GSE112985
RNA-seq analysis of A2780 and OVCAR3 human ovarian cancer cell lines after overexpression of collagen type XI alpha 1 (COL11A1)
Collagen type XI alpha 1 (COL11A1) is identified as one of the most upregulated genes in cisplatin-resistant ovarian cancer and recurrent ovarian cancer. However, the exact functions of COL11A1 in cisplatin resistance are unknown. The goal of this study is to determine molecular mechanisms by which COL11A1 confers cisplatin resistance in ovarian cancer cells. We overexpressed COL11A1 in A2780 and OVCAR3 ovarian cancer cells, which express very low endogenous levels of COL11A1. We then compared the mRNA expression levels of various genes between COL11A1-overexpressing ovarian cancer cells and control ovarian cancer cells by RNA-Seq. Our RNA-Seq data show that COL11A1 overexpression did not consistently change the expression levels of genes involved in cisplatin efflux, glutathione metabolism, and DNA repair pathways, which are known to contribute to cisplatin resistance. This result implies that COL11A1 might confer cisplatin resistance in ovarian cancer cells through other mechanisms. Overall design: We overexpressed COL11A1 in A2780 and OVCAR3 ovarian cancer cell lines (A2780-COL11A1, OVCAR3-COL11A1) and performed RNA-Seq. We also performed RNA-Seq in A2780CIS ovarian cancer cell line expressing high endogenous levels of COL11A1 and A2780-shCOL11A1 cell line where COL11A1 is knocked down with short hairpin RNA. We then compared the differential expression of mRNAs in ovarian cancer cell lines overexpressing COL11A1 (A2780-COL11A1, OVCAR3-COL11A1, and A2780CIS, ) to control cells which express no or very low COL11A1 (A2780, A2780shCOL11A1, and OVCAR3).