While it ranks fifth among cancer-related deaths in American women, ovarian cancer is the leading cause of death from gynecologic malignancy in the United States.Surgical debulking remains the treatment mainstay, followed by chemotherapy.Platinum-based agents are the preferred first-line drugs.The emergence of cancer cell drug resistance has stimulated research aimed at understanding and developing countermeasures.Among the many methods cancer cells employ in drug resistance, is a malfunctioning plasma membrane transport protein.We took the novel approach of bypassing the plasma membrane, and investigating nuclear membrane pore complexes (NPCs).We found that nuclear membrane pore constituent NUP62 protein, accumulates in early G1 phase of the cell cycle, and is required for progression through G1 phase.Knockdown of NUP62 resulted in growth arrest of cultured TOV112D high-grade ovarian carcinoma cells that was reversible upon removal ofNUP62 siRNA.Knockdown of NUP62 also conferred resistance to cisplatin in TOV112D cells.This contrasts with the fact that most cytostatic agents enhance, rather than protect against cisplatin cytotoxicity.Hence NUP62-altered TOV112D cells may employ other mechanisms.Preliminary studies have shown that NUP62 is phosphorylated in the coiled-coil domain by the protein tyrosine kinase PYK2.Activation of PYK2 is associated with chemoresistance in some tumor types, and as the coiled-coil domain mediates interactions between NUP62 and the NPC, phosphorylation of this domain may functionally alter nuclear pore architecture in a manner mimicked by NUP62 knockdown.