Related Experiment Video
Updated: Jul 4, 2026
11:02
Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
Published on: October 30, 2013
Curcumin decreases specificity protein expression in bladder cancer cells
Gayathri Chadalapaka1, Indira Jutooru, Sudhakar Chintharlapalli
1Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843-4466, USA.
Cancer Research
|July 3, 2008
Summary
Curcumin, a compound in turmeric, inhibits bladder cancer cell growth by reducing key proteins like survivin and VEGF. It achieves this by decreasing Sp transcription factors, offering a potential new cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Curcumin, the active compound in turmeric, is a polyphenol with demonstrated anticancer properties.
- It modulates multiple cellular pathways and gene expressions relevant to cancer progression.
- Previous research highlights curcumin's potential in cancer treatment, necessitating a deeper understanding of its mechanisms.
Purpose of the Study:
- To investigate the mechanism by which curcumin inhibits bladder cancer cell growth, focusing on apoptosis and angiogenesis.
- To determine the role of specificity protein (Sp) transcription factors in mediating curcumin's effects.
- To evaluate curcumin's efficacy in reducing bladder tumor growth in vivo.
Main Methods:
- Cell culture experiments using 253JB-V and KU7 bladder cancer cell lines.
- Treatment with varying concentrations of curcumin (10-25 micromol/L).
- Analysis of apoptosis, survivin, vascular endothelial growth factor (VEGF), VEGF receptor 1 (VEGFR1), and Sp protein expression (Sp1, Sp3, Sp4).
- Utilized RNA interference with small inhibitory RNAs (siRNAs) for Sp proteins.
- In vivo studies using athymic nude mice xenograft models with KU7 cells.
Main Results:
- Curcumin (10-25 micromol/L) inhibited bladder cancer cell growth, inducing apoptosis and reducing survivin, VEGF, and VEGFR1 expression.
- Curcumin treatment led to proteasome-dependent downregulation of Sp1, Sp3, and Sp4 in bladder cancer cells.
- Knockdown of Sp proteins using siRNAs mimicked and partially explained curcumin's inhibition of NF-kappaB-dependent genes (bcl-2, survivin, cyclin D1).
- Curcumin administration significantly reduced bladder tumor growth in mice, correlating with decreased Sp protein levels in tumors.
Conclusions:
- Curcumin exhibits significant anticancer activity against bladder cancer by inhibiting cell proliferation, inducing apoptosis, and reducing angiogenesis.
- A key mechanism involves the proteasome-dependent downregulation of Sp1, Sp3, and Sp4 transcription factors by curcumin.
- This reduction in Sp proteins contributes to curcumin's ability to suppress pro-survival and pro-angiogenic gene expression, highlighting its potential as a chemotherapeutic agent.