---
title: "PAX9 drives lethal autophagy and EGFR degradation to limit survival in oral squamous cell carcinoma"
id: "british-journal-of-cancer-0-pax9-activates-autophagy-through-a-transcription-dependent-mechanism-promoting"
canonical_url: "https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-pax9-activates-autophagy-through-a-transcription-dependent-mechanism-promoting"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03608-6"
published_at: "2026-09-19T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# PAX9 drives lethal autophagy and EGFR degradation to limit survival in oral squamous cell carcinoma
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-pax9-activates-autophagy-through-a-transcription-dependent-mechanism-promoting
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03608-6)
- **Published At:** 2026-09-19T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The transcription factor **PAX9** is implicated in craniofacial development and is dysregulated in oral squamous cell carcinoma (OSCC). - The study evaluated **PAX9** expression in human OSCC samples and a DMBA-induced hamster oral carcinogenesis model. - Functional experiments used PAX9 overexpression and PAX9 point mutants (L27P, I29T) in OSCC cell models to test effects on cell death, autophagy, lysosomal activity, apoptosis, EGFR degradation, and chemosensitivity. - Overexpression of **PAX9** activated autophagy, increased lysosomal function and autophagosome-lysosome fusion, and induced autophagic flux in OSCC cells. - Activation of autophagy by **PAX9** occurred via a transcription-dependent mechanism; specific transcriptional targets were not detailed in the preview. - PAX9-driven autophagy was described as “lethal autophagy” because it promoted apoptosis and reduced cell viability. - **PAX9** triggered degradation of **EGFR** through autophagy, linking autophagic activation to downregulation of a key survival receptor in OSCC. - Mutations L27P and I29T in **PAX9** prevented autophagy activation and restored cell viability, indicating these residues are functionally important for the autophagy-inducing activity. - In vitro exposure to carcinogens decreased **PAX9** expression and increased DNMT1, suggesting epigenetic (DNA methylation) regulation of **PAX9** during oral carcinogenesis. - **PAX9** expression was lower in higher-grade human oral cancers and in the DMBA hamster model, consistent with tumour-suppressive potential. - In xenograft experiments, **PAX9** overexpression enhanced cisplatin sensitivity and inhibited tumour growth in nude mice, supporting therapeutic relevance. - Data supporting the study are available from the corresponding author upon reasonable request; some data may be restricted for privacy or ethical reasons. - Figures in the article document increased expression of autophagy-related genes, lysosomal activation, autophagic flux, EGFR downregulation, apoptosis and reduced orosphere formation, lethal autophagy, cisplatin sensitisation and reduced tumour growth, and decreased PAX9 in OSCC samples and models.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [british journal of cancer](https://www.nature.com/bjc) 3. [articles](https://www.nature.com/bjc/articles?type=article) 4. article * Article * Published: 19 September 2026 Cellular and Molecular Biology # PAX9 activates autophagy through a transcription-dependent mechanism, promoting EGFR degradation to restrict cell survival in oral cancer * [Chandra Sekhar Bhol](https://www.nature.com/articles/s41416-026-03608-6#auth-Chandra_Sekhar-Bhol-Aff1-Aff2)[1](https://www.nature.com/articles/s41416-026-03608-6#Aff1),[2](https://www.nature.com/articles/s41416-026-03608-6#Aff2), * [Rakesh Kumar Kar](https://www.nature.com/articles/s41416-026-03608-6#auth-Rakesh_Kumar-Kar-Aff1)[1](https://www.nature.com/articles/s41416-026-03608-6#Aff1), * [Soumya Ranjan Mishra](https://www.nature.com/articles/s41416-026-03608-6#auth-Soumya_Ranjan-Mishra-Aff1)[1](https://www.nature.com/articles/s41416-026-03608-6#Aff1), * [Priyadarshini Mishra](https://www.nature.com/articles/s41416-026-03608-6#auth-Priyadarshini-Mishra-Aff1)[1](https://www.nature.com/articles/s41416-026-03608-6#Aff1), * [Kewal Kumar Mahapatra](https://www.nature.com/articles/s41416-026-03608-6#auth-Kewal_Kumar-Mahapatra-Aff1-Aff3)[1](https://www.nature.com/articles/s41416-026-03608-6#Aff1),[3](https://www.nature.com/articles/s41416-026-03608-6#Aff3), * [Xi