To investigate long-chain noncoding TM4SF1-AS1 in gastric cancer (GC) tissues and cells. TM4SF1-AS1 in 40 GC tissues and adjacent tissues was detected and compared using real-time fluorescence quantitative PCR (qRT-PCR). TM4SF1-AS1 in MKN28 and SGC7901 GC cells was downregulated using small interfering RNA (shRNA). The cells were grouped into an interference group (shTM4SF1-AS1 group) and a control group (shControl group). MTT and Transwell tests were applied to determine the proliferation and invasion of the cells in both groups, and flow cytometry was performed to assess the apoptosis rate in the two groups. Western blotting was performed to determine changes in key proteins in cells during the epithelial-to-mesenchymal transition (EMT) and in the TM4SF1 and PI3K-AKT signalling pathways in response to the downregulation of TM4SF1-AS1. The proliferation of MKN28 and SGC7901 in the shTM4SF1-AS1 group was significantly inhibited at 48 h and 72 h compared to that in the shControl group (all P < 0.05). In the shTM4SF1-AS1 group, the number of invaded MKN28 and SGC7901 cells was significantly lower than that in the shControl group (all P < 0.05). Apoptosis in the MKN28 and SGC7901 shTM4SF1-AS1 groups was significantly higher than that in the shControl group (all P < 0.05). Compared to those in the shControl group, levels of E-cadherin in EMT-related proteins were significantly elevated (P < 0.01), while levels of N-cadherin, Snail and Twist1 were significantly decreased (all P < 0.01). After silencing the expression of LncTM4SF1-AS1, the expression levels of TM4SF1 in the shTM4SF1-AS1 group were downregulated compared to those in the shControl group, and the p-PI3K and p-AKT proteins in the PI3K-AKT signalling pathway in the shTM4SF1-AS1 group were downregulated compared to those of the shControl group. TM4SF1-AS1 is upregulated in gastric cancer tissues and cells. Interfering with and downregulating its expression inhibit cancer cell proliferation, invasion and the EMT and promote apoptosis. The underlying mechanism for these effects is related to silencing the TM4SF1 and PI3K-AKT signalling pathways. TM4SF1-AS1 may be a potential therapeutic target for gastric cancer.

中文翻译：

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下调长链非编码RNA TM4SF1-AS1对胃癌细胞增殖、凋亡和侵袭的影响及机制

研究胃癌 (GC) 组织和细胞中的长链非编码 TM4SF1-AS1。使用实时荧光定量 PCR (qRT-PCR) 检测和比较 40 个 GC 组织和邻近组织中的 TM4SF1-AS1。使用小干扰 RNA (shRNA) 下调 MKN28 和 SGC7901 GC 细胞中的 TM4SF1-AS1。将细胞分为干扰组（shTM4SF1-AS1组）和对照组（shControl组）。采用MTT和Transwell试验检测两组细胞的增殖和侵袭能力，流式细胞仪检测两组细胞凋亡率。进行蛋白质印迹以确定上皮间质转化 (EMT) 期间细胞中关键蛋白的变化，以及响应 TM4SF1-AS1 下调的 TM4SF1 和 PI3K-AKT 信号通路中的变化。与 shControl 组相比，shTM4SF1-AS1 组 MKN28 和 SGC7901 的增殖在 48 h 和 72 h 受到显着抑制（均 P < 0.05）。shTM4SF1-AS1组侵袭的MKN28和SGC7901细胞数显着低于shControl组（均P < 0.05）。MKN28和SGC7901 shTM4SF1-AS1组的细胞凋亡明显高于shControl组（均P <0.05）。与shControl组相比，EMT相关蛋白中E-cadherin水平显着升高（P < 0.01），而N-cadherin、Snail和Twist1水平显着降低（均P < 0.01）。沉默 LncTM4SF1-AS1 的表达后，shTM4SF1-AS1 组中 TM4SF1 的表达水平与 shControl 组相比下调，与shControl组相比，shTM4SF1-AS1组PI3K-AKT信号通路中的p-PI3K和p-AKT蛋白下调。TM4SF1-AS1 在胃癌组织和细胞中上调。干扰和下调其表达抑制癌细胞增殖、侵袭和EMT并促进细胞凋亡。这些影响的潜在机制与沉默 TM4SF1 和 PI3K-AKT 信号通路有关。TM4SF1-AS1 可能是胃癌的潜在治疗靶点。这些影响的潜在机制与沉默 TM4SF1 和 PI3K-AKT 信号通路有关。TM4SF1-AS1 可能是胃癌的潜在治疗靶点。这些影响的潜在机制与沉默 TM4SF1 和 PI3K-AKT 信号通路有关。TM4SF1-AS1 可能是胃癌的潜在治疗靶点。