AI Article Synopsis
- Prion protein (PrPc) is found to be upregulated in adriamycin-resistant gastric cancer cells, showing a potential link to multidrug resistance (MDR).
- PrPc is present in various gastric cancer cell lines and tissues, and its overexpression facilitates resistance to both P-glycoprotein-related and non-related drugs by affecting drug accumulation.
- Inhibition of PrPc can partially reverse MDR, and it appears to influence apoptosis by altering the expression of key proteins like Bcl-2 and Bax, suggesting its role in the development of gastric cancer and MDR mechanisms.
Article Abstract
In our previous work, cellular prion protein (PrPc) was identified as an upregulated gene in adriamycin-resistant gastric carcinoma cell line SGC7901/ADR compared to its parental cell line SGC7901. Here we investigate the expression of PrPc in gastric cancer and whether it was involved in multidrug resistance (MDR) of gastric cancer. We demonstrated that PrPc was ubiquitously expressed in gastric cancer cell lines and tissues. PrPc conferred resistance of both P-glycoprotein (P-gp)-related and P-gp-nonrelated drugs on SGC7901, which was accompanied by decreased accumulation and increased releasing amount of adriamycin in PrPc-overexpressing cell line. Inhibition of PrPc expression by antisense or RNAi technology could partially reverse multidrug-resistant phenotype of SGC7901/ADR. PrPc significantly upregulated the expression of the classical MDR-related molecule P-gp but not multidrug resistance associated protein and glutathione S-transferase pi. The PrPc-induced MDR could be partially reversed by P-gp inhibitor verapamil. PrPc could also suppress adriamycin-induced apoptosis and alter the expression of Bcl-2 and Bax, which might be another pathway contributing to PrPc-related MDR. The further study of the biological functions of PrPc may be helpful for understanding the mechanisms of occurrence and development of clinical gastric carcinoma and PrPc-related MDR and developing possible strategies to treat gastric cancer.
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| http://dx.doi.org/10.1002/ijc.20570 | DOI Listing |
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