Research progress of HGF/c-Met signaling pathway in oral squamous cell carcinoma
Oral squamous cell carcinoma (OSCC) is a malignant tumor that seriously threatens human health. Its typical biological characteristics include strong local invasiveness, high lymph node metastasis rate, and high recurrence rate after treatment. Hepatocyte growth factor (HGF), cellular-mesenchymal to...
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Editorial Department of Journal of Prevention and Treatment for Stomatological Diseases
2025-08-01
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| Series: | 口腔疾病防治 |
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| Online Access: | https://www.kqjbfz.com/fileup/2096-1456/PDF/1754449152045-978652041.pdf |
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| author | SHI Jiafan, GONG Lingling, SUN Mingze, LIU Lulu, ZHANG Huilin, LI Ming |
| author_facet | SHI Jiafan, GONG Lingling, SUN Mingze, LIU Lulu, ZHANG Huilin, LI Ming |
| author_sort | SHI Jiafan, GONG Lingling, SUN Mingze, LIU Lulu, ZHANG Huilin, LI Ming |
| collection | DOAJ |
| description | Oral squamous cell carcinoma (OSCC) is a malignant tumor that seriously threatens human health. Its typical biological characteristics include strong local invasiveness, high lymph node metastasis rate, and high recurrence rate after treatment. Hepatocyte growth factor (HGF), cellular-mesenchymal to epithelial transition factor (c-Met), and the HGF/c-Met signaling pathway are involved in the regulation of the occurrence and development of OSCC. HGF and c-Met proteins are overexpressed in OSCC, and multiple studies have suggested that they are significantly associated with the malignant characteristics of tumors and poor prognosis. Furthermore, the abnormal activation of the HGF/c-Met signaling pathway (driven by HGF-dependent autocrine/paracrine or non-dependent mechanisms such as MET gene mutations, amplification, fusion, and protein overexpression) can synergistically promote tumor cell invasion, metastasis, and angiogenesis by activating downstream signaling pathways. However, HGF/c-Met can also mediate immune escape by promoting lactate secretion increase, inducing programmed death ligand 1 (PD-L1) expression upregulation, activating and expanding myeloid-derived suppressor cells, and promoting the proliferation of regulatory T cells (Tregs). In addition, the crosstalk between the HGF/c-Met signaling pathway and key pathways such as phosphatidylinositide 3-kinases (PI3K)/protein kinase B (AKT), epidermal growth factor receptor (EGFR), Janus kinase (JAK)/signal transducer and activator of transcription (STAT3), and non-coding RNAs can also promote tumor progression. Currently, three types of targeted drugs have been developed targeting the HGF/c-Met pathway: HGF monoclonal antibody, c-Met monoclonal antibody, and tyrosine kinase inhibitors. Some of these drugs have entered clinical trials. However, the emergence of drug resistance during treatment, especially the bidirectional compensatory activation of alternative signaling pathways such as EGFR, has become a major challenge in clinical practice. This article aims to provide an in-depth analysis of the mechanism of action of the HGF/c-Met pathway in OSCC and its interaction with other pathways, and to review the current research status of existing therapeutic drugs. The aim is to provide an important theoretical basis for developing more effective combined treatment strategies and achieving individualized precise treatment, ultimately improving the clinical prognosis and quality of life of patients. |
| format | Article |
| id | doaj-art-e691f0ba18b543d199dc5c22bdccc3d7 |
| institution | Kabale University |
| issn | 2096-1456 |
| language | zho |
| publishDate | 2025-08-01 |
| publisher | Editorial Department of Journal of Prevention and Treatment for Stomatological Diseases |
| record_format | Article |
| series | 口腔疾病防治 |
