{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu YY"],"funding":["National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["732"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11458786"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(10)"],"pubmed_abstract":["Cervical cancer (CCa) patients with lymph node (LN) metastasis face poor prognoses and have limited treatment options. Aberrant N6-methyladenosine (m<sup>6</sup>A) modification of RNAs are known to promote tumor metastasis, but their role in CCa remains unclear. Our study reveals that HNRNPC, an alternative splicing (AS) factor and m<sup>6</sup>A reader, increases tumor-related variants through m<sup>6</sup>A-dependent manner, thereby promoting lymphatic metastasis in CCa. We found that HNRNPC overexpression correlates with lymphatic metastasis and poorer prognoses in CCa patients. Functionally, knocking down HNRNPC markedly inhibited the migration and invasion of several CCa cell lines, while supplementing HNRNPC restored the malignant phenotypes of these cells. Mechanistically, HNRNPC re"],"journal":["Cell death & disease"],"pubmed_title":["HNRNPC mediates lymphatic metastasis of cervical cancer through m6A-dependent alternative splicing of FOXM1."],"pmcid":["PMC11458786"],"funding_grant_id":["81900428"],"pubmed_authors":["Liao YD","Chen ZB","Lu HW","Xia M","Liu YY","Huang H","Yuan L","Yao SZ","Pan YW","Zhang CY"],"additional_accession":[]},"is_claimable":false,"name":"HNRNPC mediates lymphatic metastasis of cervical cancer through m6A-dependent alternative splicing of FOXM1.","description":"Cervical cancer (CCa) patients with lymph node (LN) metastasis face poor prognoses and have limited treatment options. Aberrant N6-methyladenosine (m<sup>6</sup>A) modification of RNAs are known to promote tumor metastasis, but their role in CCa remains unclear. Our study reveals that HNRNPC, an alternative splicing (AS) factor and m<sup>6</sup>A reader, increases tumor-related variants through m<sup>6</sup>A-dependent manner, thereby promoting lymphatic metastasis in CCa. We found that HNRNPC overexpression correlates with lymphatic metastasis and poorer prognoses in CCa patients. Functionally, knocking down HNRNPC markedly inhibited the migration and invasion of several CCa cell lines, while supplementing HNRNPC restored the malignant phenotypes of these cells. Mechanistically, HNRNPC re","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-06-01T10:03:47.86Z","creation":"2025-04-04T02:43:47.67Z"},"accession":"S-EPMC11458786","cross_references":{"pubmed":["39375330"],"doi":["10.1038/s41419-024-07108-4"]}}