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TFAP2A facilitates aerobic glycolysis and metastasis of pancreatic cancer via IGF2BP2-mediated LDHA mA modification.

2/5 보강
Pathology, research and practice 📖 저널 OA 0.6% 2021: 0/2 OA 2022: 0/9 OA 2023: 0/9 OA 2024: 0/17 OA 2025: 0/56 OA 2026: 1/65 OA 2021~2026 2026 Vol.280() p. 156387 RNA modifications and cancer
TL;DR It is reported that TFAP2A is upregulated in PC tissues, and elevated TFAP2A expression correlates with poor prognosis in patients, and TFAP2A boosted the viability, invasion, and migration of PC cells in vitro, whereas TFAP2A depletion restrained tumor growth in vivo.
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PubMed DOI OpenAlex Semantic 마지막 보강 2026-04-30
OpenAlex 토픽 · RNA modifications and cancer Peptidase Inhibition and Analysis Cancer, Hypoxia, and Metabolism

Xu Z, Zhong X, Yang Z, Cong Z, Peng L, Zou Q

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It is reported that TFAP2A is upregulated in PC tissues, and elevated TFAP2A expression correlates with poor prognosis in patients, and TFAP2A boosted the viability, invasion, and migration of PC cell

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APA Zhiying Xu, Xingyang Zhong, et al. (2026). TFAP2A facilitates aerobic glycolysis and metastasis of pancreatic cancer via IGF2BP2-mediated LDHA mA modification.. Pathology, research and practice, 280, 156387. https://doi.org/10.1016/j.prp.2026.156387
MLA Zhiying Xu, et al.. "TFAP2A facilitates aerobic glycolysis and metastasis of pancreatic cancer via IGF2BP2-mediated LDHA mA modification.." Pathology, research and practice, vol. 280, 2026, pp. 156387.
PMID 41650847 ↗

Abstract

The hallmark of aerobic glycolysis in cancer progression is well-established, yet its specific role in pancreatic cancer (PC) remains elusive. Here, we reported that TFAP2A is upregulated in PC tissues, and elevated TFAP2A expression correlates with poor prognosis in patients. Functionally, we found that TFAP2A boosted the viability, invasion, and migration of PC cells in vitro, whereas TFAP2A depletion restrained tumor growth in vivo. Moreover, TFAP2A knockdown hindered aerobic glycolysis of PC cells. Further investigation revealed that TFAP2A deletion decreased LDHA expression in PC cells. LDHA overexpression counteracted the impacts of TFAP2A deletion on cell viability, migration, invasion, and aerobic glycolysis. Mechanistically, TFAP2A was directly bound to the promoter of IGF2BP2, upregulating its expression. Additionally, IGF2BP2 was found to bind to the mA site in LDHA mRNA, thereby enhancing its stability. Overall, TFAP2A facilitated aerobic glycolysis and PC progression via IGF2BP2-mediated stabilization of LDHA mRNA, providing novel insights for PC therapy.

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