| spelling | doaj-art-e691f0ba18b543d199dc5c22bdccc3d72025-08-20T03:44:00ZzhoEditorial Department of Journal of Prevention and Treatment for Stomatological Diseases口腔疾病防治2096-14562025-08-0133870971810.12016/j.issn.2096-1456.202550132Research progress of HGF/c-Met signaling pathway in oral squamous cell carcinomaSHI Jiafan, GONG Lingling, SUN Mingze, LIU Lulu, ZHANG Huilin, LI Ming01 School of Stomatology, Hunan University of Chinese Medicine, Changsha 410208, China;2 Changsha Stomatological Hospital, Changsha 410004, ChinaOral squamous cell carcinoma (OSCC) is a malignant tumor that seriously threatens human health. Its typical biological characteristics include strong local invasiveness, high lymph node metastasis rate, and high recurrence rate after treatment. Hepatocyte growth factor (HGF), cellular-mesenchymal to epithelial transition factor (c-Met), and the HGF/c-Met signaling pathway are involved in the regulation of the occurrence and development of OSCC. HGF and c-Met proteins are overexpressed in OSCC, and multiple studies have suggested that they are significantly associated with the malignant characteristics of tumors and poor prognosis. Furthermore, the abnormal activation of the HGF/c-Met signaling pathway (driven by HGF-dependent autocrine/paracrine or non-dependent mechanisms such as MET gene mutations, amplification, fusion, and protein overexpression) can synergistically promote tumor cell invasion, metastasis, and angiogenesis by activating downstream signaling pathways. However, HGF/c-Met can also mediate immune escape by promoting lactate secretion increase, inducing programmed death ligand 1 (PD-L1) expression upregulation, activating and expanding myeloid-derived suppressor cells, and promoting the proliferation of regulatory T cells (Tregs). In addition, the crosstalk between the HGF/c-Met signaling pathway and key pathways such as phosphatidylinositide 3-kinases (PI3K)/protein kinase B (AKT), epidermal growth factor receptor (EGFR), Janus kinase (JAK)/signal transducer and activator of transcription (STAT3), and non-coding RNAs can also promote tumor progression. Currently, three types of targeted drugs have been developed targeting the HGF/c-Met pathway: HGF monoclonal antibody, c-Met monoclonal antibody, and tyrosine kinase inhibitors. Some of these drugs have entered clinical trials. However, the emergence of drug resistance during treatment, especially the bidirectional compensatory activation of alternative signaling pathways such as EGFR, has become a major challenge in clinical practice. This article aims to provide an in-depth analysis of the mechanism of action of the HGF/c-Met pathway in OSCC and its interaction with other pathways, and to review the current research status of existing therapeutic drugs. The aim is to provide an important theoretical basis for developing more effective combined treatment strategies and achieving individualized precise treatment, ultimately improving the clinical prognosis and quality of life of patients.https://www.kqjbfz.com/fileup/2096-1456/PDF/1754449152045-978652041.pdforal squamous cell carcinoma|hepatocyte growth factor|cellular-mesenchymal to epithelial transition factor|mechanism|phosphatidylinositide 3-kinases|protein kinases b|epidermal growth factor receptor|targeted therapy|monoclonal antibodies|tyrosine kinase inhibitor |
| spellingShingle | SHI Jiafan, GONG Lingling, SUN Mingze, LIU Lulu, ZHANG Huilin, LI Ming Research progress of HGF/c-Met signaling pathway in oral squamous cell carcinoma 口腔疾病防治 oral squamous cell carcinoma|hepatocyte growth factor|cellular-mesenchymal to epithelial transition factor|mechanism|phosphatidylinositide 3-kinases|protein kinases b|epidermal growth factor receptor|targeted therapy|monoclonal antibodies|tyrosine kinase inhibitor |
| title | Research progress of HGF/c-Met signaling pathway in oral squamous cell carcinoma |
| title_full | Research progress of HGF/c-Met signaling pathway in oral squamous cell carcinoma |
| title_fullStr | Research progress of HGF/c-Met signaling pathway in oral squamous cell carcinoma |
| title_full_unstemmed | Research progress of HGF/c-Met signaling pathway in oral squamous cell carcinoma |
| title_short | Research progress of HGF/c-Met signaling pathway in oral squamous cell carcinoma |
| title_sort | research progress of hgf c met signaling pathway in oral squamous cell carcinoma |
| topic | oral squamous cell carcinoma|hepatocyte growth factor|cellular-mesenchymal to epithelial transition factor|mechanism|phosphatidylinositide 3-kinases|protein kinases b|epidermal growth factor receptor|targeted therapy|monoclonal antibodies|tyrosine kinase inhibitor |
| url | https://www.kqjbfz.com/fileup/2096-1456/PDF/1754449152045-978652041.pdf |
| work_keys_str_mv | AT shijiafangonglinglingsunmingzeliululuzhanghuilinliming researchprogressofhgfcmetsignalingpathwayinoralsquamouscellcarcinoma |