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Updated: Mar 20, 2026

Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
Published on: April 22, 2019
Roles of FGFR in oral carcinogenesis
Xiaoyan Xie1, Zhiyong Wang1, Fangman Chen1
1State Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, 610041, China.
Abstract:
Fibroblast growth factor receptors (FGFRs) play essential roles in organ development during the embryonic period, and regulate tissue repair in adults. Accumulating evidence suggests that alterations in FGFR signalling are involved in diverse types of cancer. In this review, we focus on aberrant regulation of FGFRs in pathogenesis of oral squamous cell carcinoma (OSCC), including altered expression and subcellular location, aberrant isoform splicing and mutations. We also provide an overview of oncogenic roles of each FGFR and its downstream signalling pathways in regulating OSCC cell proliferation and metastasis. Finally, we discuss potential application of FGFRs as anti-cancer targets in the preclinical environment and in clinical practice.
Insights
Altered Fibroblast Growth Factor Receptor (FGFR) signaling drives oral squamous cell carcinoma (OSCC) development. Targeting FGFRs offers promising anti-cancer strategies for OSCC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cell Signaling
Background:
- Fibroblast Growth Factor Receptors (FGFRs) are crucial for embryonic development and adult tissue repair.
- Aberrant FGFR signaling is implicated in various cancers.
- Oral Squamous Cell Carcinoma (OSCC) pathogenesis involves complex molecular alterations.
Purpose of the Study:
- To review the aberrant regulation of FGFRs in OSCC.
- To elucidate the oncogenic roles of FGFRs and their downstream pathways in OSCC.
- To discuss FGFR-targeted therapies for OSCC.
Main Methods:
- Literature review focusing on FGFRs in OSCC.
- Analysis of altered FGFR expression, splicing, and mutations in OSCC.
- Overview of FGFR signaling pathways and their impact on OSCC progression.
Main Results:
- FGFR alterations, including expression changes, aberrant splicing, and mutations, are key in OSCC pathogenesis.
- FGFR signaling promotes OSCC cell proliferation and metastasis.
- Specific FGFRs and their downstream pathways contribute to oncogenesis.
Conclusions:
- Aberrant FGFR signaling is a critical driver of OSCC.
- FGFRs represent viable therapeutic targets for OSCC.
- Targeting FGFRs holds potential for preclinical and clinical anti-cancer strategies in OSCC.
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