KDM5A regulates the growth and gefitinib drug resistance against human lung adenocarcinoma cells

KDM5A, a histone demethylase, has been shown to be involved in several cancer-related process. The present study was undertaken to explore the role and therapeutic potential of KDM5A in human lung adenocarcinoma. The results of the qRT-PCR, immunohistochemistry, and western blotting showed significant upregulation of KDM5A expression in lung adenocarcinoma tissues and cell lines. The RNA interference-mediated silencing of KDM5A in lung adenocarcinoma cell line SK-LU-1 led to significant inhibition of in vitro cell proliferation via induction of apoptosis. The induction of apoptosis in SK-LU-1 lung adenocarcinoma cells was concomitant with upregulation of Bax and downregulation of Bcl-2 expression. In contrary, overexpression of KDM5A prompted the proliferation of SK-LU-1 lung adenocarcinoma cells. Interestingly, the SK-LU-1 cancer cells showed remarkably higher sensitivity to gefitinib under KDM5A transcriptional knockdown. Taken together, KDM5A is significantly upregulated in human lung adenocarcinoma and regulates the proliferation of the lung adenocarcinoma cells. These findings suggest potential of KDM5A to act as a therapeutic target for the management of human lung adenocarcinoma.

Automated summary

This study found that KDM5A is upregulated in human lung adenocarcinoma and regulates the proliferation of cancer cells. Silencing KDM5A inhibits cell proliferation and induces apoptosis in lung adenocarcinoma cells, while also increasing their sensitivity to gefitinib.