Zhang](https://www.nature.com/articles/s41416-026-03608-6#auth-Xi-Zhang-Aff4)[4](https://www.nature.com/articles/s41416-026-03608-6#Aff4), * [Samir Kumar Patra](https://www.nature.com/articles/s41416-026-03608-6#auth-Samir_Kumar-Patra-Aff5) [ORCID: orcid.org/0000-0001-5641-1835](https://orcid.org/0000-0001-5641-1835)[5](https://www.nature.com/articles/s41416-026-03608-6#Aff5), * [Shankargouda Patil](https://www.nature.com/articles/s41416-026-03608-6#auth-Shankargouda-Patil-Aff6)[6](https://www.nature.com/articles/s41416-026-03608-6#Aff6), * [Gautam Sethi](https://www.nature.com/articles/s41416-026-03608-6#auth-Gautam-Sethi-Aff2) [ORCID: orcid.org/0000-0002-8677-8475](https://orcid.org/0000-0002-8677-8475)[2](https://www.nature.com/articles/s41416-026-03608-6#Aff2), * [Daniel J. Klionsky](https://www.nature.com/articles/s41416-026-03608-6#auth-Daniel_J_-Klionsky-Aff7) [ORCID: orcid.org/0000-0002-7828-8118](https://orcid.org/0000-0002-7828-8118)[7](https://www.nature.com/articles/s41416-026-03608-6#Aff7), * [Peter E. Lobie](https://www.nature.com/articles/s41416-026-03608-6#auth-Peter_E_-Lobie-Aff4) [ORCID: orcid.org/0000-0002-8445-184X](https://orcid.org/0000-0002-8445-184X)[4](https://www.nature.com/articles/s41416-026-03608-6#Aff4), * [Vijay Pandey](https://www.nature.com/articles/s41416-026-03608-6#auth-Vijay-Pandey-Aff4-Aff8) [ORCID: orcid.org/0000-0001-8704-0694](https://orcid.org/0000-0001-8704-0694)[4](https://www.nature.com/articles/s41416-026-03608-6#Aff4),[8](https://www.nature.com/articles/s41416-026-03608-6#Aff8) & * … * [Sujit Kumar Bhutia](https://www.nature.com/articles/s41416-026-03608-6#auth-Sujit_Kumar-Bhutia-Aff1) [ORCID: orcid.org/0000-0003-0962-3354](https://orcid.org/0000-0003-0962-3354)[1](https://www.nature.com/articles/s41416-026-03608-6#Aff1) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03608-6#citeas) [ Save article ](https://www.nature.com/articles/s41416-026-03608-6/save-research?_csrf=64WuPU3ZTDaRNLW-aqmLWn76DkF9jRcN) [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background _PAX9_ (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. ### Methods PAX9 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. ### Results Overexpression 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. ### Conclusion PAX9 activates lethal autophagy, promoting EGFR degradation and apoptosis in OSCC, highlighting its tumour-suppressive potential and therapeutic relevance. This is a preview of subscription content, [access via your institution](https://wayf.springernature.com?redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41416-026-03608-6) ## Access options [ Access through your institution ](https://wayf.springernature.com?redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41416-026-03608-6) Subscribe to this journal Receive 24 print issues and online access 251,40 € per year only 10,48 € per issue [Learn more](https://www.nature.com/bjc/subscribe) Buy this article * Purchase on SpringerLink * Instant access to the full article PDF. 39,95 € Prices may be subject to local taxes which are calculated during checkout ### Additional access options: * [Log in](https://idp.nature.com/authorize/natureuser?client_id=grover&redirect_uri=https%3A%2F%2Fwww.nature.com%2Farticles%2Fs41416-026-03608-6) * [Learn about institutional subscriptions](https://www.springernature.com/gp/librarians/licensing/license-options) * [Read our FAQs](https://support.nature.com/en/support/home) * [Contact customer support](https://www.springernature.com/gp/contact) **Fig. 1: PAX9 enhances the expression of autophagy-related genes and associated signalling pathways in OSCC.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03608-6/MediaObjects/41416_2026_3608_Fig1_HTML.png) **Fig. 2: PAX9 overexpression induces lysosomal activity and autophagosome-lysosome fusion in OSCC.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03608-6/MediaObjects/41416_2026_3608_Fig2_HTML.png) **Fig. 3: PAX9 overexpression induces autophagic flux in OSCC.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03608-6/MediaObjects/41416_2026_3608_Fig3_HTML.png) **Fig. 4: PAX9 downregulates the EGFR level through autophagy in OSCC.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03608-6/MediaObjects/41416_2026_3608_Fig4_HTML.png) **Fig. 5: PAX9 overexpression inhibits cell growth by triggering apoptosis and inhibiting orosphere formation in OSCC.