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Updated: Jun 18, 2026

Analysis of Side Population in Solid Tumor Cell Lines
Published on: February 23, 2021
Resveratrol down-regulates survivin and induces apoptosis in human multidrug-resistant SPC-A-1/CDDP cells
Weiguo Zhao1, Pengtao Bao, Haowen Qi
1Department of Respiratory Medicine, The Second Affiliated Hospital of Chinese PLA General Hospital, Beijing, P.R. China. zhaowg2008@qq.com
Abstract:
We studied the effect of resveratrol treatment on multidrug-resistant human non-small cell lung cancer cells. Human multidrug-resistant SPC-A-1/CDDP cells were treated with resveratrol at a concentration of 25, 50, or 100 microM in in vitro studies and nude mice were implanted with multidrug-resistant SPC-A-1/and fed a special diet that included resveratrol at a dose of either 1 g/kg/day or 3 g/kg/day in in vivo studies. No adverse toxicological effects of resveratrol treatment were observed. The rate of cell proliferation, apoptosis ratio, cell cycle phase distribution, IC50 values of cisplatin, gefitinib, and paclitaxel, implanted tumour volume, and expression of survivin in resveratrol-treated and control mice were then determined. Resveratrol significantly inhibited the proliferation of SPC-A-1/CDDP cells, induced apoptosis, arrested the cell cycle phase between G0-G1 and S phase or at the G2/M phase, decreased the IC50 values of multiple chemotherapeutic drugs, and showed anti-tumour effects in nude mice that had been implanted with SPC-A-1/CDDP cells. In additional, resveratrol affected the proliferation of SPC-A-1/CDDP cells in a dose- and time-dependent manner. Expression of survivin in SPC-A-1/CDDP cells decreased after they were treated with all concentrations of resveratrol and resveratrol was also found to have a dose-dependent effect on survivin expression. Resveratrol can induce apoptosis in multidrug-resistant human NSCLC SPC-A-1/CDDP cells by down-regulating the expression of survivin.
Insights
Resveratrol effectively combats multidrug-resistant lung cancer by inhibiting cell growth and inducing apoptosis. This natural compound also enhances chemotherapy efficacy and reduces tumor size in preclinical models.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Multidrug resistance (MDR) in non-small cell lung cancer (NSCLC) poses a significant therapeutic challenge.
- Resveratrol, a natural polyphenol, has demonstrated potential anti-cancer properties.
- Investigating resveratrol's efficacy against MDR NSCLC is crucial for developing novel treatment strategies.
Purpose of the Study:
- To evaluate the in vitro and in vivo effects of resveratrol on multidrug-resistant human non-small cell lung cancer (NSCLC) cells (SPC-A-1/CDDP).
- To determine resveratrol's impact on cell proliferation, apoptosis, cell cycle, chemosensitivity, and tumor growth.
- To elucidate the role of survivin expression in resveratrol-mediated anti-cancer effects.
Main Methods:
- In vitro treatment of SPC-A-1/CDDP cells with varying concentrations of resveratrol.
- In vivo studies using nude mice xenograft models implanted with SPC-A-1/CDDP cells, treated with resveratrol orally.
- Assessment of cell proliferation, apoptosis, cell cycle distribution, drug IC50 values, tumor volume, and survivin expression.
Main Results:
- Resveratrol significantly inhibited SPC-A-1/CDDP cell proliferation and induced apoptosis in a dose- and time-dependent manner.
- Resveratrol treatment led to cell cycle arrest at G0-G1 and G2/M phases.
- Resveratrol decreased the IC50 values of cisplatin, gefitinib, and paclitaxel, indicating enhanced chemosensitivity, and reduced tumor volume in vivo.
- Resveratrol downregulated survivin expression in a dose-dependent manner, correlating with apoptosis induction.
Conclusions:
- Resveratrol exhibits significant anti-proliferative and pro-apoptotic effects against multidrug-resistant human NSCLC cells.
- Resveratrol enhances the efficacy of conventional chemotherapeutic agents and possesses anti-tumor activity in vivo.
- Downregulation of survivin expression is a key mechanism by which resveratrol induces apoptosis in MDR NSCLC.
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