ArticleJournal of experimental & clinical cancer research : CR2021
CPSF6 links alternative polyadenylation to metabolism adaption in hepatocellular carcinoma progression.
Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Single-cell profiling and genetic regulation of alternative polyadenylation in the human brain.Nature genetics · 2026Article
- SERPINE1 Alternative Polyadenylation Influences Gastric Cancer Prognosis via N6-Methyladenosine Modification.Cancer science · 2026Article
- Article
- IGF2BP2 binding to CPSF6 facilitates m6A-mediated alternative polyadenylation of PUM2 and promotes malignant progression in ovarian cancer.Clinical and translational medicine · 2025Article
- SLC27A5 inhibits cancer stem cells by inducing alternative polyadenylation of METTL14 in hepatocellular carcinoma.Genes & diseases · 2025Article
- IGF2BP3 recruits NUDT21 to regulate SPTBN1 alternative polyadenylation and drive ovarian cancer progression.Communications biology · 2025Article
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
- Crosstalk between RNA-binding proteins and non-coding RNAs in tumors: molecular mechanisms, and clinical significance.International journal of biological sciences · 2025Review
- The roles and mechanisms of coding and noncoding RNA variations in cancer.Experimental & molecular medicine · 2024Review
- Disruption of PABPN1 phase separation by SNRPD2 drives colorectal cancer cell proliferation and migration through promoting alternative polyadenylation of CTNNBIP1.Science China. Life sciences · 2024Article
- RNA processing modification mediated subtypes illustrate the distinctive features of tumor microenvironment in hepatocellular carcinoma.Genes and immunity · 2024Article
- Nudt21-mediated alternative polyadenylation of MZT1 3'UTR contributes to pancreatic cancer progression.iScience · 2024Article
- Downregulation of CPSF6 leads to global mRNA 3' UTR shortening and enhanced antiviral immune responses.PLoS pathogens · 2024Article
- Multiplexed screening reveals how cancer-specific alternative polyadenylation shapes tumor growth in vivo.Nature communications · 2024Article
- Negative Regulation of CPSF6 Suppresses the Warburg Effect and Angiogenesis Leading to Tumor Progression Via c-Myc Signaling Network: Potential Therapeutic Target for Liver Cancer Therapy.International journal of biological sciences · 2024Article
- Alternative polyadenylation factor CPSF6 regulates temperature compensation of the mammalian circadian clock.PLoS biology · 2023Article
- Integrative transcriptome analysis reveals alternative polyadenylation potentially contributes to GCRV early infection.Frontiers in microbiology · 2023Article
- Heterogeneity characterization of hepatocellular carcinoma based on the sensitivity to 5-fluorouracil and development of a prognostic regression model.Frontiers in pharmacology · 2023Article
- U1 snRNP proteins promote proximal alternative polyadenylation sites by directly interacting with 3' end processing core factors.Journal of molecular cell biology · 2022Article
- Circular RNAs hsa_circ_0001438 and hsa_circ_0000417 are downregulated and upregulated, respectively, in hepatocellular carcinoma.International journal of experimental pathology · 2022Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlternative polyadenylation (APA) is an important mechanism of gene expression regulation through generation of RNA isoforms with distinct 3' termini. Increasing evidence has revealed that APA is actively involved in development and disease, including hepatocellular carcinoma (HCC). However, how APA functions in tumor formation and progression remains elusive. In this study, we investigated the role of cleavage factor I (CFIm) subunit CPSF6 in human hepatocellular carcinoma (HCC).
methodsExpression levels of CPSF6 in clinical tissues and cell lines were determined by qRT-PCR and western blot. Functional assays, including the cell number, MTT, colony formation and transwell, were used to determine the oncogenic role of CPSF6 in HCC. Animal experiments were used to determine the role of CPSF6 in HCC tumorigenicity in vivo. Deep sequencing-based 3 T-seq was used to profile the transcriptome-wide APA sites in both HCC cells and CPSF6 knockdown HCC cells. The function of CPSF6-affected target NQO1 with distinct 3'UTRs was characterized by metabolism assays.
resultsWe observed CPSF6 was upregulated in HCC and the high expression of CPSF6 was associated with poor prognosis in patients. Overexpression of CPSF6 promoted proliferation, migration and invasion of HCC cells in vitro and in vivo. Transcriptome-wide APA profiling analysis indicated that high expression of CPSF6 promoted the favorable usage of the proximal poly(A) site in the 3'UTR of NQO1. We demonstrated CPSF6-induced tumorigenic activities were mediated by the NQO1 isoform with short 3'UTR. Furthermore, we found that CPSF6 induced metabolic alterations in liver cells through NQO1.
conclusionCPSF6 plays a critical role in HCC progression by upregulating NQO1 expression through APA. These findings provide evidence to demonstrate that APA of NQO1 contributes to HCC progression and may have implications for developing new therapeutic strategy against this disease.
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