Evidence map›Paper›PMID 39891222›Full record

ArticleCancer cell international2025

MTMR6 downregulation contributes to cisplatin resistance in oral squamous cell carcinoma.

Kah Young Lee, Su Young Oh, Heon-Jin Lee, Tae-Geon Kwon, Jin-Wook Kim, Chang-Geol Shin, Su-Hyung Hong, So-Young Choi

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Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 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

8 authors.

Kah Young LeeDepartment of Microbiology and Immunology, School of Dentistry, Kyungpook National University, Daegu, South Korea.
Su Young OhDepartment of Microbiology and Immunology, School of Dentistry, Kyungpook National University, Daegu, South Korea.
Heon-Jin LeeDepartment of Microbiology and Immunology, School of Dentistry, Kyungpook National University, Daegu, South Korea.
Tae-Geon KwonDepartment of Oral and Maxillofacial Surgery, School of Dentistry, Kyungpook National University, Daegu, South Korea.
Jin-Wook KimDepartment of Oral and Maxillofacial Surgery, School of Dentistry, Kyungpook National University, Daegu, South Korea.
Chang-Geol ShinDepartment of Oral and Maxillofacial Surgery, School of Dentistry, Kyungpook National University, Daegu, South Korea.
Su-Hyung HongDepartment of Microbiology and Immunology, School of Dentistry, Kyungpook National University, Daegu, South Korea. hongsu@knu.ac.kr.ORCID http://orcid.org/0000-0001-5569-3826
So-Young ChoiDepartment of Oral and Maxillofacial Surgery, School of Dentistry, Kyungpook National University, Daegu, South Korea. dentalchoi@knu.ac.kr.ORCID http://orcid.org/0000-0002-2563-3539

Funding

National Research Foundation of Korea 2021R1A2C4002660National Research Foundation of Korea 2022R1A2C2006728
6 · The paper itself

Abstract

backgroundThe therapeutic effectiveness of cisplatin, a widely used chemotherapy drug for oral squamous cell carcinoma (OSCC), is often compromised by resistance, making it difficult to predict treatment outcomes. The role of myotubularin and myotubularin-related (MTMR) genes in cisplatin resistance remains unclear. We aimed to elucidate the molecular mechanisms underlying MTMR6 with cisplatin resistance in OSCC.

methodsMTMR6 expression was compared between UMSCC1 and cisplatin-resistant UM-Cis cells. Gain- and loss-of-function experiments involving MTMR6 was performed to evaluate its impact on cisplatin resistance. The regulatory role of hsa-miR-544a on MTMR6 expression was explored via antagomir and miRNA mimic assays. The relationship between MTMR6 protein levels and cisplatin sensitivity was assessed in OSCC patient tissues classified as sensitive or resistant to cisplatin monotherapy. A survival analysis based on The Cancer Genome Atlas (TCGA) head and neck squamous cell carcinoma (HNSCC) dataset was performed to evaluate the correlation between MTMR6 expression and patient outcomes following cisplatin treatment. In vivo cisplatin resistance was examined using mouse xenografts derived from MTMR6-knockdown UMSCC1 cells.

resultsMTMR6 expression was markedly reduced in cisplatin-resistant UM-Cis cells compared to UMSCC1 cells. Functional analyses revealed that modulating MTMR6 activity alters cisplatin resistance. A luciferase assay confirmed that hsa-miR-544a regulates MTMR6 gene expression. Additionally, antagomir and miRNA mimics demonstrated that hsa-miR-544a enhances cisplatin resistance by suppressing MTMR6 expression. In OSCC patient tissues, higher MTMR6 protein levels were associated with cisplatin sensitivity, while cisplatin-resistant tissues had lower MTMR6 expression. Survival analysis of the TCGA HNSCC dataset indicated that low MTMR6 expression correlates with poorer outcomes in cisplatin-treated patients compared to those with high MTMR6 expression. Mouse xenografts derived from MTMR6-knockdown UMSCC1 cells exhibited increased resistance to cisplatin compared to controls.

conclusionAssessing mRNA levels of MTMR6 and has-miR-544a in biopsy samples could help predict cisplatin responsiveness in OSCC.

Indexed as

Cisplatin resistanceClinical tissuesHsa-miR-544aMTMR6Oral squamous cell carcinomaOSCC organoid

Identifiers

PMID39891222
PMCPMC11783708

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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.