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Up-regulation of kin17 is essential for proliferation of breast cancer Zeng T; Gao H; Yu P; He H; Ouyang X; Deng L; Zhang YPLoS One 2011[]; 6 (9): e25343BACKGROUND: Kin17 is ubiquitously expressed at low levels in human tissue and participates in DNA replication, DNA repair and cell cycle control. Breast cancer cells are characterized by enabling replicative immortality and accumulated DNA damage. However, whether kin17 contributes to breast carcinogenesis remains unknown. METHODOLOGY/PRINCIPAL FINDINGS: In this study, we show for the first time that kin17 is an important molecule related to breast cancer. Our results show that kin17 expression was markedly increased in clinical breast tumors and was associated with tumor grade, Ki-67 expression, p53 mutation status and progesterone receptor expression, which were assessed in a clinicopathologic characteristics review. Knockdown of kin17 inhibited DNA replication and repair, blocked cell cycle progression and inhibited anchorage-independent growth, while increasing sensitivity to chemotherapy in breast cancer cells. Moreover, kin17 silencing decreased EGF-stimulated cell growth. Furthermore, overexpression of kin17 promoted DNA replication and cell proliferation in MCF-10A. CONCLUSIONS/SIGNIFICANCE: Our findings indicate that up-regulation of kin17 is strongly associated with cellular proliferation, DNA replication, DNA damage response and breast cancer development. The increased level of kin17 was not only a consequence of immortalization but also associated with tumorigenesis. Therefore, kin17 could be a novel therapeutic target for inhibiting cell growth in breast cancer.|*Up-Regulation[MESH]|Adult[MESH]|Breast Neoplasms/genetics/*metabolism/*pathology[MESH]|Cell Cycle/drug effects/genetics[MESH]|Cell Line, Tumor[MESH]|Cell Proliferation/drug effects[MESH]|DNA Repair/drug effects/genetics[MESH]|DNA Replication/drug effects/genetics[MESH]|DNA-Binding Proteins/deficiency/genetics/*metabolism[MESH]|Disease Progression[MESH]|Epidermal Growth Factor/pharmacology[MESH]|Female[MESH]|Gene Knockdown Techniques[MESH]|Humans[MESH]|RNA-Binding Proteins/genetics/*metabolism[MESH] |
