ArticleAnnals of translational medicine2020
Sam68 promotes aerobic glycolysis in colorectal cancer by regulating PKM2 alternative splicing.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 60 citations in OpenAlex.
- CircLAMA5 traps Sam68 in the cytoplasm to regulate alternative splicing and drive sunitinib resistance in ccRCC.Oncogene · 2026Article
- Targeting colorectal cancer and T‑cell metabolism for the treatment of colorectal cancer (Review).Oncology reports · 2026Review
- The glycolysis-H4K12la-PKM2 positive feedback loop drives M2 polarization of macrophages in colorectal cancer.Clinical epigenetics · 2026Article
- [Glycolytic Reprogramming in Lung Adenocarcinoma: Molecular Mechanisms, Metabolic Biomarkers and Targeted Therapeutic Strategies].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Review
- Article
- Alternative Splicing at the Crossroad of Inflammatory Bowel Diseases and Colitis-Associated Colon Cancer.Cancers · 2025Review
- Alternative splicing factor RAB3IP as a novel risk signature to predict the prognosis of colorectal cancer.Journal of Cancer · 2025Article
- Predictive Value of Normalized Lactate Load for Patients with Acute Type A Aortic Dissection: Based on the MIMIC-IV Database.Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia · 2025Article
- Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025Review
- Role of glucose metabolic reprogramming in colorectal cancer progression and drug resistance.Translational oncology · 2024Review
- SHP2 mutations promote glycolysis and inhibit apoptosis via PKM2/hnRNPK signaling in colorectal cancer.iScience · 2024Article
- The ratio of PKM1/PKM2 is the key factor affecting the glucose metabolism and biological function of colorectal cancer cells.Translational cancer research · 2024Article
- The Regulatory Network of hnRNPs Underlying RegulatingBiomolecules · 2024Review
- Sam68 is a druggable vulnerability point in cancer stem cells.Cancer metastasis reviews · 2024Review
- Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024Review
- LINC01852 inhibits the tumorigenesis and chemoresistance in colorectal cancer by suppressing SRSF5-mediated alternative splicing of PKM.Molecular cancer · 2024Article
- Nucleolin promotes tumor growth in colorectal cancer by enhancing hnRNPA1-mediated PKM2 alternative splicing.Genes & diseases · 2023Article
- Targeted splicing therapy: new strategies for colorectal cancer.Frontiers in oncology · 2023Review
- LNCAROD enhances hepatocellular carcinoma malignancy by activating glycolysis through induction of pyruvate kinase isoform PKM2.Journal of experimental & clinical cancer research : CR · 2021Article
- CD44 alternative splicing senses intragenic DNA methylation in tumors via direct and indirect mechanisms.Nucleic acids research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSam68, an RNA-binding protein, exerts oncogenic functions in several types of cancer. However, the specific functions and mechanisms of Sam68 in colorectal cancer (CRC) had not been previously clarified. Pyruvate kinase muscle (PKM)2 is the key rate-limiting enzyme in glycolysis, and PKM2 maintains the glycolysis-dominant energy metabolism in most cancer cells.
methodsCCK8 assay was performed to show the effect of Sam68 on cell growth. Pyruvate kinase activity and lactate detection assays were performed to analyze the effects of Sam68 on aerobic glycolysis. RNA immunoprecipitation (RIP) was used to detect the binding of Sam68 to the
resultsGain-of-function and loss-of-function studies showed that ectopic expression of Sam68 promoted glycolysis and cell proliferation in CRC cells, whereas Sam68 knockdown inhibited glycolysis and cell proliferation. Mechanically, Sam68 modulated the expression profile of pyruvate kinase (PKM2 or PKM1) by regulating its alternative splicing. Overexpression of Sam68 was associated with decreased
conclusionsThese findings suggested that Sam68 affected cell growth and glycolysis pathway by regulating the alternative splicing and expression of PKM2 in CRC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.