RRS1 silencing suppresses colorectal cancer cell proliferation and tumorigenesis by inhibiting G2/M progression and angiogenesis
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Xin-Lin Wu1, Zhi-Wen Yang1, Li He1, Pei-De Dong1, Ming-Xing Hou1, Xing-Kai Meng2, Hai-Ping Zhao2, Zhao-Yang Wang1, Feng Wang1, Baoluri3,4, Wurenqimuge3,4, Agudamu1, Yong-Feng Jia3,4 and Lin Shi3,4
1Department of Gastrointestinal Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China
2Department of Hepatobiliary Surgery, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China
3Department of Pathology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China
4Institute of Pathology and Pathophysiology, Inner Mongolia Medical University, Hohhot 010059, Inner Mongolian Autonomous Region, China
Lin Shi, email: [email protected]
Keywords: colorectal cancer, RRS1, angiogenesis, cell cycle arrest, apoptosis
Received: March 06, 2017 Accepted: August 26, 2017 Published: September 15, 2017
Colorectal cancer (CRC) is one of the most common malignancies worldwide. Ribosome biogenesis regulatory protein homolog (RRS1) is an essential factor involved in ribosome biogenesis, while its role in CRC remains largely unclear. Here, we found that RRS1 expression was significantly higher in CRC tissues compared with adjacent normal tissues. RRS1 High expression also predicted poor overall survival of CRC patients. Knockdown of RRS1 induced the G2/M cell cycle arrest, apoptosis and suppressed the proliferation of RKO and HCT-116 CRC cells. Furthermore, angiogenesis was also reduced in CRC cells after RRS1 knockdown. In addition, suppression of RRS1 blunted the tumor formation of CRC cells in nude mice. At the molecular level, silencing of RRS1 decreased the expression of M-phase inducer phosphatase 3 (CDC25C), Cyclin-dependent kinase 1 (CDK1), antigen KI-67 (KI67) and increased the protein level of cyclin-dependent kinase inhibitor 1 (CDKN1A) and tumor suppressor p53 (p53). Taken together, our findings provide evidence that RRS1 may promote the development of colon cancer. Therefore, targeting RRS1 may be a promising therapeutic strategy for CRC patients.
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