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LncDBH-AS1 敲低通过 miR-155/AXIN1 轴激活 Wnt 信号通路增强非小细胞肺癌细胞的增殖。

LncDBH-AS1 knockdown enhances proliferation of non-small cell lung cancer cells by activating the Wnt signaling pathway via the miR-155/AXIN1 axis.

机构信息

Affiliated Hospital of Shaoxing University, Zhejiang Province, China.

出版信息

Eur Rev Med Pharmacol Sci. 2021 Jan;25(1):139-144. doi: 10.26355/eurrev_202101_24377.

Abstract

OBJECTIVE

Dys-regulated long noncoding RNAs (lncRNAs) are involved in the cell growth of several malignancies and their aggressive phenotypes. LncRNA DBH-AS1 plays an important role in the advancement of various malignant tumors, but its contribution to non-small cell lung cancer (NSCLC) is still unexplored. This study intends to elucidate the role of the regulatory network of lncRNA DBH-AS1 in NSCLC progression.

PATIENTS AND METHODS

The LncDBH-AS1 expression in 32 paired NSCLC patients' tissue samples and NSCLC cell lines were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The role of LncDBH-AS1 in NSCLC was investigated through cell counting kit-8 (CCK-8) assay and colony formation assay in vitro. Besides, the interaction between LncDBH-AS1 and miR-155 was also analyzed.

RESULTS

The DBH-AS1 expression was significantly down-regulated in NSCLC cell lines and tissue samples. Decreased DBH-AS1 levels promoted the in vitro proliferation of the NSCLC cells. The mechanism was that DBH-AS1 regulated AXIN1 expression by sponging miR-155 in NSCLC cell lines. Importantly, LncDBH-AS1 might inhibit WNT/β-CATENIN activation in NSCLC cells.

CONCLUSIONS

The progression of NSCLC is facilitated by DBH-AS1 via miR-155 interaction and up-regulation of AXIN1 expression.

摘要

目的

失调的长非编码 RNA(lncRNA)参与了几种恶性肿瘤的细胞生长及其侵袭表型。lncRNA DBH-AS1 在多种恶性肿瘤的进展中发挥着重要作用,但它在非小细胞肺癌(NSCLC)中的作用仍未被探索。本研究旨在阐明 lncRNA DBH-AS1 调控网络在 NSCLC 进展中的作用。

患者和方法

通过定量逆转录聚合酶链反应(qRT-PCR)检测 32 对 NSCLC 患者组织样本和 NSCLC 细胞系中的 LncDBH-AS1 表达。通过细胞计数试剂盒-8(CCK-8)试验和体外集落形成试验研究 LncDBH-AS1 在 NSCLC 中的作用。此外,还分析了 LncDBH-AS1 与 miR-155 之间的相互作用。

结果

DBH-AS1 在 NSCLC 细胞系和组织样本中的表达明显下调。降低 DBH-AS1 水平促进了 NSCLC 细胞的体外增殖。其机制是 DBH-AS1 通过在 NSCLC 细胞系中海绵吸附 miR-155 来调节 AXIN1 的表达。重要的是,LncDBH-AS1 可能抑制 NSCLC 细胞中 WNT/β-CATENIN 的激活。

结论

DBH-AS1 通过与 miR-155 的相互作用和 AXIN1 表达的上调促进了 NSCLC 的进展。

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