PEITC reverse multi-drug resistance of human gastric cancer SGC7901/DDP cell line
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Tao Tang1, Xin Song, Yu-Fen Liu
1Department of Gastrointestinal Surgery, China-Japan Friendship Hospital, Beijing, 100029, China.
Abstract:
Gastric cancer is one of the leading causes of cancer death in the world and nearly all patients who respond initially to cisplatin later develop drug resistance, indicating multi-drug resistance is an essential aspect of the failure of treatment. Phenethyl isothiocyanate (PEITC) has been implicated in inhibiting metastasis of several types of human cancer. However, the effect and potential mechanism of PEITC reversed multi-drug resistance of human gastric cancer is not fully clear. We have identified the role of PEITC in multi-drug resistance reversal of human gastric cancer SGC7901/DDP cell line. PEITC inhibited cisplatin-resistant human SGC7901/DDP cell growth in a dose-dependent manner, causing increased apoptosis, ROS generation, glutathione depletion, accumulation of Rhodamine-123, decreased expression of P-glycoprotein and cell cycle arrest. mRNA and protein expression of the multi-drug resistance gene (MDR1), multi-drug resistance-associated protein (MRP1), excision repair cross-complementing gene 1 (ERCC1), survivin, and Mad2 was decreased, and phosphorylation of Akt and transcriptional activation of NF-κB were suppressed. PEITC may be useful as the therapeutic strategy for overcoming multi-drug resistance through suppressing the PI3K-Akt pathway in human gastric cancer.
Insights
Phenethyl isothiocyanate (PEITC) reverses multi-drug resistance in human gastric cancer cells. This compound inhibits cancer cell growth and overcomes cisplatin resistance by suppressing key molecular pathways.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Gastric cancer is a leading cause of cancer mortality worldwide.
- Acquired cisplatin resistance is a major challenge in gastric cancer treatment.
- Phenethyl isothiocyanate (PEITC) shows potential in inhibiting cancer metastasis.
Purpose of the Study:
- To investigate the efficacy of PEITC in reversing multi-drug resistance in human gastric cancer.
- To elucidate the underlying molecular mechanisms of PEITC's action.
Main Methods:
- Utilized the cisplatin-resistant human gastric cancer cell line SGC7901/DDP.
- Assessed cell viability, apoptosis, reactive oxygen species (ROS) generation, glutathione levels, and P-glycoprotein expression.
- Quantified Rhodamine-123 accumulation and cell cycle progression.
- Analyzed mRNA and protein expression of key drug resistance genes (MDR1, MRP1, ERCC1, survivin, Mad2).
- Investigated the PI3K-Akt signaling pathway, including Akt phosphorylation and NF-κB activation.
Main Results:
- PEITC demonstrated dose-dependent inhibition of SGC7901/DDP cell growth.
- PEITC treatment increased apoptosis, ROS generation, and Rhodamine-123 accumulation.
- PEITC reduced glutathione levels, P-glycoprotein expression, and induced cell cycle arrest.
- PEITC downregulated MDR1, MRP1, ERCC1, survivin, and Mad2 expression at both mRNA and protein levels.
- PEITC suppressed Akt phosphorylation and NF-κB transcriptional activation, indicating PI3K-Akt pathway inhibition.
Conclusions:
- PEITC effectively reverses cisplatin resistance in human gastric cancer cells.
- PEITC exerts its effects by inducing apoptosis, depleting glutathione, and inhibiting key drug resistance genes.
- PEITC's therapeutic potential lies in its ability to overcome multi-drug resistance via suppression of the PI3K-Akt pathway.
