PLX078232

GSE143147: Cyclin K interacts with -catenin to induce Cyclin D1 expression and facilitate tumorigenesis and radioresistance in lung cancer

• Organsim mouse
• Type RNASEQ
• Target gene
• Project ARCHS4

Radioresistance has remained the major cause of local relapse and distant metastasis in lung cancer. However, the underlying molecular mechanisms remain poorly defined. In this study, we report that Cyclin K is frequently overexpressed and correlated with poor prognosis in lung cancer patients. Functionally, we demonstrate that Cyclin K depletion exhibits reduced proliferation, defective G2/M checkpoint and enhanced radiosensitivity in lung cancer. Mechanistically, we reveal that Cyclin K interacts with and stimulates the transcriptional activity of -catenin, thereby upregulating the expression of Cyclin D1. More importantly, we show that Cyclin D1 is the major effector which mediates the biological functions of Cyclin K in lung cancer. Collectively, our findings suggest that Cyclin K positively modulates -catenin/Cyclin D1 axis to promote tumorigenesis and radioresistance in lung cancer, indicating Cyclin K may be a novel attractive biomarker for lung cancer radiotherapy. SOURCE: Yao Guojun (m201775548@hust.edu.cn) - Hua Zhong University of science and technology