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IGF2BP2-modified circular RNA circARHGAP12 promotes cervical cancer progression by interacting m⁶A/FOXM1 manner.

ABSTRACT: Emerging evidence indicates that circular RNA (circRNA) and N⁶-methyladenosine (m⁶A) play critical roles in cervical cancer. However, the synergistic effect of circRNA and m⁶A on cervical cancer progression is unclear. In the present study, our sequencing data revealed that a novel m⁶A-modified circRNA (circARHGAP12, hsa_circ_0000231) upregulated in the cervical cancer tissue and cells. Interestingly, the m⁶A modification of circARHGAP12 could amplify its enrichment. Functional experiments illustrated that circARHGAP12 promoted the tumor progression of cervical cancer in vivo and vitro. Furthermore, MeRIP-Seq illustrated that there was a remarkable m⁶A site in FOXM1 mRNA. CircARHGAP12 interacted with m⁶A reader IGF2BP2 to combine with FOXM1 mRNA, thereby accelerating the stability of FOXM1 mRNA. In conclusion, we found that circARHGAP12 exerted the oncogenic role in cervical cancer progression through m⁶A-dependent IGF2BP2/FOXM1 pathway. These findings may provide new concepts for cervical cancer biology and pathological physiology.

SUBMITTER: Ji F

PROVIDER: S-EPMC8364552 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature

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IGF2BP2-modified circular RNA circARHGAP12 promotes cervical cancer progression by interacting m6A/FOXM1 manner.

Ji Fei F Lu Yang Y Chen Shaoyun S Yu Yan Y Lin Xiaoling X Zhu Yuanfang Y Luo Xin X

Cell death discovery 20210814 1

Emerging evidence indicates that circular RNA (circRNA) and N6-methyladenosine (m6A) play critical roles in cervical cancer. However, the synergistic effect of circRNA and m6A on cervical cancer progression is unclear. In the present study, our sequencing data revealed that a novel m6A-modified circRNA (circARHGAP12, hsa_circ_0000231) upregulated in the cervical cancer tissue and cells. Interestingly, the m6A modification of circARHGAP12 cou ...[more]

PMID: 34392306

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Project description:BackgroundN6-methyladenosine (m6A) is the most common post-transcriptional modification at the RNA level. However, the exact molecular mechanisms of m6A epigenetic regulation in breast cancer remain largely unknown and need to be fully elucidated.Methods The integrating bioinformatics analyses were used to screen clinical relevance and dysregulated m6A "reader" protein YTHDF1 in breast cancer from TCGA databases, which was further validated in a cohort of clinical specimens. Furthermore, functional experiments such as the CCK-8 assay, EdU assay, wound healing assay, transwell invasion assay and cell cycle assay were used to determine the biological role of YTHDF1 in breast cancer. RIP, m6A-IP, and CLIP assays were used to find the target of YTHDF1 and further verification by RT-qPCR, western blot, polysome profiling assay. The protein-protein interaction between YTHDF1 and FOXM1 was detected via co-immunoprecipitation.ResultsOur study showed that YTHDF1 was overexpressed in breast cancer cells and clinical tissues specimens. At the same time, the high expression level of YTHDF1 was positively correlated with tumor size, lymph node invasion, and distant metastasis in breast cancer patients. YTHDF1 depletion repressed the proliferation, invasion and epithelial-mesenchymal transformation (EMT) and induced G0/G1 phase cell cycle arrest of breast cancer cells in vitro and in vivo. We also demonstrated that FOXM1 is a target of YTHDF1. Through recognizing and binding to the m6A-modified mRNA of FOXM1, YTHDF1 accelerated the translation process of FOXM1 and promoted breast cancer metastasis. Whereas overexpression of FOXM1 in breast cancer cells partially counteracted the tumor suppressed effects caused by YTHDF1 silence, which further verified the regulatory relationship between YTHDF1 and FOXM1.ConclusionOur study reveals a novel YTHDF1/FOXM1 regulatory pathway that contributes to metastasis and progression of breast cancer, suggesting that YTHDF1 might be applied as a potential biomarker and therapeutic target. That also advances our understanding of the tumorigenesis for breast cancer from m6A epigenetic regulation.

Dataset Information

IGF2BP2-modified circular RNA circARHGAP12 promotes cervical cancer progression by interacting m⁶A/FOXM1 manner.

Publications

IGF2BP2-modified circular RNA circARHGAP12 promotes cervical cancer progression by interacting m<sup>6</sup>A/FOXM1 manner.

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