Evidence map›Paper›PMID 40651179›Full record

ArticleTranslational oncology2025

Mitochondrial apoptosis induced by MNAT1 in laryngeal squamous cell carcinoma cells reverses drug resistance.

Ran An, Fan Yang, Yujian Teng, Yan Guo, Rui Zhao, Jing Cao, Yaohui Liu, Yue Wang, Pengyan Liu, Ming Liu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

  1. Review
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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

11 authors.

Ran AnDepartment of Otorhinolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Fan YangDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Yujian TengDepartment of Otorhinolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Yan GuoDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Rui ZhaoDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Jing CaoDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Yaohui LiuDepartment of Otorhinolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Yue WangDepartment of Otorhinolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Pengyan LiuDepartment of Otorhinolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Ming LiuDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China. Electronic address: liumingorg@163.com.
Linli TianDepartment of Otorhinolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, 150086, China. Electronic address: tianlinli78@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLaryngeal squamous cell carcinoma (LSCC), the predominant histological subtype of laryngeal cancer with a poor diagnosis, requires further exploration of its molecular mechanisms and potential therapeutic targets.

methodsThe expression of MNAT1 in LSCC was detected by western blotting and IHC. EDU analysis, colony formation assay, scratch assay, transwell assay and flow cytometry were used to detect cell proliferation, migration, invasion and apoptosis. The downstream genes of MNAT1 were predicted by RNA-seq. The interaction between MNAT1 and GDF15 was verified by Co-immunoprecipitation assay. The effect of MNAT1 on mitochondrial activity in LSCC cells was determined by ROS, JC-1, and lysosomal mitochondrial activity. The effect of MNAT1 and GDF15 on tumor growth of drug-resistant cells was evaluated in vivo.

resultsMNAT1 was highly expressed in LSCC tissues. After MNAT1-knockdown, the proliferation, migration and invasion of LSCC cells were inhibited, the level of apoptosis was significantly increased, and the resistance to cisplatin was decreased. MNAT1 interacts with GDF15. MNAT1 affects cell proliferation, migration and invasion through GDF15, and further affects mitochondrial apoptosis through AMPK pathway. In addition, MNAT1-knockdown and GDF15-knockdown reduced the tumor growth rate and enhanced the sensitivity of cisplatin in vivo.

conclusionsMNAT1 promoted GDF15-mediated changes in AMPK pathway to affect mitochondrial apoptosis, which reveals the progression of LSCC and the mechanism of chemotherapy resistance, providing a new understanding of the mechanism of mitochondrial apoptosis and chemotherapy resistance in LSCC.

Indexed as

AMPKCisplatin resistanceGDF15Mitochondrial apoptosisMNAT1

Identifiers

PMID40651179
PMCPMC12274886

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