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CORRECTION article

Front. Cell Dev. Biol., 10 September 2025

Sec. Cancer Cell Biology

Volume 13 - 2025 | https://doi.org/10.3389/fcell.2025.1684892

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

This article is a correction to:

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

    1. Read original article
Lifeng Gan,,Lifeng Gan1,2,3Peiyue Luo,,Peiyue Luo1,2,3Junrong Zou,Junrong Zou2,3Wei Li,,Wei Li1,2,3Qi Chen,,Qi Chen1,2,3Le Cheng,,Le Cheng1,2,3Fangtao Zhang,,Fangtao Zhang1,2,3Haidong Zhong,,Haidong Zhong1,2,3Yiran LuYiran Lu1Liying Zheng Liying Zheng4*Biao Qian, Biao Qian2,3*
  • 1The First Clinical College, Gannan Medical University, Ganzhou, Jiangxi, China
  • 2Department of Urology, The First Affiliated hospital of Gannan Medical University, Ganzhou, Jiangxi, China
  • 3Department of Urology and Andrology, The Key Laboratory of the First Clinical Medical College of Gannan Medical University, Ganzhou, Jiangxi, China
  • 4Department of Graduate, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China

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

by Gan L, Luo P, Zou J, Li W, Chen Q, Cheng L, Zhang F, Zhong H, Lu Y, Zheng L and Qian B (2025). Front. Cell Dev. Biol. 13:1611889. doi: 10.3389/fcell.2025.1611889

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.

Figure 1. 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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Keywords: hypoxia, HIF, lncRNA, digestive system tumors, liver cancer, colorectal cancer, gastric cancer, pancreatic cancer

Citation: Gan L, Luo P, Zou J, Li W, Chen Q, Cheng L, Zhang F, Zhong H, Lu Y, Zheng L and Qian B (2025) Correction: Crosstalk between hypoxia-inducible factor (HIF) and lncRNAs in digestive tumors: from molecular mechanisms to clinical translation. Front. Cell Dev. Biol. 13:1684892. doi: 10.3389/fcell.2025.1684892

Received: 13 August 2025; Accepted: 04 September 2025;
Published: 10 September 2025.

Edited and reviewed by:

Federico Pio Fabrizio, Kore University of Enna, Italy

Copyright © 2025 Gan, Luo, Zou, Li, Chen, Cheng, Zhang, Zhong, Lu, Zheng and Qian. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Liying Zheng, NTEyMTg2NTBAcXEuY29t; Biao Qian, cWIyMDAzXzIwMDBAMTYzLmNvbQ==

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.