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长链非编码RNA通过-miR-206轴调节食管癌细胞的增殖、迁移和凋亡。

Long non-coding RNA regulates the proliferation, migration, and apoptosis of esophageal cancer cells via the -miR-206- axis.

作者信息

Gai Ling, Huang Yeqing, Zhao Lingling, Li Feng, Zhuang Zhixiang

机构信息

Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Department of Chemotherapy, Affiliated Hospital of Nantong University, Nantong, China.

出版信息

J Gastrointest Oncol. 2021 Oct;12(5):2093-2108. doi: 10.21037/jgo-21-586.

Abstract

BACKGROUND

Esophageal cancer (EC) is a common malignant tumor of the digestive tract, the treatment of which involves surgery combined with radiotherapy and chemotherapy, as well as other comprehensive types of treatment. The pathogenesis of EC remains unclear, which hinders the development of clinical therapy and the identification of molecular targets for this disease. Long non-coding RNAs (lncRNAs) have been shown to be associated with the malignant biological behavior of EC, but the specific molecular mechanisms underlying the carcinogenesis of EC are not fully understood.

METHODS

Reverse transcription-quantitative PCR (RT-qPCR) was applied to measure the lncRNA HAGLR opposite strand lncRNA () levels in EC cell lines and tissues. Cell Counting Kit-8 (CCK-8) detection, scratch test, and Transwell assay were performed to determine the proliferation, migration and invasion of EC cell. The interaction between , microRNA (miR)-206, and notch receptor 3 () was confirmed by RNA immunoprecipitation and dual luciferase reporter gene assays.

RESULTS

is upregulated in esophageal squamous cell carcinoma (ESCC) tissues and predicts poor prognosis. Silent is negatively associated with malignant behavior in EC cells. Low expression of can induce decreased invasive and migratory abilities in EC cells. Downregulated significantly inhibits the proliferation of EC cells and accelerates apoptosis. promotes EC cell tumorigenesis . participates in the /miR-206/ regulatory axis in EC cells.

CONCLUSIONS

may play a role in the progression of EC by modulating the miR-206/ signaling axis, and may be a novel target for the diagnosis and treatment of EC.

摘要

背景

食管癌(EC)是一种常见的消化道恶性肿瘤,其治疗包括手术联合放疗和化疗以及其他综合治疗方式。EC的发病机制仍不清楚,这阻碍了临床治疗的发展以及该疾病分子靶点的识别。长链非编码RNA(lncRNAs)已被证明与EC的恶性生物学行为相关,但EC致癌的具体分子机制尚未完全阐明。

方法

应用逆转录定量PCR(RT-qPCR)检测EC细胞系和组织中lncRNA HAGLR反义链lncRNA()水平。采用细胞计数试剂盒-8(CCK-8)检测、划痕试验和Transwell试验来确定EC细胞的增殖、迁移和侵袭能力。通过RNA免疫沉淀和双荧光素酶报告基因试验证实了、微小RNA(miR)-206和Notch受体3()之间的相互作用。

结果

在食管鳞状细胞癌(ESCC)组织中上调,并预测预后不良。沉默与EC细胞的恶性行为呈负相关。的低表达可导致EC细胞侵袭和迁移能力下降。下调显著抑制EC细胞的增殖并加速细胞凋亡。促进EC细胞肿瘤发生。在EC细胞中参与/miR-206/信号轴。

结论

可能通过调节miR-206/信号轴在EC进展中发挥作用,并且可能是EC诊断和治疗的新靶点。

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