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03608-6/MediaObjects/41416_2026_3608_Fig5_HTML.png) **Fig. 6: PAX9 induces lethal autophagy in OSCC.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03608-6/MediaObjects/41416_2026_3608_Fig6_HTML.png) **Fig. 7: PAX9 enhances cisplatin sensitivity and inhibits tumour growth in xenograft nude mice.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03608-6/MediaObjects/41416_2026_3608_Fig7_HTML.png) **Fig. 8: PAX9 is downregulated in OSCC.** ![](https://media.springernature.com/m312/springer-static/image/art%3A10.1038%2Fs41416-026-03608-6/MediaObjects/41416_2026_3608_Fig8_HTML.png) ### Explore related subjects Discover the latest articles and news in related subjects. * [Cancer](https://www.nature.com/subjects/cancer) * [Oral cancer](https://www.nature.com/subjects/oral-cancer) ## Data availability The data supporting the findings of this study will be available from the corresponding author upon reasonable request. Some data may not be available because of privacy or ethical restrictions. ## References 1. Ren ZH, Hu CY, He HR, Li YJ, Lyu J. Global and regional burdens of oral cancer from 1990 to 2017: results from the global burden of disease study. Cancer Commun. 2020;40:81–92. [Article](https://doi.org/10.1002%2Fcac2.12009) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=Global%20and%20regional%20burdens%20of%20oral%20cancer%20from%201990%20to%202017%3A%20results%20from%20the%20global%20burden%20of%20disease%20study&journal=Cancer%20Commun&doi=10.1002%2Fcac2.12009&volume=40&pages=81-92&publication_year=2020&author=Ren%2CZH&author=Hu%2CCY&author=He%2CHR&author=Li%2CYJ&author=Lyu%2CJ) 2. Bhol CS, Mishra SR, Patil S, Sahu SK, Kirtana R, Manna S, et al. PAX9 reactivation by inhibiting DNA methyltransferase triggers antitumor effect in oral squamous cell carcinoma. Biochim Biophys Acta Mol Basis Dis. 2022;1868:166428. [Article](https://doi.org/10.1016%2Fj.bbadis.2022.166428) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BB38XhtlSmsb7J) [PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=35533906) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=PAX9%20reactivation%20by%20inhibiting%20DNA%20methyltransferase%20triggers%20antitumor%20effect%20in%20oral%20squamous%20cell%20carcinoma&journal=Biochim%20Biophys%20Acta%20Mol%20Basis%20Dis&doi=10.1016%2Fj.bbadis.2022.166428&volume=1868&publication_year=2022&author=Bhol%2CCS&author=Mishra%2CSR&author=Patil%2CS&author=Sahu%2CSK&author=Kirtana%2CR&author=Manna%2CS) 3. Mahapatra KK, Mishra SR, Dhiman R, Bhutia SK. Stonin 2 activates lysosomal-mTOR axis for cell survival in oral cancer. Toxicol In Vitro. 2023;88:105561. [Article](https://doi.org/10.1016%2Fj.tiv.2023.105561) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BB3sXitlyqtbw%3D) [PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=36702439) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=Stonin%202%20activates%20lysosomal-mTOR%20axis%20for%20cell%20survival%20in%20oral%20cancer&journal=Toxicol%20In%20Vitro&doi=10.1016%2Fj.tiv.2023.105561&volume=88&publication_year=2023&author=Mahapatra%2CKK&author=Mishra%2CSR&author=Dhiman%2CR&author=Bhutia%2CSK) 4. Bhol CS, Senapati PK, Kar RK, Chew G, Mahapatra KK, Lee E, et al. Autophagy paradox: Genetic and epigenetic control of autophagy in cancer progression. Cancer Lett. 2025;630:217909. [Article](https://doi.org/10.1016%2Fj.canlet.2025.217909) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BB2MXhsF2mtLrM) [PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=40645397) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=Autophagy%20paradox%3A%20Genetic%20and%20epigenetic%20control%20of%20autophagy%20in%20cancer%20progression&journal=Cancer%20Lett&doi=10.1016%2Fj.canlet.2025.217909&volume=630&publication_year=2025&author=Bhol%2CCS&author=Senapati%2CPK&author=Kar%2CRK&author=Chew%2CG&author=Mahapatra%2CKK&author=Lee%2CE) 5. Bhol CS, Panigrahi DP, Praharaj PP, Mahapatra KK, Patra S, Mishra SR, et al. Epigenetic modifications of autophagy in cancer and cancer therapeutics. Semin Cancer Biol. 2020;66:22–33. 6. Hu X, Sui X, Li L, Huang X, Rong R, Su X, et al. Protocadherin 17 acts as a tumour suppressor inducing tumour cell apoptosis and autophagy, and is frequently methylated in gastric and colorectal cancers. J Pathol. 