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FGFR Like1 drives esophageal cancer progression via EMT, PI3K/Akt, and notch signalling: insights from clinical data
Aprajita Srivastava1, Anoop Saraya2, Deepak Gunjan2
1University School of Biotechnology, Guru Gobind Singh Indraprastha University, New Delhi, India.
Abstract:
FGFRL1, one of the least explored FGFRs, has recently been shown to have implications in cancer, but its functional significance in esophageal cancer (EC) remains largely unexplored. We evaluated FGFRL1 expression in EC patients (n = 106) using immunohistochemistry, observing a significant increase in preneoplastic and neoplastic tissues (P < 0.001, OR = 73.2; AUC = 0.817). RNAi-coupled next-generation sequencing revealed enrichment of EMT, PI3K/Akt, and Notch pathways. Quantitative RT-PCR validated the downregulation of top cluster and Notch pathway genes (P < 0.05). Western blot showed decreased phospho-GSK3β, phospho-Akt, and mesenchymal markers. TCGA data supported a positive correlation with EMT. Functional assays demonstrated FGFRL1's oncogenic role, showing G1 phase arrest, and reduced proliferation, migration, and invasion (P < 0.001). Our study highlights FGFRL1 as a key driver of EC progression.
Insights
Fibroblast Growth Factor Receptor Like 1 (FGFRL1) is upregulated in esophageal cancer (EC), driving tumor progression. Its inhibition halts cell cycle and reduces cancer cell migration and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Fibroblast Growth Factor Receptor Like 1 (FGFRL1) is an understudied member of the FGFR family.
- Emerging evidence suggests FGFRL1's involvement in various cancers.
- Its specific role in esophageal cancer (EC) pathogenesis is largely unknown.
Purpose of the Study:
- To investigate the expression and functional significance of FGFRL1 in esophageal cancer.
- To elucidate the molecular pathways influenced by FGFRL1 in EC.
- To determine FGFRL1's potential as a therapeutic target in EC.
Main Methods:
- Immunohistochemistry to assess FGFRL1 expression in EC tissues.
- RNAi-coupled next-generation sequencing to identify associated pathways.
- Quantitative RT-PCR and Western blot for gene and protein expression analysis.
- TCGA data analysis for correlation with EMT.
- Functional assays to evaluate FGFRL1's impact on cell cycle and invasion.
Main Results:
- FGFRL1 expression is significantly elevated in EC tissues compared to normal tissues.
- FGFRL1 upregulation correlates with EMT, PI3K/Akt, and Notch pathway activation.
- Knockdown of FGFRL1 leads to G1 cell cycle arrest.
- FGFRL1 inhibition reduces esophageal cancer cell proliferation, migration, and invasion.
Conclusions:
- FGFRL1 acts as an oncogene in esophageal cancer.
- FGFRL1 promotes EC progression through EMT and signaling pathways.
- FGFRL1 represents a potential therapeutic target for esophageal cancer treatment.
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