miR-335的过表达赋予结肠癌细胞增殖和肿瘤生长能力。
Overexpression of miR-335 confers cell proliferation and tumour growth to colorectal carcinoma cells.
作者信息
Lu Yanxia, Yang Hui, Yuan Li, Liu Guobing, Zhang Chao, Hong Min, Liu Yan, Zhou Min, Chen Fang, Li Xuenong
机构信息
Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, Guangdong Province, China.
Department of Pathology, Xi'an 141 Hospital, Xi'an, 710089, Shanxi Province, China.
出版信息
Mol Cell Biochem. 2016 Jan;412(1-2):235-45. doi: 10.1007/s11010-015-2630-9. Epub 2015 Dec 26.
The involvement of miR-335 in csolorectal cancer (CRC) development remains controversial. Here, we found that miR-335 was highly up-regulated in CRC specimens relative to normal mucosa, and high miR-335 expression level was markedly associated with the tumour size and differentiation of CRC. The overexpression of miR-335 in CRC cells facilitated cell proliferation in vitro and tumour growth in vivo. RASA1 was validated as a target of miR-335 that was downregulation in CRC. Forced expression of miR-335 silenced RASA1 and triggered Ras/ERK cascade in CRC. Together, miR-335-RASA1 contributes to cell growth in CRC, and elucidation of downstream pathway will provide new insights into the molecular mechanisms of CRC progression.
miR - 335在结直肠癌（CRC）发展中的作用仍存在争议。在此，我们发现相对于正常黏膜，miR - 335在CRC标本中高度上调，且miR - 335高表达水平与CRC的肿瘤大小和分化显著相关。miR - 335在CRC细胞中的过表达促进了体外细胞增殖和体内肿瘤生长。RASA1被验证为miR - 335的靶标，其在CRC中表达下调。miR - 335的强制表达使RASA1沉默并在CRC中触发Ras/ERK级联反应。总之，miR - 335 - RASA1促进CRC中的细胞生长，阐明其下游通路将为CRC进展的分子机制提供新见解。
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