METTL3/YTHDC1-mediated upregulation of LINC00294 promotes hepatocellular carcinoma progression

Zhang, Rulin; Yang, Rui; Huang, Zhuodeng; Xu, Xiang; Lv, Siang; Guan, Xin; Li, Hao; Wu, Jun

doi:10.1016/j.heliyon.2023.e22595

Heliyon

2023

DOI: 10.1016/j.heliyon.2023.e22595

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METTL3/YTHDC1-mediated upregulation of LINC00294 promotes hepatocellular carcinoma progression

Rulin Zhang,

Rui Yang,

Zhuodeng Huang

et al.

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2024

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Cited by 6 publications

References 39 publications

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RNA methylase RBM15 facilitates malignant progression of colorectal cancer through regulating E2F2 in an m6A modification‐dependent manner

Zhang,

Li,

Zhou

et al. 2024

J Biochem & Molecular Tox

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Recently, RBM15 has emerged as an oncogenic factor in a majority of tumors. However, the mechanism is unclear that accounts for how RBM15‐induces colorectal cancer (CRC) progression and it is in need of further study. We determined RBM15 expression through the UALCAN database and RT‐qPCR. The role of RBM15 in inducing the malignant and aggressive cancerous phenotype was characterized based on the results of the western blot, RT‐qPCR, CCK‐8 and transwell assays. The target genes of RBM15 were screened by LinkedOmics. m6A methylation kit was applied to analyze the methylation levels of mRNA. SRAMP website was employed to predict m6A sites of targeted mRNA. RIP, dual luciferase reporter gene and actinomycin D assay were conducted to verify the interactions between RBM15 and its targeted gene, and the presence of m6A modification site of its targeted mRNA, respectively. We confirmed the augmentation of RBM15 expression in CRC, which also has a high clinical diagnostic value for CRC. Functionally, RBM15 silencing clearly restrained malignant cellular processes in CRC cells. Mechanistically, RBM15 bound to E2F2 which increased its m6A binding and stabilized the corresponding E2F2 mRNA formation. Excessive E2F2 largely restored the repression malignant phenotype of tumor cells caused by RBM15 silencing. RBM15 regulated E2F2 in an m6A modification‐dependent manner thereby boosting malignant cellular processes in CRC. The RBM15/E2F2 axis may be a novel target for CRC therapy.

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RNA methylase RBM15 facilitates malignant progression of colorectal cancer through regulating E2F2 in an m6A modification‐dependent manner

Zhang,

Li,

Zhou

et al. 2024

J Biochem & Molecular Tox

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Overexpression of lncRNA LINC00294 Induces Cell Cycle Arrest and Apoptosis in Colorectal Cancer by Regulating the miR‐499a‐5p/LARP4B Axis

Wang,

Nie,

Wang

et al. 2024

J Biochem & Molecular Tox

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Increasing long noncoding RNAs (lncRNAs) have been found to participate in regulating the progression of colorectal cancer (CRC), which is a common gastrointestinal malignancy. Here, the specific role and mechanisms of lncRNA LINC00294 were investigated in CRC. The expression levels of LINC00294, miR‐499a‐5p, and La‐related protein 4B (LARP4B) in CRC cells (HCT116 and SW620) and tissues were assessed by RT‐qPCR. The viability, proliferation, cell cycle, and apoptosis of HCT116 and SW620 cells were determined by CCK‐8, EdU, and flow cytometry assays. Protein levels of cell cycle and cell apoptosis markers were measured by western blot analysis. FISH assay was performed to evaluate the subcellular localization of LINC00294 in CRC cells. Luciferase reporter assay, RNA pull‐down assay, as well as RIP assay verified the interactions between miR‐499a‐5p and LINC00294 (or LARP4B). The xenograft model was established in mice to investigate the function of LINC00294 in vivo. LINC00294 presented a decreased expression level in CRC cells and tissues. LINC00294 overexpression suppressed the cell proliferative capacity, promoted cell cycle arrest, and induced cell apoptosis in CRC HCT116 and SW620 cells. LINC00294 interacted with miR‐499a‐5p, and miR‐499a‐5p targeted LARP4B. MiR‐499a‐5p was upregulated while LARP4B was downregulated in CRC cells. In rescue assays, LARP4B knockdown reversed the inhibition of LINC00294 overexpression on malignant phenotypes of HCT116 and SW620 cells. In the xenograft model, LINC00294 overexpression inhibited tumor growth in vivo. LINC00294 exerted an antitumor function in CRC by forming a LINC00294/miR‐499a‐5p/LARP4B regulatory network.

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Crosstalk between m6A modification and non-coding RNAs in HCC

Qiu,

Yuan,

Wang

et al. 2024

Cellular Signalling

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METTL3/YTHDC1-mediated upregulation of LINC00294 promotes hepatocellular carcinoma progression

Cited by 6 publications

References 39 publications

RNA methylase RBM15 facilitates malignant progression of colorectal cancer through regulating E2F2 in an m6A modification‐dependent manner

RNA methylase RBM15 facilitates malignant progression of colorectal cancer through regulating E2F2 in an m6A modification‐dependent manner

Overexpression of lncRNA LINC00294 Induces Cell Cycle Arrest and Apoptosis in Colorectal Cancer by Regulating the miR‐499a‐5p/LARP4B Axis

Crosstalk between m6A modification and non-coding RNAs in HCC

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