Overexpression of miR-335 confers cell proliferation and tumour growth to colorectal carcinoma cells
Overexpression of miR-335 confers cell proliferation and tumour growth to colorectal carcinoma cells
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miR-335 的过度表达赋予结直肠癌细胞细胞增殖和肿瘤生长
DOI：
10.1007/s11010-015-2630-9
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发表时间：
2016-01-01
影响因子：
4.3
通讯作者：
Li, Xuenong
中科院分区：
文献类型：
--
作者：
Lu, Yanxia;Yang, Hui;Li, Xuenong
MiR-335在直肠癌(CRC)发生中的作用仍存在争议。在此，我们发现miR-335在大肠癌组织中较正常粘膜高度上调，并且miR-335的高表达水平与结直肠癌的肿瘤大小和分化程度显著相关。在结直肠癌细胞中过表达miR-335促进了细胞的体外增殖和体内肿瘤的生长。RASA1被确认为miR-335的靶点，这是CRC下调的目标。强制表达miR-335使RASA1沉默，并触发RAS/ERK级联反应。总之，miR-335-RASA1促进了结直肠癌细胞的生长，阐明其下游通路将为进一步研究结直肠癌的分子机制提供新的思路。
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.