| Title: |
Glypican-3 knockdown inhibits the cell growth, stemness, and glycolysis development of hepatocellular carcinoma cells under hypoxic microenvironment through lactylation. |
| Authors: |
Yao, Gebing1 (AUTHOR), Yang, Zihua1 (AUTHOR) dryangzihua@hotmail.com |
| Source: |
Archives of Physiology & Biochemistry. Oct2024, Vol. 130 Issue 5, p546-554. 9p. |
| Subject Terms: |
*HEPATOCELLULAR carcinoma, *PROTEIN stability, *GENE expression, *POLYMERASE chain reaction, *PROTEIN expression |
| Abstract: |
Context: Hepatocellular carcinoma (HCC) is a common malignant tumour in China. Glypican-3 (GPC3) is reported to be closely related to the occurrence and development of various tumours. Objective: This study aimed to explore the role of GPC3 in HCC. Materials and methods: The cell behaviours were investigated using Cell Counting Kit-8 (CCK-8), Traswell, and sphere formation assays. The protein and mRNA expression levels were detected using western blot and Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR) assays. Results: The results showed that GPC3 knockdown decreased the cell viability and stemness, glucose uptake, lactate production, and extracellular acidification rate (ECAR), while increased the oxygen consumption rate (OCR) in hypoxia-treated HCC cells. Additionally, GPC3 knockdown decreased the global lactylation and c-myc lactylation, which further decreased the protein stability and expressions of c-myc. Discussion and conclusion: GPC3-mediated lactylation modification may be a new direction in HCC treatment in the future. [ABSTRACT FROM AUTHOR] |
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