SAM68 promotes tumorigenesis in lung adenocarcinoma by regulating metabolic conversion via PKM alternative splicing
Song Zhu, Weiping Chen, Jizhong Wang, Ling Qi, Hui‐Lin Pan, Zhengfu Feng, Dongbo Tian
Abstract
splicing, contributing to increased oncogene PKM2 isoform formation and inhibition of PKM1 isoform formation. SAM68 is therefore a promising therapeutic target for the treatment of LUAD.
Topics & Concepts
CarcinogenesisPKM2Cancer researchAlternative splicingBiologyAdenocarcinomaMetastasisLung cancerGlycolysisCancerCell biologyMolecular biologyExonPyruvate kinaseMedicineInternal medicineBiochemistryMetabolismGeneGeneticsRNA Research and SplicingRNA modifications and cancerCancer-related molecular mechanisms research