Abstract

Our previous study manifested that lanthanum chloride (LaCl3) can enhance the anticancer ability of cisplatin (DDP) in ovarian cancer cells. Here, ovarian cancer cells SKOV3 and SKOV3/DDP were subjected to DDP and LaCl3. Cell viability, apoptosis, DNA repair, and PI3K/Akt pathway were detected. LaCl3 induced more cell death and apoptosis caused by DDP in two cell lines, accompanied by upregulation of Bax and Cleaved caspase 3 proteins, and downregulation of Bcl-2 protein. LaCl3 also could decrease RAD51 protein by inactivation of the PI3K/Akt pathway. These data indicated that LaCl3 could be a potential drug to modulate DDP resistance by inactivating of PI3K/Akt pathway and attenuating DNA repair in ovarian cancer.

Highlights

  • Ovarian cancer is the most lethal gynecologic cancer

  • The percentages of survival cells were more than 90% in SKOV3 and SKOV3/DDP cells after exposure to LaCl3 (0.5, 1, and 1.5 μmol/L)

  • DDP resistance is a key obstacle for the treatment of ovarian cancer

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Summary

Introduction

Ovarian cancer is the most lethal gynecologic cancer. The first-line treatment for ovarian cancer is cisplatin (DDP)-based chemotherapy after cytoreductive surgery. The DDP resistance of ovarian cancer during the treatment is an important reason for the treatment failure. Cisplatin (DDP) often attacks DNA to cause DNA damage and lead to cell apoptosis; an enhanced DNA repair plays a key role in DDP resistance [3, 4]. Survival pathways were necessary for cell survival and involved in chemoresistance. The PI3K/Akt survival pathway was a way to play an important role in cell survival and DDP resistance in ovarian cancer. Lots of research target the DNA repair and PI3K/Akt pathway to explore new drugs to reverse the DDP resistance and improve the prognosis of ovarian cancer [8, 9]. It is important to explore novel drugs to conquer the resistance of DDP

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