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<p>Chemoresistance remains a significant barrier to the treatment of esophageal cancer (EC), regulated by metabolic and signaling adaptations. Fibroblast Growth Factor Receptor-Like 1 (FGFRL1) is a key regulator of cancer progression; however, its involvement in chemoresistance remains poorly understood. This study investigates the functional significance of FGFRL1 in chemo-resistant EC cells and its association with response to chemotherapy. FGFRL1 expression was analysed in cisplatin-resistant EC cells using real-time PCR and Western blotting. FGFRL1 protein levels were examined in clinical specimens from EC patients post-neoadjuvant chemotherapy (NACT) to evaluate their correlation with treatment response using immunohistochemistry. Significantly decreased expression of FGFRL1 was observed in cisplatin-resistant EC cells (<i>p</i> &lt; 0.05). Interestingly, overexpression of FGFRL1 suppressed proliferation, migration, and clonogenic potential (<i>p</i> &lt; 0.05), while activating Notch signaling via JAG1, DLL1, DLL4, NOTCH1, NOTCH2, and HES1 (<i>p</i> &lt; 0.05) in cisplatin-resistant EC cells. FGFRL1 overexpression also shifted glucose metabolism toward glycogen synthesis, involving regulators GFPT2, AQP3, and GALNT5 (<i>p</i> &lt; 0.05). In patient specimens, high FGFRL1 expression was significantly associated with chemotherapy response, observed in 80% of complete responders (CR)versus 36.4% of partial + non-responders (PR + NR) EC patients (<i>p</i> = 0.000, OR = 8.61). We report for the first time that FGFRL1 regulates metabolic and signalling pathways in chemo-resistant EC.</p>

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FGFRL1 Modulates Glucose-Glycogen Homeostasis and Signaling Pathway Genes to Suppress Chemoresistance in Esophageal Carcinoma

  • 期刊论文

  • 发表日期：

    2026年4月7日

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  • Aprajita,
  • Prerna Pandey,
  • N.R Dash,
  • Rinu Sharma

摘要

Chemoresistance remains a significant barrier to the treatment of esophageal cancer (EC), regulated by metabolic and signaling adaptations. Fibroblast Growth Factor Receptor-Like 1 (FGFRL1) is a key regulator of cancer progression; however, its involvement in chemoresistance remains poorly understood. This study investigates the functional significance of FGFRL1 in chemo-resistant EC cells and its association with response to chemotherapy. FGFRL1 expression was analysed in cisplatin-resistant EC cells using real-time PCR and Western blotting. FGFRL1 protein levels were examined in clinical specimens from EC patients post-neoadjuvant chemotherapy (NACT) to evaluate their correlation with treatment response using immunohistochemistry. Significantly decreased expression of FGFRL1 was observed in cisplatin-resistant EC cells (p < 0.05). Interestingly, overexpression of FGFRL1 suppressed proliferation, migration, and clonogenic potential (p < 0.05), while activating Notch signaling via JAG1, DLL1, DLL4, NOTCH1, NOTCH2, and HES1 (p < 0.05) in cisplatin-resistant EC cells. FGFRL1 overexpression also shifted glucose metabolism toward glycogen synthesis, involving regulators GFPT2, AQP3, and GALNT5 (p < 0.05). In patient specimens, high FGFRL1 expression was significantly associated with chemotherapy response, observed in 80% of complete responders (CR)versus 36.4% of partial + non-responders (PR + NR) EC patients (p = 0.000, OR = 8.61). We report for the first time that FGFRL1 regulates metabolic and signalling pathways in chemo-resistant EC.