CAVIN2 is frequently silenced by CpG methylation and sensitizes lung cancer cells to paclitaxel and 5-FU

Author:

Peng Mingyu1,Ye Lin2,Yang Li1,Liu Xinzhu1,Chen Yuhan1,Huang Guichuan1,Jiang Yu2,Wang Yan2,Li Dairong1,He Jin2,Qiu Zhu2,Xiang Tingxiu2,Guo Shuliang1

Affiliation:

1. Department of Respiratory & Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China

2. Chongqing Key Laboratory of Molecular Oncology & Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China

Abstract

Aim: To explore the biological functions and clinical significance of CAVIN2 in lung cancer. Materials & methods: Methylation-specific PCR was used to measure promoter methylation of CAVIN2. The function of CAVIN2 was tested by Cell Counting Kit-8, colony formation, Transwell, flow cytometric analysis, acridine orange/ethidium bromide, chemosensitivity assay and xenograft assay. Results:  CAVIN2 is significantly downregulated by promoter methylation in lung cancer. CAVIN2 overexpression inhibits lung cancer cell migration and invasion. Furthermore, ectopic expression of CAVIN2 inhibits cell proliferation in vivo and in vitro by inducing G2/M cell cycle arrest, which sensitizes the chemosensitivity of lung cancer cells to paclitaxel and 5-fluorouracil, but not cisplatin. Conclusion:  CAVIN2 is a tumor suppressor in non-small-cell lung cancer and can sensitize lung cancer cells to paclitaxel and 5-fluorouracil.

Funder

Chongqing Science and Technology Commission

National Natural Science Foundation of China

Natural Science Foundation of Chongqing

Publisher

Future Medicine Ltd

Subject

Cancer Research,Genetics

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