ArticleJournal of physiology and biochemistry2021
FOXA2 inhibits doxorubicin-induced apoptosis via transcriptionally activating HBP rate-limiting enzyme GFPT1 in HCC cells.
Article in Journal of physiology and biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- O-GlcNAcylation: the metabolic-immune translator in tumor evolution and treatment.Molecular medicine (Cambridge, Mass.) · 2026Review
- FOXA2 suppresses ESCC proliferation and metastasis by inhibiting PSMB9 expression, thereby attenuating proteasome activity.Cancer cell international · 2026Article
- FOXA2 in cancer: from fundamental biology to clinical translation.Frontiers in oncology · 2026Review
- Abnormal glycosylation changes in brain tissue of kainic acid-induced epileptic rats.Scientific reports · 2025Article
- GFAT1 promotes the progression of hepatocellular carcinoma via enhancing the O-GlcNAcylation of VEZF1.Cell death & disease · 2025Article
- Exploring the metabolic signaling network of GFPT in cancer.Cell death discovery · 2025Review
- Identifying potential signatures of immune cells in hepatocellular carcinoma using integrative bioinformatics approaches and machine-learning strategies.Immunologic research · 2025Article
- The Prognostic Value and Immunotherapeutic Characteristics of GFPT2 in Pan-cancer.Combinatorial chemistry & high throughput screening · 2025Article
- Unveiling therapeutic targets for spinal stenosis from genetic insights: a Mendelian randomization analysis.Scientific reports · 2024Article
- Regulation of protein O-GlcNAcylation by circadian, metabolic, and cellular signals.The Journal of biological chemistry · 2024Review
- Current knowledge and potential intervention of hexosamine biosynthesis pathway in lung cancer.World journal of surgical oncology · 2023Review
- Article
- TargetingFrontiers in oncology · 2022Review
- O-GlcNAcylation links oncogenic signals and cancer epigenetics.Discover oncology · 2021Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis plays an important role in both carcinogenesis and cancer treatment. Understanding the mechanisms through which resistance to apoptosis occurs in cancer cells has huge implications for cancer treatment. Although pieces of evidence have shown that elevated levels of global O-GlcNAcylation play an anti-apoptotic role in myriad cancers, the underlying mechanism is still ambiguous. In this study, we demonstrated that FOXA2, an essential transcription factor for liver homeostasis and hepatocellular carcinoma (HCC) development, inhibits doxorubicin (DOX)-induced apoptosis through elevating cellular O-GlcNAcylation in HCC cells. In response to DOX treatment, elevated FOXA2 and global O-GlcNAcylation level was observed in HCC cells, and higher FOXA2 levels indicated lower levels of DOX-induced apoptosis. Subsequently, we demonstrated that FOXA2 is a direct transcriptional activator of the hexosamine biosynthetic pathway (HBP) rate-limiting enzyme GFPT1. The upregulation of FOXA2 expression induced the synthesis of intracellular UDP-GlcNAc, which is the sugar substrate of O-GlcNAcylation produced by the HBP. The flux through the HBP elevated the global O-GlcNAcylation level and led to the activation of survival signaling pathways in HCC cells. Furthermore, GFPT1 was proved to be an important downstream regulator of FOXA2-mediated apoptotic suppression. These results provide insights into the molecular mechanism by which FOXA2 inhibits DOX-induced HCC cell apoptosis and suggest that targeting FOXA2 might offer a new strategy for HCC treatment.
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