Translational cancer research · 2026
Role of podoplanin in tongue squamous cell carcinoma and the regulation of malignant cellular behaviors via the ERK/MMP-2 signaling axis.
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Sheng Xiaowei, Ding Liping, Zhang Qiang, Lu Yong, Guo Jun
Аннотация
BACKGROUND: The prognostic significance and functional role of podoplanin (PDPN) in tongue squamous cell carcinoma (TSCC) remain incompletely defined. This study investigated PDPN expression, prognostic relevance, effects on malignant cellular behaviors, and involvement of the ERK/MMP-2 signaling axis.
METHODS: PDPN levels in TSCC and matched surrounding noncancerous tissues were detected via immunohistochemistry. The link between PDPN levels and clinicopathological parameters was analyzed, and the prognostic value of PDPN was evaluated. Functional assays were conducted via PDPN knockdown and overexpression models in SCC-9 and CAL-27 cells, respectively. Extracellular matrix (ECM) adhesion, wound healing, cell proliferation, and Transwell migration and invasion analyses were conducted. Bioinformatics prediction, Western blot analysis, and treatment with a specific ERK inhibitor were integrated to clarify the regulatory effects of PDPN on MMP-2 via the MAPK-ERK axis. Furthermore, a xenograft model was established in nude mice to verify the tumor-promoting effects of PDPN in vivo.
RESULTS: PDPN was significantly upregulated in TSCC tissues and correlated with poor differentiation, advanced tumor-node-metastasis (TNM) stage, and lymphatic invasion. Multivariate Cox regression analysis identified PDPN as an independent unfavorable prognostic factor for patients with TSCC. Functional assays revealed that PDPN promoted cell migration, proliferation, and invasion, which were mediated through the ERK/MMP-2 pathway. In vivo, PDPN knockdown reduced tumor growth and decreased MMP-2 expression.
CONCLUSIONS: PDPN is overexpressed in TSCC and possesses independent prognostic value. PDPN promotes TSCC progression via the ERK/MMP-2 signaling axis, which suggests its utility as a prognostic biomarker and therapeutic target for patients with TSCC.
METHODS: PDPN levels in TSCC and matched surrounding noncancerous tissues were detected via immunohistochemistry. The link between PDPN levels and clinicopathological parameters was analyzed, and the prognostic value of PDPN was evaluated. Functional assays were conducted via PDPN knockdown and overexpression models in SCC-9 and CAL-27 cells, respectively. Extracellular matrix (ECM) adhesion, wound healing, cell proliferation, and Transwell migration and invasion analyses were conducted. Bioinformatics prediction, Western blot analysis, and treatment with a specific ERK inhibitor were integrated to clarify the regulatory effects of PDPN on MMP-2 via the MAPK-ERK axis. Furthermore, a xenograft model was established in nude mice to verify the tumor-promoting effects of PDPN in vivo.
RESULTS: PDPN was significantly upregulated in TSCC tissues and correlated with poor differentiation, advanced tumor-node-metastasis (TNM) stage, and lymphatic invasion. Multivariate Cox regression analysis identified PDPN as an independent unfavorable prognostic factor for patients with TSCC. Functional assays revealed that PDPN promoted cell migration, proliferation, and invasion, which were mediated through the ERK/MMP-2 pathway. In vivo, PDPN knockdown reduced tumor growth and decreased MMP-2 expression.
CONCLUSIONS: PDPN is overexpressed in TSCC and possesses independent prognostic value. PDPN promotes TSCC progression via the ERK/MMP-2 signaling axis, which suggests its utility as a prognostic biomarker and therapeutic target for patients with TSCC.