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长链非编码RNA FENDRR通过影响c-Myc mRNA水平抑制黑色素瘤生长。

LncRNA FENDRR Suppresses Melanoma Growth via Influencing c-Myc mRNA Level.

作者信息

Niu Changying, Tan Shenxing

机构信息

Dermatological Department, Affiliated Hospital of Weifang Medical University, Weifang, People's Republic of China.

Plastic Surgery, Affiliated Hospital of Weifang Medical University, Weifang, People's Republic of China.

出版信息

Clin Cosmet Investig Dermatol. 2023 Aug 9;16:2119-2128. doi: 10.2147/CCID.S409622. eCollection 2023.

Abstract

BACKGROUND

Long non-coding RNAs (lncRNAs) play an important role in the occurrence of melanoma. However, the specific molecular mechanisms that regulate its biological function are still poorly understood. Therefore, the main purpose of this study is to elucidate the internal mechanism of lncRNA-FENDRR as a biological marker for the occurrence of SKCM and its influence on its proliferation.

RESULTS

FENDRR is low expressed in skin cutaneous melanoma (SKCM) tissues and appears to be at an even lower level as the tumor progresses. However, the high expression of FENDRR can affect the proliferation of SKCM cell line A375. The results of flow cytometry showed that after overexpression of FENDRR, the cell cycle was arrested in the G1/G0 phase. Bioinformatics analysis and RIP results showed that FENDRR could be combined with YTHDF1. Together, these complexes regulate c-Myc mRNA level and determine cell proliferation.

CONCLUSION

We found that overexpression of FENDRR can effectively inhibit SKCM, which provides a new theoretical basis for new therapeutic approaches and targeted RNA drugs.

摘要

背景

长链非编码RNA(lncRNAs)在黑色素瘤的发生中起重要作用。然而,调节其生物学功能的具体分子机制仍知之甚少。因此,本研究的主要目的是阐明lncRNA-FENDRR作为皮肤黑色素瘤(SKCM)发生的生物学标志物的内在机制及其对其增殖的影响。

结果

FENDRR在皮肤黑色素瘤(SKCM)组织中低表达,并且随着肿瘤进展似乎处于更低水平。然而,FENDRR的高表达可影响SKCM细胞系A375的增殖。流式细胞术结果显示,FENDRR过表达后,细胞周期停滞在G1/G0期。生物信息学分析和RIP结果表明,FENDRR可与YTHDF1结合。这些复合物共同调节c-Myc mRNA水平并决定细胞增殖。

结论

我们发现FENDRR过表达可有效抑制SKCM,这为新的治疗方法和靶向RNA药物提供了新的理论依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a893/10423570/bac927260de4/CCID-16-2119-g0001.jpg

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