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SNHG16/miR-30a 轴通过调节 RRM2 促进乳腺癌细胞增殖和侵袭。

The SNHG16/miR-30a axis promotes breast cancer cell proliferation and invasion by regulating RRM2.

机构信息

Zibo Vocational Institute, Zibo, China.

出版信息

Neoplasma. 2020 May;67(3):567-575. doi: 10.4149/neo_2020_190625N550. Epub 2020 Feb 28.

Abstract

Long noncoding RNAs (lncRNAs) have been suggested to play vital roles in tumor initiation and progression. Recent studies have reported that the lncRNA small nucleolar RNA host gene 16 (SNHG16) is highly expressed in breast cancer tissue. In the present study, we demonstrated that SNHG16 is an oncogene involved in cell proliferation and invasion in breast cancer. First, we examined the functional role of SNHG16 in breast cancer cells by knocking down SNHG16 expression via siRNA. We found that SNHG16 inhibition reduced the proliferation and invasion of breast cancer cells in vitro. Then, based on bioinformatic prediction and functional assay validation, we demonstrated SNHG16 interaction with miR-30a and its role in breast cancer cells. Finally, we examined the functional role of RRM2 in breast cancer cells by knocking down RRM2 expression via siRNA. Our results indicated that the SNHG16/miR-30a axis regulated the expression of ribonucleotide reductase M2 (RRM2) in breast cancer cells. These results provide novel insight into breast cancer tumorigenesis and suggest that SNHG16 could serve as a therapeutic target in breast cancer.

摘要

长链非编码 RNA(lncRNA)被认为在肿瘤的发生和发展中起着至关重要的作用。最近的研究报道,小核仁 RNA 宿主基因 16(SNHG16)lncRNA 在乳腺癌组织中高度表达。在本研究中,我们证明 SNHG16 是一种参与乳腺癌细胞增殖和侵袭的癌基因。首先,我们通过 siRNA 敲低 SNHG16 表达来检测 SNHG16 在乳腺癌细胞中的功能作用。我们发现 SNHG16 抑制可减少乳腺癌细胞的体外增殖和侵袭。然后,基于生物信息学预测和功能测定验证,我们证明了 SNHG16 与 miR-30a 的相互作用及其在乳腺癌细胞中的作用。最后,我们通过 siRNA 敲低 RRM2 表达来检测 RRM2 在乳腺癌细胞中的功能作用。我们的结果表明,SNHG16/miR-30a 轴调节乳腺癌细胞中核糖核苷酸还原酶 M2(RRM2)的表达。这些结果为乳腺癌的肿瘤发生提供了新的见解,并表明 SNHG16 可作为乳腺癌的治疗靶点。

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