Effects of CD133 expression on chemotherapy and drug sensitivity of adenoid cystic carcinoma.

Abstract

The cellular resistance of tumors is a major obstacle for successful tumor therapy. Cluster of differentiation (CD)133 plays an important role in the regulation of drug resistance in gastric and colon cancers. However, its effect on chemotherapeutic sensitivity in adenoid cystic carcinoma (ACC) has not been fully explored. The present study discussed the specific role of CD133 in ACC drug-resistant sensitive cells. KOA-1 cells were treated with 5-fluorouracil (5-FU) and pingyangmycin (PYM) to form drug-resistant cell lines. A Cell Counting Kit-8 assay was used to detect the cell survival rate. Cell invasion was measured using a Transwell assay. The expression levels of CD133 were detected by reverse transcription-quantitative (RT-q) PCR. The expression levels of drug-resistant mRNAs and proteins were detected by RT-qPCR and immunofluorescence analyses, respectively. The CD133 were inhibited by small interfering RNA technology. The survival rate and invasive ability of KOA-1 cells were increased following the induction of drug resistance. The expression levels of CD133, multidrug resistance protein (MDR)1 and multidrug resistance-associated protein (MRP)1 were significantly increased in drug-resistant cell lines. Knockdown of CD133 expression in the resistant cell lines, KOA-1/5-FU and KOA-1/PYM, decreased the survival rate and invasive ability. The expression levels of MDR1 and MRP1 were also significantly decreased. Knockdown of CD133 expression in ACC drug-resistant cells could inhibit the viability and invasion of tumors and enhance the sensitivity of drug-resistant cells to chemotherapeutic drugs.