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pmid:37215982

Increased methylation of ZNF671 suppresses tumor progression by promoting MAPK6 transcription in laryngeal carcinoma.

Wei Zhang · Ting Liu · Xinyi Li · Tianshu Li · Xiangchi Ma · Dongxu Zhao · Xudong Zhao

International journal of biological sciences · 2023 doi:10.7150/ijbs.82692

Paper

complete

Experiment

partial

Data

partial

Analysis

partial

Execution

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title
Increased methylation of ZNF671 suppresses tumor progression by promoting MAPK6 transcription in laryngeal carcinoma.
doi
10.7150/ijbs.82692
pmid
37215982
authors array · 7 items
[0]
Wei Zhang
[1]
Ting Liu
[2]
Xinyi Li
[3]
Tianshu Li
[4]
Xiangchi Ma
[5]
Dongxu Zhao
[6]
Xudong Zhao
journal
International journal of biological sciences
year
2023
abstract
Background: Laryngeal squamous cell carcinoma (LSCC) is a malignant tumor of the head and neck, the exact mechanism of which has not been explored. Methods: By analyzing the GEO data, we found the highly methylated and low expression gene ZNF671. The expression level of ZNF671 in clinical samples was verified by RT-PCR, western blotting and methylation-specific PCR. The function of ZNF671 in LSCC was detected by cell culture and transfection, MTT, Edu, TUNEL assays and flow cytometry analysis. The binding sites of ZNF671 to MAPK6 promoter region were detected and verified by luciferase reporter gene and chromatin immunoprecipitation. Finally, the effect of ZNF671 on LSCC tumors was tested in vivo. Results: In this study, by analyzing GEO data GSE178218 and GSE59102, we found that zinc finger protein (ZNF671) expression was decreased, and DNA methylation level was increased in laryngeal cancer. Moreover, the abnormal expression of ZNF671 was associated with poor survival prognosis of patients. In addition, we found that overexpression of ZNF671 could inhibit the viability, proliferation, migration and invasion of LSCC cells, while promoting cell apoptosis. In contrast, the opposite effects were observed after knockdown of ZNF671. Through the prediction website and chromatin immunoprecipitation and luciferase reporter experiments, it was found that ZNF671 could bind to the promoter region of MAPK6, thereby inhibiting the expression of MPAK6. In vivo experiments confirmed that overexpression of ZNF671 could inhibit tumor growth. Conclusion: Our study found that ZNF671 expression was down-regulated in LSCC. ZNF671 up-regulates the expression of MAPK6 by binding to its promoter region, thus participating in cell proliferation, migration and invasion in LSCC. Our study may provide new ideas for early prediction and treatment of LSCC.
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DNA methylation analysis of laryngeal squamous cell carcinoma
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HOX genes: potential candidates furthering the development of larynx squamous cell carcinoma.
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in clinical samples was verified by RT-PCR, western blotting and methylation-specific PCR. The function o
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671 in LSCC was detected by cell culture and transfection, MTT, Edu, TUNEL assays and flow cytometry a
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invasion of LSCC cells, while promoting cell apoptosis. In contrast, the opposite effects were obse
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and transfection, MTT, Edu, TUNEL assays and flow cytometry analysis. The binding sites of ZNF671 to MAP
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e effect of ZNF671 on LSCC tumors was tested in vivo. Results: In this study, by analyzing GEO da
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:37215982", "kind": "science-record", "revision": 4, "content_hash": "sha256:5484ada24bf10ecfbd1c7eccec254d41b302e85cfe2112d449dade5d39d08371", "created_at": "2026-11-01T19:01:55Z", "updated_at": "2026-11-01T22:51:58Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Increased methylation of ZNF671 suppresses tumor progression by promoting MAPK6 transcription in laryngeal carcinoma.", "doi": "10.7150/ijbs.82692", "pmid": "37215982", "authors": ["Wei Zhang", "Ting Liu", "Xinyi Li", "Tianshu Li", "Xiangchi Ma", "Dongxu Zhao", "Xudong Zhao"], "journal": "International journal of biological sciences", "year": 2023, "abstract": "Background: Laryngeal squamous cell carcinoma (LSCC) is a malignant tumor of the head and neck, the exact mechanism of which has not been explored. Methods: By analyzing the GEO data, we found the highly methylated and low expression gene ZNF671. The expression level of ZNF671 in clinical samples was verified by RT-PCR, western blotting and methylation-specific PCR. The function of ZNF671 in LSCC was detected by cell culture and transfection, MTT, Edu, TUNEL assays and flow cytometry analysis. The binding sites of ZNF671 to MAPK6 promoter region were detected and verified by luciferase reporter gene and chromatin immunoprecipitation. Finally, the effect of ZNF671 on LSCC tumors was tested in vivo. Results: In this study, by analyzing GEO data GSE178218 and GSE59102, we found that zinc finger protein (ZNF671) expression was decreased, and DNA methylation level was increased in laryngeal cancer. Moreover, the abnormal expression of ZNF671 was associated with poor survival prognosis of patients. In addition, we found that overexpression of ZNF671 could inhibit the viability, proliferation, migration and invasion of LSCC cells, while promoting cell apoptosis. In contrast, the opposite effects were observed after knockdown of ZNF671. Through the prediction website and chromatin immunoprecipitation and luciferase reporter experiments, it was found that ZNF671 could bind to the promoter region of MAPK6, thereby inhibiting the expression of MPAK6. In vivo experiments confirmed that overexpression of ZNF671 could inhibit tumor growth. Conclusion: Our study found that ZNF671 expression was down-regulated in LSCC. ZNF671 up-regulates the expression of MAPK6 by binding to its promoter region, thus participating in cell proliferation, migration and invasion in LSCC. 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