Chemotherapy resistance of cancer mainly has innate resistance and acquired drug resistance, which is mainly caused by the gene mutation induced by chemotherapy drugs. Alternative splicing of CD44 has been shown to be associated with the occurrence and development of tumors especially the multidrug resistance, but the underlying mechanism of CD44 in drug resistance remains unclear. Previous studies have found CD44 variants could significantly improve tumor resistance, therefore, we hypothesized the CD44v16, a CD44 variant found in our lab, might confer drug resistance in K562 cell. Through lentiviral expression system, the CD44v16 gene was introduced into the sensitive K562 cell, and the result indicated it could remarkably improve the drug resistance index. Real-time PCR and western blot experiments showed the expressions of protein p65, Bcl-2, Snail, and IKKβ in CD44v16-positive cell group were higher than the CD44v16-negative group. Therefore, we suggest the CD44v16 could induce the K562 cell acquired with resistance to adriamycin via NF-κB/Snail/Bcl-2 pathway, which paved the way for further study the function of CD44v16 in drug resistance.
Keywords: Adriamycin; CD44v16; Drug resistance; K562.
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