2013;229:62–73. [Article](https://doi.org/10.1002%2Fpath.4093) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BC38XhvVOrtr%2FE) [PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=22926751) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=Protocadherin%2017%20acts%20as%20a%20tumour%20suppressor%20inducing%20tumour%20cell%20apoptosis%20and%20autophagy%2C%20and%20is%20frequently%20methylated%20in%20gastric%20and%20colorectal%20cancers&journal=J%20Pathol&doi=10.1002%2Fpath.4093&volume=229&pages=62-73&publication_year=2013&author=Hu%2CX&author=Sui%2CX&author=Li%2CL&author=Huang%2CX&author=Rong%2CR&author=Su%2CX) 7. You Y, Yang W, Qin X, Wang F, Li H, Lin C, et al. ECRG4 acts as a tumor suppressor and as a determinant of chemotherapy resistance in human nasopharyngeal carcinoma. Cell Oncol. 2015;38:205–14. [Article](https://link.springer.com/doi/10.1007/s13402-015-0223-y) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BC2MXps1Slsro%3D) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=ECRG4%20acts%20as%20a%20tumor%20suppressor%20and%20as%20a%20determinant%20of%20chemotherapy%20resistance%20in%20human%20nasopharyngeal%20carcinoma&journal=Cell%20Oncol&doi=10.1007%2Fs13402-015-0223-y&volume=38&pages=205-14&publication_year=2015&author=You%2CY&author=Yang%2CW&author=Qin%2CX&author=Wang%2CF&author=Li%2CH&author=Lin%2CC) 8. Liu X, Hu X, Kuang Y, Yan P, Li L, Li C, et al. BCLB, methylated in hepatocellular carcinoma, is a starvation stress sensor that induces apoptosis and autophagy through the AMPK-mTOR signaling cascade. Cancer Lett. 2017;395:63–71. [Article](https://doi.org/10.1016%2Fj.canlet.2017.02.030) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BC2sXjvFWrsrc%3D) [PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=28259820) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=BCLB%2C%20methylated%20in%20hepatocellular%20carcinoma%2C%20is%20a%20starvation%20stress%20sensor%20that%20induces%20apoptosis%20and%20autophagy%20through%20the%20AMPK-mTOR%20signaling%20cascade&journal=Cancer%20Lett&doi=10.1016%2Fj.canlet.2017.02.030&volume=395&pages=63-71&publication_year=2017&author=Liu%2CX&author=Hu%2CX&author=Kuang%2CY&author=Yan%2CP&author=Li%2CL&author=Li%2CC) 9. Bhol CS, Patil S, Sahu BB, Patra SK, Bhutia SK. The clinical significance and correlative signaling pathways of paired box gene 9 in development and carcinogenesis. Biochim Biophys Acta Rev Cancer. 2021;1876:188561. [Article](https://doi.org/10.1016%2Fj.bbcan.2021.188561) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BB3MXhtFSkurjJ) [PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=33965511) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=The%20clinical%20significance%20and%20correlative%20signaling%20pathways%20of%20paired%20box%20gene%209%20in%20development%20and%20carcinogenesis&journal=Biochim%20Biophys%20Acta%20Rev%20Cancer&doi=10.1016%2Fj.bbcan.2021.188561&volume=1876&publication_year=2021&author=Bhol%2CCS&author=Patil%2CS&author=Sahu%2CBB&author=Patra%2CSK&author=Bhutia%2CSK) 10. Bonczek O, Balcar VJ, Šerý OJCG. PAX9 gene mutations and tooth agenesis: a review. Clin Genet. 2017;92:467–76. [Article](https://doi.org/10.1111%2Fcge.12986) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BC2sXhs1WitrnN) [PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=28155232) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=PAX9%20gene%20mutations%20and%20tooth%20agenesis%3A%20a%20review&journal=Clin%20Genet&doi=10.1111%2Fcge.12986&volume=92&pages=467-76&publication_year=2017&author=Bonczek%2CO&author=Balcar%2CVJ&author=%C5%A0er%C3%BD%2COJCG) 11. Shi M, Ren S, Chen H, Li J, Huang C, Li Y, et al. Alcohol drinking inhibits NOTCH–PAX9 signaling in esophageal squamous epithelial cells. J Pathol. 2021;253:384–95. [Article](https://doi.org/10.1002%2Fpath.5602) [CAS](https://www.nature.com/articles/cas-redirect/1:CAS:528:DC%2BB3MXmslGnsrc%3D) [PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=33314197) [PubMed Central](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7987830) [ Google Scholar](http://scholar.google.com/scholar_lookup?&title=Alcohol%20drinking%20inhibits%20NOTCH%E2%80%93PAX9%20signaling%20in%20esophageal%20squamous%20epithelial%20cells&journal=J%20Pathol&doi=10.1002%2Fpath.5602&volume=253&pages=384-95&publication_year=2021&author=Shi%2CM&author=Ren%2CS&author=Chen%2CH&author=Li%2CJ&author=Huang%2CC&author=Li%2CY) 12. Xiong Z, Ren S, Chen H, Liu Y, Huang C, Zhang YL, et al. PAX9 regulates squamous cell differentiation
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