Evidence map›Paper›PMID 36139430›Full record

ArticleCells2022

MYH9 Facilitates Cell Invasion and Radioresistance in Head and Neck Cancer via Modulation of Cellular ROS Levels by Activating the MAPK-Nrf2-GCLC Pathway.

Guo-Rung You, Joseph T Chang, Yan-Liang Li, Chi-Wei Huang, Yu-Liang Tsai, Kang-Hsing Fan, Chung-Jan Kang, Shiang-Fu Huang, Po-Hung Chang, Ann-Joy Cheng

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 37 citations in OpenAlex.

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  17. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
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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

10 authors at 2 institutions in 1 country.

Guo-Rung YouDepartment of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Joseph T ChangDepartment of Radiation Oncology, Chang Gung Memorial Hospital-Linkou, Taoyuan 33305, Taiwan.
Yan-Liang LiDepartment of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Chi-Wei HuangDepartment of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Yu-Liang TsaiDepartment of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Kang-Hsing FanDepartment of Radiation Oncology, Chang Gung Memorial Hospital-Linkou, Taoyuan 33305, Taiwan.
Chung-Jan KangSchool of Medicine, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Shiang-Fu HuangSchool of Medicine, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Po-Hung ChangDepartment of Otorhinolaryngology, Chang Gung Memorial Hospital-LinKou, Taoyuan 33305, Taiwan.
Ann-Joy ChengDepartment of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.ORCID 0000-0002-1317-0725
Chang Gung University · TWChang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The MYH9 (Myosin heavy chain 9), an architecture component of the actomyosin cytoskeleton, has been reported to be dysregulated in several types of cancers. However, how this molecule contributes to cancer development is still obscure. This study deciphered the molecular function of MYH9 in head and neck cancer (HNC). Cellular methods included clonogenic survival, wound-healing migration, and Matrigel invasion assays. Molecular techniques included RT-qPCR, western blot, luciferase reporter assays, and flow cytometry. Clinical association studies were undertaken by TCGA data mining, Spearman correlation, and Kaplan-Meier survival analysis. We found that MYH9 was overexpressed in tumors and associated with poor prognosis in HNC patients. MYH9 promoted cell motility along with the modulation of the extracellular matrix (fibronectin, ITGA6, fascin, vimentin, MMPs). Also, MYH9 contributed to radioresistance and was related to the expression of anti-apoptotic and DNA repairing molecules (XIAP, MCL1, BCL2L1, ATM, RAD50, and NBN). Mechanically, MYH9 suppressed cellular ROS levels, which were achieved by activating the pan-MAPK signaling molecules (Erk, p38, and JNK), the induction of Nrf2 transcriptional activity, and the up-regulation of antioxidant enzymes (GCLC, GCLM, GPX2). The antioxidant enzyme GCLC was further demonstrated to facilitate cell invasion and radioresistance in HNC cells. Thus, MYH9 exerts malignant functions in HNC by regulating cellular ROS levels via activating the MAPK-Nrf2-GCLC signaling pathway. As MYH9 contributes to radioresistance and metastasis, this molecule may serve as a prognostic biomarker for clinical application. Furthermore, an in vivo study is emergent to support the therapeutic potential of targeting MYH9 to better manage refractory cancers.

Indexed as

Head and Neck NeoplasmsMyosin Heavy ChainsNF-E2-Related Factor 2ActomyosinAntioxidantsBiomarkersFibronectinsGlutamate-Cysteine LigaseHumansMyeloid Cell Leukemia Sequence 1 ProteinReactive Oxygen SpeciesVimentinActomyosinAntioxidantsBiomarkersFibronectinsGCLC protein, humanGlutamate-Cysteine LigaseMyeloid Cell Leukemia Sequence 1 ProteinMYH9 protein, humanMyosin Heavy ChainsNF-E2-Related Factor 2Reactive Oxygen SpeciesVimentincell invasionGCLChead and neck cancerMAPK signaling pathwayMYH9Nrf2prognosisradioresistancereactive oxygen species

Identifiers

PMID36139430
PMCPMC9497050
OpenAlexW4295845728

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.