PRRX1 Regulates Cellular Phenotype Plasticity and Dormancy of Head and Neck Squamous Cell Carcinoma Through miR-642b-3p
Open accessAbstract
BACKGROUND: Dormancy is one characteristic of cancer cells to make patients remain asymptomatic before metastasis and relapse, which is closely related to the survival rate of cancer patients, including head and neck squamous cell carcinoma (HNSCC). PRRX1 has previously been implicated in the invasion and metastasis of the epithelial-mesenchymal transition (EMT) process in different types of human carcinoma. However, whether PRRX1 can regulate cancer dormancy and its reactivation, leading to the migration and invasion of HNSCC cells, remains elusive. The aim of this study was to determine the role of PRRX1 in cellular phenotype plasticity and cancer dormancy of HNSCC cells and its association with miRNAs in HNSCC. METHODS: The expression of PRRX1 was detected by immunohistochemical staining in primary HNSCC samples and the metastatic lymph nodes. Meanwhile, the role of PRRX1 and its relationship with miR-642b-3p and EMT in cellular phenotype plasticity and cancer dormancy of HNSCC were investigated in vitro and in vivo. RESULTS: PRRX1 was significantly higher at the invasive front of HNSCC samples compared with the metastatic lymph nodes, and such switch process was accompanied by the cellular phenotype plasticity and cell dormancy activation. In HNSCC cell lines, PRRX1 positively promoted the expression of known EMT inducers and cooperated with activated TGF-β1 to contribute to EMT and migration and invasion of HNSCC cells. Then, we found that overexpression of miR-642b-3p, one of the most significantly downregulated miRNAs in PRRX1-overexpressed cells, significantly reduced the migration and invasion, and increased cell proliferation and apoptosis. And miR-642b-3p restoration reversed PRRX1-induced cell dormancy and EMT of HNSCC cells through TGF-β2 and p38. Finally, we demonstrated that overexpressed PRRX1 was closely correlated with miR-642b-3p downregulation and the upregulation of TGF-β2 and p38 in a xenograft model of HNSCC. CONCLUSIONS: Our findings showed that PRRX1 may be one of the main driving forces for the cellular phenotype plasticity and tumor dormancy of HNSCC. Therefore, we can raise the possibility that EMT may help to keep cancer cell in dormant state and mesenchymal-epithelial transition may resurge dormancy in HNSCC.
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Long term LY2109761 treatment of mice harboring chemically induced SCCs resulted in outgrowth of tumors with increased, drug-refractile Smad2 activation and phenotypes suggestive of elevated TGF-β signaling.
“Long term LY2109761 treatment of mice harboring chemically induced SCCs resulted in outgrowth of tumors with increased, drug-refractile Smad2 activation and phenotypes suggestive of elevated TGF-β signaling336.”
From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [336]
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- Authors
- Jiang, J., Zheng, M., Zhang, M., Yang, X., Li, L., Wang, S.-S., Wu, J.-S., Yu, X.-H., Wu, J.-B., Pang, X., Tang, Y.-J., Tang, Y.-L., & Liang, X.-H.
- Affiliations
- University of Electronic Science and Technology of China (CN)
- Wenzhou Medical University (CN)
- Sichuan University (CN)
- Corresponding author
- Liang, Xin-hua
- ORCID
- Venue
- Neoplasia
- Publisher
- Elsevier BV
- Published
- 2019-02
- Volume
- 21
- Issue
- 2
- Pages
- 216-229
- ISSN
- 1476-5586 (ISSN-L)
- PMC
- PMC6324219
- OpenAlex
- W2910117544
- Cited by
- 54
- References
- 43
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 13 · 2023: 6 · 2022: 7 · 2021: 15 · 2020: 6 · 2019: 3
- FWCI
- 3.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Neoplasia (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Natural Science Foundation of China (81672672, 81502357, 81572650, 81772891, 81372891)
- National Program on Key Research Project of China (2016YFC0902700)
- Natural Science Foundation of Zhejiang Province (Q142114001)
- Fundamental Research Funds for the Central Universities
- Topics
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Otorhinolaryngology › Head and Neck Cancer Studies
- Keywords
- PRRX1, head and neck squamous cell carcinoma, tumor dormancy, epithelial-mesenchymal transition, TGF-beta2, p38 MAPK, cell migration and invasion, metastasis, microRNA regulation, apoptosis, cell proliferation, metastatic lymph nodes, xenografts
- MeSH terms
- Squamous Cell Carcinoma of Head and Neck, Adult, Aged, Animals, Disease Models, Animal, Female, Humans, Male, Middle Aged, Neoplasm Staging, Protein Binding, Biomarkers, Gene Expression Regulation, Neoplastic, Homeodomain Proteins, Proto-Oncogene Proteins c-met, Gene Expression Profiling, Xenograft Model Antitumor Assays, RNA Interference, MicroRNAs, p38 Mitogen-Activated Protein Kinases, Mice, Transforming Growth Factor beta1, Transforming Growth Factor beta2, Gene Knockdown Techniques, Asymptomatic Diseases, Epithelial-Mesenchymal Transition, Neoplasm Grading
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