Evidence map›Paper›PMID 42763310›Full record

ArticleBritish journal of cancer2026

PAX9 activates autophagy through a transcription-dependent mechanism, promoting EGFR degradation to restrict cell survival in oral cancer.

Chandra Sekhar Bhol, Rakesh Kumar Kar, Soumya Ranjan Mishra, Priyadarshini Mishra, Kewal Kumar Mahapatra, Xi Zhang, Samir Kumar Patra, Shankargouda Patil, Gautam Sethi, Daniel J Klionsky and 3 more

Abstract read
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In one paragraph

Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

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4 · The record

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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

13 authors.

Chandra Sekhar BholCancer and Cell Death Laboratory, Department of Life Science, National Institute of Technology Rourkela, Sundergarh, India.
Rakesh Kumar KarCancer and Cell Death Laboratory, Department of Life Science, National Institute of Technology Rourkela, Sundergarh, India.
Soumya Ranjan MishraCancer and Cell Death Laboratory, Department of Life Science, National Institute of Technology Rourkela, Sundergarh, India.
Priyadarshini MishraCancer and Cell Death Laboratory, Department of Life Science, National Institute of Technology Rourkela, Sundergarh, India.
Kewal Kumar MahapatraCancer and Cell Death Laboratory, Department of Life Science, National Institute of Technology Rourkela, Sundergarh, India.
Xi ZhangInstitute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, PR China.
Samir Kumar PatraEpigenetics and Cancer Research Laboratory, Department of Life Science, National Institute of Technology Rourkela, Sundergarh, India.ORCID http://orcid.org/0000-0001-5641-1835
Shankargouda PatilCollege of Dental Medicine, Roseman University of Health Sciences, South Jordan, UT, USA.
Gautam SethiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0002-8677-8475
Daniel J KlionskyLife Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0002-7828-8118
Peter E LobieInstitute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, PR China.ORCID http://orcid.org/0000-0002-8445-184X
Vijay PandeyInstitute of Biopharmaceutical and Health Engineering, Tsinghua Shenzhen International Graduate School, Tsinghua University, Shenzhen, PR China.ORCID http://orcid.org/0000-0001-8704-0694
Sujit Kumar BhutiaCancer and Cell Death Laboratory, Department of Life Science, National Institute of Technology Rourkela, Sundergarh, India. sujitb@nitrkl.ac.in.ORCID http://orcid.org/0000-0003-0962-3354

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPAX9 (paired box 9) gene, a transcription factor belonging to the PAX family, is associated with craniofacial development. Dysregulation of PAX9 is associated with oral squamous cell carcinoma (OSCC), and its functional regulation in OSCC remains unknown.

methodsPAX9 expression was evaluated in human OSCC tissues and a DMBA-induced hamster oral carcinogenesis model, and its functional role in cell death and autophagy was assessed using PAX9 overexpression and PAX9 mutants in OSCC. Autophagy, lysosomal activity, apoptosis, EGFR degradation, and chemosensitivity were analysed in vitro and in an OSCC xenograft model.

resultsOverexpression of PAX9 activated autophagy and enhanced lysosomal function through a transcription-dependent mechanism, thereby inducing apoptosis in OSCC. Mutations at L27P and I29T in PAX9 blocked autophagy and restored cell viability in OSCC. Interestingly, PAX9 was shown to activate lethal autophagy, which degrades EGFR, thereby inducing cell death and chemosensitisation in OSCC. Moreover, PAX9 expression decreased in higher-grade human oral cancers and in DMBA-induced hamster oral carcinogenesis, and in vitro exposure to carcinogens reduced PAX9 while increasing DNMT1, suggesting that DNA methylation may regulate PAX9 during oral carcinogenesis.

conclusionPAX9 activates lethal autophagy, promoting EGFR degradation and apoptosis in OSCC, highlighting its tumour-suppressive potential and therapeutic relevance.

Identifiers

PMID42763310

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