to reactive oxygen species. Biochemical and biophysical research communications, 2012, Aug-17, Volume: 425, Issue:1 Reactive oxygen species modulate cell fate in a context-dependent manner. Sublethal doses of H(2)O(2) decreased the level of proliferating cell nuclear antigen (PCNA) in normal cells (including primary human dermal fibroblasts and IMR-90 cells) without affecting cyclin-dependent kinase 2 (CDK2) activity, leading to cell cycle arrest and subsequent senescence. In contrast, exposure of cancer cells (such as HeLa and MCF7 cells) to H(2)O(2) increased CDK2 activity with no accompanying change in the PCNA level, leading to cell proliferation. A CDK2 inhibitor, CVT-313, prevented H(2)O(2)-induced cancer cell proliferation. These results support the notion that the cyclin/CDK2/p21(Cip1)/PCNA complex plays an important role as a regulator of cell fate decisions. Topics: Cell Line, Tumor; Cell Proliferation; Cellular Senescence; Cyclin-Dependent Kinase 2; Cyclin-Dependent Kinase Inhibitor p21; HeLa Cells; Humans; Hydrogen Peroxide; Neoplasms; Proliferating Cell Nuclear Antigen; Purines; Reactive Oxygen Species	2012

Article

Year

CDK2 differentially controls normal cell senescence and cancer cell proliferation upon exposure to reactive oxygen species.

Biochemical and biophysical research communications, 2012, Aug-17, Volume: 425, Issue:1

Reactive oxygen species modulate cell fate in a context-dependent manner. Sublethal doses of H(2)O(2) decreased the level of proliferating cell nuclear antigen (PCNA) in normal cells (including primary human dermal fibroblasts and IMR-90 cells) without affecting cyclin-dependent kinase 2 (CDK2) activity, leading to cell cycle arrest and subsequent senescence. In contrast, exposure of cancer cells (such as HeLa and MCF7 cells) to H(2)O(2) increased CDK2 activity with no accompanying change in the PCNA level, leading to cell proliferation. A CDK2 inhibitor, CVT-313, prevented H(2)O(2)-induced cancer cell proliferation. These results support the notion that the cyclin/CDK2/p21(Cip1)/PCNA complex plays an important role as a regulator of cell fate decisions.

Topics: Cell Line, Tumor; Cell Proliferation; Cellular Senescence; Cyclin-Dependent Kinase 2; Cyclin-Dependent Kinase Inhibitor p21; HeLa Cells; Humans; Hydrogen Peroxide; Neoplasms; Proliferating Cell Nuclear Antigen; Purines; Reactive Oxygen Species

2012