Evidence map›Paper›PMID 36867943›Full record

ArticleRedox biology2023

Hyperoxia induces glucose metabolism reprogramming and intracellular acidification by suppressing MYC/MCT1 axis in lung cancer.

Xiucheng Liu, Hao Qin, Li Zhang, Caili Jia, Zhixiang Chao, Xichun Qin, Hao Zhang, Chang Chen

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Redox biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  6. The Warburg Effect and Aerobic Glycolysis in Tumors.Cancer treatment and research · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Function of antigen-presenting cells in non-small-cell lung cancer (NSCLC).Medical oncology (Northwood, London, England) · 2025
    Review
  11. Article
  12. Article
  13. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Xiucheng LiuDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China; Thoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, Jiangsu, 221006, China.
Hao QinThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, Jiangsu, 221006, China; Department of Thoracic Surgery, Affiliated Hospital of Xuzhou Medical University, 99 West Huaihai Road, Xuzhou, 221006, Jiangsu, China.
Li ZhangThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, Jiangsu, 221006, China.
Caili JiaThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, Jiangsu, 221006, China.
Zhixiang ChaoThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, Jiangsu, 221006, China.
Xichun QinThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, Jiangsu, 221006, China.
Hao ZhangThoracic Surgery Laboratory, Xuzhou Medical University, Xuzhou, Jiangsu, 221006, China; Department of Thoracic Surgery, Affiliated Hospital of Xuzhou Medical University, 99 West Huaihai Road, Xuzhou, 221006, Jiangsu, China. Electronic address: zhanghao@xzhmu.edu.cn.
Chang ChenDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, 200433, China; Shanghai Engineering Research Center of Lung Transplantation, Shanghai, China. Electronic address: chenthoracic@163.com.
Xuzhou Medical College · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The perils and promises of inspiratory hyperoxia (IH) in oncology are still controversial, especially for patients with lung cancer. Increasing evidence shows that hyperoxia exposure is relevant to the tumor microenvironment. However, the detailed role of IH on the acid-base homeostasis of lung cancer cells remains unclear. In this study, the effects of 60% oxygen exposure on intra- and extracellular pH were systematically evaluated in H1299 and A549 cells. Our data indicate that hyperoxia exposure reduces intracellular pH, which might be expected to reduce the proliferation, invasion, and epithelial-to-mesenchymal transition of lung cancer cells. RNA sequencing, Western blot, and PCR analysis reveal that monocarboxylate transporter 1 (MCT1) mediates intracellular lactate accumulation and intracellular acidification of H1299 and A549 cells at 60% oxygen exposure. In vivo studies further demonstrate that MCT1 knockdown dramatically reduces lung cancer growth, invasion, and metastasis. The results of luciferase and ChIP-qPCR assays further confirm that MYC is a transcription factor of MCT1, and PCR and Western blot assays confirm that MYC is downregulated under hyperoxic conditions. Collectively, our data reveal that hyperoxia can suppress the MYC/MCT1 axis and cause the accumulation of lactate and intracellular acidification, thereby retarding tumor growth and metastasis.

Indexed as

HyperoxiaLung NeoplasmsSymportersCell Line, TumorGlucoseHumansHydrogen-Ion ConcentrationLactic AcidOxygenTumor MicroenvironmentGlucoseLactic AcidOxygenSymportersAcid-base hemostasisInspiratory hyperoxiaLung cancerMonocarboxylate transporter 1

Identifiers

PMID36867943
PMCPMC10011425
OpenAlexW4322505023

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.