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FAM162A Promotes Osteosarcoma Progression Via Activating HIF-1α to Enhance Glycolysis
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DOI：10.1002/mc.70112.png)
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Abstract
En 中文
Osteosarcoma (OS) [1] is the most prevalent primary bone cancer and is highly prone to both local invasion and metastasis. FAM162A, a protein implicated in cell growth transformation, is recognized as an oncogene in various cancers. Its role in osteosarcoma, however, remains poorly understood. This study investigates the role of FAM162A in the OS development. We identified that FAM162A was observably upregulated in osteosarcoma and inversely correlated with the prognosis of patients using bioinformatics and immunohistochemical analysis. The CCK-8, colony formation, scratch, and trans-well migration assays were performed to detect the effects of FAM162A on OS cell proliferation and migration. Then we found FAM162A-associated pathways in OS using GO and KEGG analyses and verified and used the downstream factor HIF-1 alpha inhibitor to restore the OS cell proliferation induced by FAM162A overexpression to detect the mechanism of FAM162A in OS. Mechanistically, FAM162A facilitates glycolysis by activating HIF-1 alpha and subsequently PKM2, a critical glycolytic gene, thereby advancing OS progression. These insights elucidated FAM162A's involvement in OS and its impact on glucose metabolism reprogramming, underscoring its potential as a therapeutic target.
Keywords:
FAM162A
glycolysis
HIF1 alpha
osteosarcoma
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