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Radiotherapy ( RT ) can be used as preoperative treatment to downstage initially unresectable locally rectal carcinoma, but radioresistance and recurrence remain significant problems. Retinoblastoma binding protein 6 ( RBBP 6) has been implicated in the regulation of cell cycle, apoptosis and chemoresistance both in vitro and in vivo. The present study investigated whether the inhibition of  RBBP 6 expression would improve radiosensitivity in human colorectal cancer cells. After  SW 620 and  HT 29 cells were exposed to radiation, the levels of  RBBP 6  mRNA  and protein increased over time in both cells. Moreover, a significant reduction in clonogenic survival and a decrease in cell viability in parallel with an obvious increase in cell apoptosis were demonstrated in irradiated  RBBP 6‐knockdown cells. Transfection with  RBBP 6 sh RNA  improved the levels of G2‐M phase arrest, which blocked the cells in a more radiosensitive period of the cell cycle. These observations indicated that cell cycle and apoptosis mechanisms may be connected with tumor cell survival following radiotherapy. In vivo, the tumor growth rate of nude mice in the  RBBP 6‐knockdown group was significantly slower than that in other groups. These results indicated that  RBBP 6 overexpression could resist colorectal cancer cells against radiation by regulating cell cycle and apoptosis pathways, and inhibition of  RBBP 6 could enhance radiosensitivity of human colorectal cancer.

RBBP 6 increases radioresistance and serves as a therapeutic target for preoperative radiotherapy in colorectal cancer