Mechanism of RBM15 in the malignant proliferation of colorectal cancer cells through regulating the stability of LncRNA FGD5-AS1 via m6A modification.

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research Pub Date : 2024-12-17 DOI:10.1016/j.yexcr.2024.114384

Lin Ma, Weihua Liu, Xin Wang, Dezheng Li, Chuankui Wei

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引用次数: 0

Abstract

Colorectal cancer (CRC) is the third most prevalent cancer all around the world. This study explored the mechanism of RBM15-mediated m6A modification in CRC cell malignant proliferation. The expression of RBM15, LncRNA FGD5-AS1, and HOXC10 was detected in CRC cells. m6A levels in cells and m6A enrichment on FGD5-AS1 RNA were analyzed. FGD5-AS1 RNA stability and localization in CRC cells were analyzed. The binding of LncRNA FGD5-AS1 to YBX1 and YBX1 to the HOXC10 promoter was analyzed. Combined experiments were conducted to validate the mechanism. Tumor xenografts in nude mice were used to verify the mechanism of RBM15 in vivo. RBM15 was highly expressed in CRC cells. RBM15 inhibition suppressed CRC cell proliferation and reduced PCNA expression. RBM15 increased m6A modification on FGD5-AS1 RNA, enhancing FGD5-AS1 stability and expression. FGD5-AS1 promoted HOXC10 expression by recruiting YBX1 to the HOXC10 promoter. YBX1 inhibition suppressed HOXC10 expression. Overexpression of FGD5-AS1 or HOXC10 partially reversed the alleviative effect of RBM15 inhibition on CRC cell proliferation. RBM15 downregulation attenuated in vivo CRC cell proliferation by inhibiting the FGD5-AS1/HOXC10 axis. In conclusion, RBM15 promotes the FGD5-AS1/HOXC10 axis via m6A modification to promote CRC cell proliferation.

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来源期刊

Experimental cell research 医学-细胞生物学

CiteScore

7.20

自引率

0.00%

发文量

295

审稿时长

30 days

期刊介绍： Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.