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. 2025 Sep 10;13:1684892. doi: 10.3389/fcell.2025.1684892

Correction: Crosstalk between hypoxia-inducible factor (HIF) and lncRNAs in digestive tumors: from molecular mechanisms to clinical translation

Lifeng Gan 1,2,3, Peiyue Luo 1,2,3, Junrong Zou 2,3, Wei Li 1,2,3, Qi Chen 1,2,3, Le Cheng 1,2,3, Fangtao Zhang 1,2,3, Haidong Zhong 1,2,3, Yiran Lu 1, Liying Zheng 4,*, Biao Qian 2,3,*
PMCID: PMC12457903  PMID: 41000073

There was a mistake in Figure 1 as published. The oxygen concentration labels for “Normoxia” and “Hypoxia” were inadvertently swapped. The original figure incorrectly labeled: Normoxia as “0.1%–1%” and Hypoxia as “21%”. The corrected Figure 1 appears below.

FIGURE 1.

Diagram illustrating the HIF signaling pathway. On the left, under normoxia (approximately twenty-one percent oxygen), HIF-1α undergoes prolyl hydroxylation, binds to VHL, and degrades. On the right, under hypoxia (approximately 0.1 to one percent oxygen), HIF-1α stabilizes, pairs with HIF-1β, binds to HRE on DNA, and activates hypoxia-responsive genes. Non-coding RNAs, including circRNA, miRNA, and lncRNA, further modulate gene expression, leading to protein translation.

HIF-1α responds to gene transcription under hypoxic activation. VHL: Von Hippel-Lindau; HRE: hypoxia response element; PHD: Prolyl hydroxylase; FIH: Factor-inhibiting HIF.

The original article has been updated.

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