Kim, Hyunju Kim, Seong Ho Hwang, Dohyeon An, Jinsu Chung, Hak Suk Yang, Eun Gyeong Kim, So Yeon 2024-01-19T18:00:42Z 2024-01-19T18:00:42Z 2021-09-05 2020-04 0829-8211 https://pubs.kist.re.kr/handle/201004/118799 Extensive studies have been reported the non-canonical functions of pyruvate kinase M2 (PKM2) as a kinase, transcriptional regulator, and even cell-to-cell communicator, emphasizing its importance in various signaling pathways. However, the role of secreted PKM2 in cancer progression and its signaling pathway is yet to be elucidated. In this study, we found that extracellular PKM2 enhanced the migration of low-metastatic, benign colon cancer cells by upregulating claudin-1 expression and internalizing it to the cytoplasm and nucleus. Knock-down of claudin-1 significantly reduced extracellular PKM2-induced cell migration. Inhibition of either protein kinase C (PKC) or epidermal growth factor receptor (EGFR) resulted in a reduction of extracellular PKM2-mediated claudin-1 expression, suggesting EGFR-PKC-claudin-1 as a signaling pathway in the extracellular PKM2-mediated tumorigenesis of colon cancer cells. English CANADIAN SCIENCE PUBLISHING Extracellular pyruvate kinase M2 facilitates cell migration by upregulating claudin-1 expression in colon cancer cells Article 10.1139/bcb-2019-0139 1 BIOCHEMISTRY AND CELL BIOLOGY, v.98, no.2, pp.219 - 226 BIOCHEMISTRY AND CELL BIOLOGY 98 2 219 226 N scie scopus 000525369100017 2-s2.0-85083003449 Biochemistry & Molecular Biology Cell Biology Biochemistry & Molecular Biology Cell Biology Article GENE-TRANSCRIPTION PROTEIN PROMOTES PATHWAY OVEREXPRESSION TUMORIGENESIS CONTRIBUTES MELANOMA MARKER PKC extracellular PKM2 claudin-1 EGFR PKC cell migration colon cancer