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MicroRNA-216b 通过与 cyclin T2 相互作用调控胃癌细胞增殖、侵袭和周期进程。

MicroRNA-216b regulates cell proliferation, invasion and cycle progression via interaction with cyclin T2 in gastric cancer.

机构信息

Department of General Surgery, The First Affiliated Hospital of Soochow University, Soochow.

Department of General Surgery, Affiliated Hospital of Nantong University, Nantong.

出版信息

Anticancer Drugs. 2020 Jul;31(6):623-631. doi: 10.1097/CAD.0000000000000915.

Abstract

Gastric cancer has become the second most common malignant tumor in the world, revealing the molecular mechanism of gastric cancer development is essential for the treatment of gastric cancer and improvement of prognosis. Recent studies have shown that microRNAs may play a carcinogenic or tumor-suppressive role in many types of cancer. It has been detected that miR-216b is down-regulated in many cancer types, indicating that miR-216b can be used as a prognostic marker for these particular types of cancer. However, the effect of miR-216b on gastric cancer remains unclear. In the present study, miR-216 was observed to be significantly down-regulated in cancer tissues compared to normal tissues, and the level of miR-216b in various gastric cancer cell lines was decreased. In addition, miR-216b overexpression inhibits proliferation, migration, invasion, cell cycle and apoptosis of gastric cancer cells. We further verified that the inhibitory effect of miR-216b on proliferation and invasion of gastric cancer cells is mediated by cyclin T2. Overexpression of cyclin T2 can reverse the anti-cancer effect of miR-216b mimics. The results further enriched the mechanism of miR-216b in the development and progression of gastric cancer.

摘要

胃癌已成为全球第二大常见恶性肿瘤,揭示胃癌发生的分子机制对于胃癌的治疗和预后的改善至关重要。最近的研究表明,microRNAs 可能在多种癌症中发挥致癌或肿瘤抑制作用。已经检测到 miR-216b 在许多癌症类型中下调,表明 miR-216b 可以作为这些特定类型癌症的预后标志物。然而,miR-216b 对胃癌的影响尚不清楚。本研究观察到 miR-216 在癌症组织中明显下调,而在各种胃癌细胞系中 miR-216b 的水平降低。此外,miR-216b 的过表达抑制胃癌细胞的增殖、迁移、侵袭、细胞周期和凋亡。我们进一步验证了 miR-216b 通过 cyclin T2 抑制胃癌细胞增殖和侵袭的抑制作用。cyclin T2 的过表达可以逆转 miR-216b 模拟物的抗癌作用。这些结果进一步丰富了 miR-216b 在胃癌发生和发展中的作用机制。

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