Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Department of General Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Int J Biol Macromol. 2019 Feb 1;122:1046-1052. doi: 10.1016/j.ijbiomac.2018.09.051. Epub 2018 Sep 15.
Gastric cancer (GC) severely threatens human life, and METase seemed to inhibit tumor growth. However, the potential mechanism underlying it is still unclear.
Both clinical tissues and cell lines were used in the present study. SNHG5 and miR-20a expressions were determined using real-time PCR. Western blot was performed to determine the expression of autophagy-related proteins. The interaction between miR-20a and SNHG5 was determined using luciferase reporter assay and RNA immunoprecipitation (RIP).
The expression of SNHG5 was decreased in GC tissues and cell lines. Overexpressed METase significantly promoted cell apoptosis and autophagy, as well as the expression of SNHG5. SNHG5 directly regulated the expression of miR-20a. GC cells transfected with pcDNA-SNHG5 significantly promoted cell apoptosis and autophagy, while the co-transfected with miR-20a mimic dramatically reversed the effects of pcDNA-SNHG5. Overexpressed METase significantly promoted cell autophagy, which was abolished by down-regulated SNHG5.
Overexpressed METase promoted cell apoptosis and autophagy via up-regulating the expression of SNHG5 and down-regulating miR-20a in GC.
胃癌（GC）严重威胁人类生命，METase 似乎能抑制肿瘤生长。然而，其潜在机制尚不清楚。
本研究同时使用临床组织和细胞系。采用实时 PCR 测定 SNHG5 和 miR-20a 的表达。采用 Western blot 测定自噬相关蛋白的表达。采用荧光素酶报告实验和 RNA 免疫沉淀（RIP）测定 miR-20a 和 SNHG5 之间的相互作用。
SNHG5 在 GC 组织和细胞系中的表达降低。过表达 METase 可显著促进细胞凋亡和自噬，以及 SNHG5 的表达。SNHG5 可直接调节 miR-20a 的表达。转染 pcDNA-SNHG5 的 GC 细胞可显著促进细胞凋亡和自噬，而共转染 miR-20a 模拟物则可显著逆转 pcDNA-SNHG5 的作用。过表达 METase 可显著促进细胞自噬，而下调 SNHG5 则可消除这种作用。
过表达 METase 通过上调 SNHG5 和下调 miR-20a 在 GC 中促进细胞凋亡和自噬。
