GSE211529
Role of lamin A in regulation of DNA Damage Response pathways in ovarian cancer
A-type lamins, the key structural components of the nucleus, are emerging as regulators in the maintenance of nuclear architecture and genome organization. Extensive research for the last two decades has enormously contributed in understanding the roles of lamins in various signaling mechanisms which frequently go awry in neoplasias. It is interesting to know that alteration in lamin A/C expression and distribution drives tumorigenesis thus modifying its expression can be a potent therapeutic approach. One of the important signatures of a cancer cell is its inability to repair DNA damage which befalls due to a number of genomic defects that transform the cells to be sensitive to chemotherapeutic agents. Also, the errors in DNA repair mechanism are accompanied by high replication rate. This genomic and chromosomal instability is the most conventional feature found in cases of high grade ovarian serous carcinoma. Here, we report elevated levels of lamins in OVCAR3 cells (High grade ovarian serous carcinoma cell line) with respect to IOSE (Immortalised ovarian surface epithelial cells) and the altered damage repair machineries in both the cell lines. We have analysed the changes in global gene expression in sequel to DNA damage induced by etoposide in lamin A upregulated ovarian carcinoma background and reported a number of differentially expressed genes associated with pathways conferring cellular proliferation and chemoresistance. We highlight new avenues unravelling the role of an upregulated lamin A in confronting chemically induced genomic instability in the context of ovarian cancer. Overall design: Comparative gene expression profiling of RNA Sequencing data of DMSO(Vehicle/Mock) treated and Etoposide treated OVCAR3 (High grade ovarian serous carcinoma cell line) cells. All the samples were studied in duplicates.