Abstract
PurposeAssessment of miR-424-3p mimic capability to sensitize SK-OV-3 and TOV-21G ovarian cancer cells to cisplatin by decreasing the expression of galectin-3, which is an anti-apoptotic protein overexpressed in ovarian cancer and associated with resistance to chemotherapy.MethodsWe performed a reverse transfection of miR-424-3p mimic into SK-OV-3 and TOV-21G ovarian cancer cells, followed by Real Time™ RT-PCR analysis of the expression of miR-424-3p and galectin-3 mRNA as well as ELISA assay for galectin-3 protein level. Next, we studied the viability (XTT assay), proliferation (EdU incorporation assay), and apoptosis (ELISA assay) of the both cell lines transfected with the mimic and treated with cisplatin.ResultsWe demonstrated that miR-424-3p mimic effectively transfects into SK-OV-3 and TOV-21G ovarian cancer cells in which it significantly suppresses the expression of galectin-3 at the protein level, but not at the mRNA level. Reverse transfection of both cell lines with the mimic, followed by treatment with cisplatin, resulted in a reduction in cell viability and proliferation as well as an increase in the induction of apoptosis.ConclusionsMiR-424-3p mimic sensitizes SK-OV-3 and TOV-21G ovarian cancer cells to cisplatin by decreasing the expression of galectin-3.
Highlights
Ovarian cancer is the fifth leading cause of cancer death among women worldwide, and by that, it is considered to be one of the most deadly gynecological cancers [1,2,3]
The NWGR anti-death motif suppresses apoptosis of cancer cells induced by chemotherapeutic agents, such as cisplatin, and galectin-3 plays an important role in the resistance to anticancer drugs [6, 8]
We estimated the reverse transfection efficiency to be approximately 97% in SK-OV-3 and TOV-21G ovarian cancer cell lines based on the ratio of cells successfully transfected with 5′-FAM-labeled miR-424-3p mimic to the total number of cells in three different fields
Summary
Ovarian cancer is the fifth leading cause of cancer death among women worldwide, and by that, it is considered to be one of the most deadly gynecological cancers [1,2,3]. The clinical response rate after chemotherapy is often high, but frequently occurring relapses lead to an acquired resistance to Galectin-3 (coded by LGALS3 gene) is a lectin-containing an N-terminal domain that regulates its cellular function, an α-collagen-like sequence, and a C-terminal carbohydrate recognition domain (CRD) that binds to β-galactosides [3, 6]. The C-terminal domain includes the NWGR (Asp–Trp–Gly–Arg) anti-death motif, which is a part of highly conserved BH1 domain specific to the BCL-2 protein family. The NWGR anti-death motif suppresses apoptosis of cancer cells induced by chemotherapeutic agents, such as cisplatin, and galectin-3 plays an important role in the resistance to anticancer drugs [6, 8]. Increasing evidence suggests that galectin-3 promotes chemoresistance in prostate cancer, cholangiocarcinoma, thyroid carcinoma [9], lung cancer [5], and ovarian cancer [3, 5] as well as protects BT549
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