Short-form RON (sf-RON) enhances glucose metabolism to promote cell proliferation via activating β-catenin/SIX1 signaling pathway in gastric cancer.
Short-form RON (sf-RON) enhances glucose metabolism to promote cell proliferation via activating β-catenin/SIX1 signaling pathway in gastric cancer.
复制标题
短型 RON (sf-RON) 通过激活胃癌中的 β-catenin/SIX1 信号通路增强葡萄糖代谢，促进细胞增殖
DOI：
10.1007/s10565-020-09525-5
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发表时间：
2021-03
影响因子：
6.1
通讯作者：
Zhang Z
中科院分区：
文献类型：
--
作者：
Wang Z;Yang Y;Hu S;He J;Wu Z;Qi Z;Huang M;Liu R;Lin Y;Tan C;Xu M;Zhang Z
受体d 'origine nantais（罗恩）与多种人类恶性肿瘤的细胞增殖、转移和化学抗性有关。罗恩转录本编码的短型罗恩（sf-罗恩）在胃癌组织中过表达，但其调控功能尚不清楚。在此，我们发现sf-RON通过增强葡萄糖代谢促进胃癌细胞增殖。此外，sf-RON还通过AKT 1/GSK 3 β信号通路诱导β-catenin的表达。同时，在SIX 1的启动子区发现了β-catenin的结合位点，并证实β-catenin正调控SIX 1的表达。SIX 1增强了葡萄糖代谢中关键蛋白如GLUT 1和LDHA的启动子活性。结果表明，sf-RON通过参与sf-RON/β-catenin/SIX 1信号轴调控胃癌细胞增殖和糖代谢，对胃癌治疗靶点的选择具有重要意义。本文的在线版本（10.1007/s10565-020-09525-5）包含补充材料，可供授权用户使用。
Recepteur d’origine nantais (RON) has been implicated in cell proliferation, metastasis, and chemoresistance of various human malignancies. The short-form RON (sf-RON) encoded by RON transcripts was overexpressed in gastric cancer tissues, but its regulatory functions remain illustrated. Here, we found that sf-RON promoted gastric cancer cell proliferation by enhancing glucose metabolism. Furthermore, sf-RON was proved to induce the β-catenin expression level through the AKT1/GSK3β signaling pathway. Meanwhile, the binding sites of β-catenin were identified in the promoter region of SIX1 and it was also demonstrated that β-catenin positively regulated SIX1 expression. SIX1 enhanced the promoter activity of key proteins in glucose metabolism, such as GLUT1 and LDHA. Results indicated that sf-RON regulated the cell proliferation and glucose metabolism of gastric cancer by participating in a sf-RON/β-catenin/SIX1 signaling axis and had significant implications for choosing the therapeutic target of gastric cancer. The online version of this article (10.1007/s10565-020-09525-5) contains supplementary material, which is available to authorized users.
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