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Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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RNA interference-mediated vascular endothelial growth factor-C reduction suppresses malignant progression and

Hui-hui Zhang1, Fan Qi, Ying-rui Shi

  • 1Department of Urology, Xiangya Hospital, Central South University, Changsha, Hunan, P.R. China.

Cancer Biotherapy & Radiopharmaceuticals
|September 10, 2011
PubMed

Insights

Vascular endothelial growth factor-C (VEGF-C) promotes bladder cancer cell proliferation and invasion. Inhibiting VEGF-C with RNA interference suppressed tumor growth and enhanced chemosensitivity, suggesting it as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Vascular endothelial growth factor-C (VEGF-C) is implicated in lymphangiogenesis and metastasis in human cancers.
  • Understanding VEGF-C's role in bladder cancer progression is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the function of VEGF-C in the malignant progression of the human bladder cancer T24 cell line.
  • To evaluate the therapeutic potential of inhibiting VEGF-C in bladder cancer.

Main Methods:

  • Western blotting to detect VEGF-C expression.
  • MTT assay to assess cell proliferation after rhVEGF-C treatment.
  • Lentivirus-based RNA interference (RNAi) to inhibit VEGF-C expression.
  • Evaluation of cell proliferation, invasiveness, and mitomycin C (MMC)-induced apoptosis.

Main Results:

  • Recombinant human VEGF-C (rhVEGF-C) increased T24 cell proliferation in a dose-dependent manner.
  • VEGF-C RNAi significantly reduced VEGF-C mRNA and protein levels, inhibiting cell growth and invasiveness.
  • VEGF-C inhibition enhanced MMC-induced apoptosis, involving modulation of Bcl-2/Bax ratio, Caspase-3 activation, MMP-9 expression, and p38 MAPK/Akt phosphorylation.

Conclusions:

  • VEGF-C promotes bladder cancer cell proliferation and invasion by suppressing apoptosis and facilitating migration.
  • Targeting VEGF-C via RNAi effectively suppresses malignant progression and enhances chemosensitivity in T24 cells.
  • Inhibition of VEGF-C represents a promising therapeutic strategy for bladder cancer.

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