Evidence map›Paper›PMID 32767829›Full record

ArticleCancer science2020

DRP1 promotes lactate utilization in KRAS-mutant non-small-cell lung cancer cells.

Mangze Hu, Yu Zhao, Yuejiao Cao, Qianru Tang, Ziqin Feng, Jun Ni, Xiaorong Zhou

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. [Advances in Lactate Metabolic Reprogramming in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026
    Review
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  17. The effects of freshFrontiers in pharmacology · 2022
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  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Mangze HuDepartment of Immunology, School of Medicine, Nantong University, Nantong, China.
Yu ZhaoDepartment of Immunology, School of Medicine, Nantong University, Nantong, China.
Yuejiao CaoDepartment of Rehabilitation, The Affiliated Hospital of Nantong University, Nantong, China.
Qianru TangDepartment of Immunology, School of Medicine, Nantong University, Nantong, China.
Ziqin FengDepartment of Immunology, School of Medicine, Nantong University, Nantong, China.
Jun NiDepartment of Rehabilitation, The Affiliated Hospital of Nantong University, Nantong, China.
Xiaorong ZhouDepartment of Immunology, School of Medicine, Nantong University, Nantong, China.ORCID https://orcid.org/0000-0002-6120-7318
Nantong University · CNFujian Medical University · CN

Funding

Jiangsu Key Foundation of Social Development BE2018670Jiangsu Six Elite Units Foundation WSW-058Nantong Science and technology project XG202008-5National Natural Science Foundation of China 81771681
6 · The paper itself

Abstract

Metabolic alterations are well documented in various cancers. Non-small-cell lung cancers (NSCLCs) preferentially use lactate as the primary carbon source, but the underlying mechanisms are not well understood. We developed a lactate-dependent cell proliferation assay and found that dynamin-related protein (DRP1), which is highly expressed in KRAS-mutant NSCLC, is required for tumor cells to proliferate and uses lactate as fuel, demonstrating the critical role of DRP1 in the metabolic reprogramming of NSCLC. Metabolic and transcriptional profiling suggests that DRP1 orchestrates a supportive metabolic network to promote lactate utilization and redox homeostasis in lung cancer cells. DRP1 suppresses the production of reactive oxygen species (ROS) and protects cells against oxidative damage by enhancing lactate utilization. Moreover, targeting DRP1 not only reduces HSP90 expression but also enhances ROS-induced HSP90 cleavage, thus inhibiting activation of mitogen activated protein kinase and PI3K pathways and leading to suppressed lactate utilization and increased ROS-induced cell death. Taken together, these results suggest that DRP1 is a crucial regulator of lactate metabolism and redox homeostasis in KRAS-mutant lung cancer, and that targeting lactate utilization by modulating DRP1 activity might be an effective treatment for lung cancer.

Indexed as

A549 CellsApoptosisCarcinoma, Non-Small-Cell LungCell DeathCell Line, TumorCell ProliferationDynaminsGene Expression Regulation, NeoplasticHumansLactic AcidLung NeoplasmsMitogen-Activated Protein KinasesMutationOxidation-ReductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)DNM1L protein, humanDynaminsKRAS protein, humanLactic AcidMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)Reactive Oxygen Speciescancer metabolismDRP1KRAS mutationlactatelung cancer

Identifiers

PMID32767829
PMCPMC7540982
OpenAlexW3047724530

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.