MALAT1 通过招募 SF2/ASF 促进胃癌细胞增殖。
MALAT1 promotes cell proliferation in gastric cancer by recruiting SF2/ASF.
作者信息
Wang Junqing, Su Liping, Chen Xuehua, Li Pu, Cai Qu, Yu Beiqin, Liu Bingya, Wu Weize, Zhu Zhenggang
机构信息
Department of Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai 20025, People's Republic of China; Shanghai Key Laboratory of Gastric Neoplasms, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai 20025, People's Republic of China; Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai 20025, People's Republic of China.
Shanghai Key Laboratory of Gastric Neoplasms, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai 20025, People's Republic of China; Shanghai Institute of Digestive Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197, Rui Jin Er Road, Shanghai 20025, People's Republic of China.
出版信息
Biomed Pharmacother. 2014 Jun;68(5):557-64. doi: 10.1016/j.biopha.2014.04.007. Epub 2014 Apr 28.
The functions of long non-coding RNAs (lncRNAs) in gastric cancer (GC) remain largely unknown. MALAT1 is a kind of lncRNA that had been validated as a pivotal metastasis and prognosis mark in lung adenocarcinoma. In this study, we found that MALAT1 was aberrantly highly expressed in GC cell lines (SGC-7901, MKN-45 and SUN-16), and induced specific distribution and over-expression of SF2/ASF in nucleolus. Knock-down of MALAT1 or SF2/ASF in SGC-7901 cells respectively induced significant arrest of cell cycle in G0/G1 phase along with a remarkable suppression of cell proliferation, and the nuclear distribution and expression of SF2/ASF was significantly impaired when MALAT1 was depleted. However, over-expression of SF2/ASF exhibited no effect on rescuing the cell proliferation suppression by MALAT1 depletion. These results suggest that MALAT1 may function as a promoter of GC cell proliferation partly by regulating SF2/ASF, and our findings may provide us a likely biomarker and a potential target for GC diagnosis and therapeutic treatment.
长链非编码RNA（lncRNAs）在胃癌（GC）中的功能在很大程度上仍不清楚。MALAT1是一种lncRNA，已被证实是肺腺癌中关键的转移和预后标志物。在本研究中，我们发现MALAT1在胃癌细胞系（SGC-7901、MKN-45和SUN-16）中异常高表达，并诱导剪接因子2/精氨酸/丝氨酸富集蛋白（SF2/ASF）在核仁中特异性分布和过表达。在SGC-7901细胞中分别敲低MALAT1或SF2/ASF会诱导细胞周期在G0/G1期显著停滞，同时细胞增殖受到显著抑制，并且当MALAT1被耗尽时，SF2/ASF的核分布和表达会显著受损。然而，过表达SF2/ASF对挽救因MALAT1缺失导致的细胞增殖抑制没有作用。这些结果表明，MALAT1可能部分通过调节SF2/ASF发挥胃癌细胞增殖促进因子的作用，我们的发现可能为我们提供一种可能的生物标志物以及胃癌诊断和治疗的潜在靶点。
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