CHD1L knockdown suppresses bladder cancer cell growth in vitro

Abstract

Abstract Purpose CHD1L is a DNA helicase protein which is involved in recombinant chromatin and DNA damage repair. As a oncogene, how CHD1L was expressed and functioned in human bladder cancer cells were still not clear. This study was conducted to investigate how CHD1L is expressed and functions in human bladder cancer cells. Materials and methods We detected the expression level of CHD1L in human bladder cancer 5637 cells using qPCR. Through transfecting shCHD1L-harboring lentivirus and constructing CHD1L-knockdown cell models, MTT assay and flow cytometry assay were employed to detect the changes in cell proliferation, cell cycle and cell apoptosis, respectively. Cellular ability of migration was then tested using wound-healing assay and Transwell assay. Results We found that CHD1L was upregulated in bladder cancer 5637 cells. Knocking down CHD1L blocked cell cycle in G1/S transition and thus suppressed cell proliferation and cell migration, but accelerated cell apoptosis. Further exploration in the molecular mechanism indicated that dysfunctions of shCHD1L-harboring cells resulted from CHD1L downexpression may be involved in the reduction of phosphorylation levels of AKT and ERK proteins. Conclusions This study highlighted the tumor-promoting role of CHD1L played in bladder cancer cells, which provided a primary insight into further and deeper on related topics.