Silencing vascular endothelial growth factor C increases the radiosensitivity in nasopharyngeal carcinoma CNE-2 cells

Area of Science:

• Oncology
• Molecular Biology
• Radiotherapy Research

Background:

• Vascular endothelial growth factor C (VEGF-C) is implicated in nasopharyngeal carcinoma (NPC) progression, including lymphatic vessel density, tumor staging, and metastasis.
• VEGF-C contributes to treatment failure in NPC following radiotherapy.
• Targeting VEGF-C may offer a strategy to overcome radioresistance in NPC.

Purpose of the Study:

• To investigate the effects of VEGF-C on radiotherapy response in human NPC cell lines.
• To elucidate the underlying molecular mechanisms by which VEGF-C influences radiosensitivity.
• To evaluate VEGF-C as a potential therapeutic target for enhancing NPC radiosensitivity.

Main Methods:

• Stable knockdown of VEGF-C was achieved in CNE-2 NPC cells using small interfering RNA (si-VEGFC).
• Cells were treated with si-VEGFC and 8 Gy X-ray irradiation.
• Cell proliferation (CCK-8), colony formation, DNA damage (comet assay), and apoptosis (flow cytometry) were assessed.
• Signaling pathways were analyzed using PCR array, RT-qPCR, and Western blot.

Main Results:

• Silencing VEGF-C significantly inhibited proliferation and colony formation in irradiated NPC cells.
• VEGF-C knockdown combined with radiation increased DNA damage and apoptosis.
• These combined treatments promoted radiosensitivity in CNE-2 cells.
• VEGF-C knockdown appeared to activate the NF-kB signaling pathway.

Conclusions:

• VEGF-C plays a critical role in NPC radioresistance.
• Silencing VEGF-C enhances NPC radiosensitivity by promoting DNA damage and apoptosis.
• Activation of the NF-kB signaling pathway is likely involved in the mechanism of VEGF-C knockdown-mediated radiosensitization.
• VEGF-C represents a promising therapeutic target for improving radiotherapy outcomes in NPC.