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Background <p>Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors worldwide. In this study, we aimed to investigate the pathophysiological mechanism through which F‑box and leucine-rich repeat protein&#xa0;18 (FBXL18) promotes the progression of ESCC.</p> Methods <p>ESCC cell lines KYSE150 and TE‑1 were infected with PLVX-FBXL18 or shFBXL18-derived lentivirus to overexpress or knock down FBXL18. A&#xa0;Cell-Counting Kit&#xa0;8 and colony-forming assay were used to assess cell viability and proliferation. Cells were irradiated with varying doses of X‑ray (IR) to determine whether FBXL18 influenced the radiosensitivity of ESCC cells. KYSE450 cells, stably transduced with shNC or shFBXL18-derived lentivirus, were injected into nude mice to assess whether FBXL18 affected ESCC tumor growth. KYSE150 and TE-1&#xa0;cells overexpressing FBXL18 were lysed for Western blot analysis to evaluate protein expression.</p> Results <p>FBXL18 overexpression enhanced cell viability and colony formation, and proliferation of ESCC cells. In contrast, FBXL18 knockdown inhibited tumor growth <i>in vivo</i>. Additionally, FBXL18 overexpression reduced the radiosensitivity of ESCC cells. Mechanistically, FBXL18 was found to exert its effects by suppressing the expression of FBXL7 in ESCC cells.</p> Conclusion <p>FBXL18 promotes cell proliferation and diminishes radiosensitivity in ESCC cells. Most likely, it exerts its pro-tumorigenic effects by downregulating FBXL7.</p>

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FBXL18 increases cell proliferation and reduces cell radiosensitivity in esophageal squamous cell carcinoma

  • 期刊论文

  • 发表日期：

    2025年2月19日

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  • Yahui Kang,
  • Ning Ge,
  • Xiaolong Yuan,
  • Bihong Zhan,
  • Hongbo Zhang

摘要

Background

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors worldwide. In this study, we aimed to investigate the pathophysiological mechanism through which F‑box and leucine-rich repeat protein 18 (FBXL18) promotes the progression of ESCC.

Methods

ESCC cell lines KYSE150 and TE‑1 were infected with PLVX-FBXL18 or shFBXL18-derived lentivirus to overexpress or knock down FBXL18. A Cell-Counting Kit 8 and colony-forming assay were used to assess cell viability and proliferation. Cells were irradiated with varying doses of X‑ray (IR) to determine whether FBXL18 influenced the radiosensitivity of ESCC cells. KYSE450 cells, stably transduced with shNC or shFBXL18-derived lentivirus, were injected into nude mice to assess whether FBXL18 affected ESCC tumor growth. KYSE150 and TE-1 cells overexpressing FBXL18 were lysed for Western blot analysis to evaluate protein expression.

Results

FBXL18 overexpression enhanced cell viability and colony formation, and proliferation of ESCC cells. In contrast, FBXL18 knockdown inhibited tumor growth in vivo. Additionally, FBXL18 overexpression reduced the radiosensitivity of ESCC cells. Mechanistically, FBXL18 was found to exert its effects by suppressing the expression of FBXL7 in ESCC cells.

Conclusion

FBXL18 promotes cell proliferation and diminishes radiosensitivity in ESCC cells. Most likely, it exerts its pro-tumorigenic effects by downregulating FBXL7.