Department of Thoracic Surgery, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou China.
Bioengineered. 2022 Feb;13(2):4397-4410. doi: 10.1080/21655979.2022.2033412.
Esophageal cancer (EC) is one type of aggressive gastrointestinal cancers. The treatment of EC is challenging. Effective therapeutic targets require development. Long non-coding RNA TRPM2 antisense RNA (LncRNA TRPM2-AS) is considering a novel biomarker and therapeutic target for various types of cancer. However, the role of lncRNA TRPM2-AS in EC remains unknown. This study aimed to illustrate effects of LncRNA TRPM2-AS on EC growth and metastasis and potential underlying molecular mechanisms. LncRNA TRPM2-AS expression was determined in both EC tissues and cell lines by quantitative real-time polymerase-chain reaction (qRT-PCR). Cell proliferation ability was evaluated by cell counting kit-8 and colony formation assays. Cell apoptosis was analyzed by flow cytometry. Cell migration and invasion were determined using transwell. Epithelial-mesenchymal transition (EMT)-related markers expression were determined using qRT-PCR and Western blotting. Furthermore, potential lncRNA TRPM2-AS targeting miRNAs were predicted by public databases. The expression of five selected miRNAs were validated by qRT-PCR. We found that lncRNA TRPM2-AS expression was increased in EC tissues and cell lines compared with respective control. Silencing lncRNA TRPM2-AS suppressed EC cell proliferation, migration, and invasion while promoted cell apoptosis. Moreover, lncRNA TRPM2-AS knockdown reduced neural cadherin, vimentin, and matrix metallopeptidase 9 gene and protein expressions while increased epithelial cadherin expression. Furthermore, lncRNA TRPM2-AS knockdown promoted microRNA (miR)-1291, miR-6852-5p, and miR-138-5p expressions. Taken together, this study for the first time demonstrates that upregulation of lncRNA TRPM2-AS in EC promotes the growth and metastasis of EC likely through interacting with miR-1291, miR-6852-5p, and miR-138-5p.
食管癌（EC）是一种侵袭性胃肠道癌症。EC 的治疗具有挑战性。需要开发有效的治疗靶点。长链非编码 RNA TRPM2 反义 RNA（LncRNA TRPM2-AS）被认为是各种癌症的新型生物标志物和治疗靶点。然而，LncRNA TRPM2-AS 在 EC 中的作用尚不清楚。本研究旨在阐明 LncRNA TRPM2-AS 对 EC 生长和转移的影响及其潜在的分子机制。通过实时定量聚合酶链反应（qRT-PCR）确定 EC 组织和细胞系中 LncRNA TRPM2-AS 的表达。通过细胞计数试剂盒-8 和集落形成测定评估细胞增殖能力。通过流式细胞术分析细胞凋亡。通过 Transwell 测定细胞迁移和侵袭。通过 qRT-PCR 和 Western blot 测定上皮-间充质转化（EMT）相关标志物的表达。此外，通过公共数据库预测潜在的 LncRNA TRPM2-AS 靶向 miRNA。通过 qRT-PCR 验证了五个选定 miRNA 的表达。结果发现，与相应的对照相比，LncRNA TRPM2-AS 在 EC 组织和细胞系中的表达增加。沉默 LncRNA TRPM2-AS 抑制 EC 细胞增殖、迁移和侵袭，同时促进细胞凋亡。此外，LncRNA TRPM2-AS 敲低降低了神经钙黏蛋白、波形蛋白和基质金属蛋白酶 9 基因和蛋白的表达，而增加了上皮钙黏蛋白的表达。此外，LncRNA TRPM2-AS 敲低促进了 microRNA（miR）-1291、miR-6852-5p 和 miR-138-5p 的表达。总之，本研究首次证明，在 EC 中上调 LncRNA TRPM2-AS 可能通过与 miR-1291、miR-6852-5p 和 miR-138-5p 相互作用，促进 EC 的生长和转移。
