BACKGROUND
MicroRNA (miR)-106a was involved in the
tumorigenesis and highly expressed in
gastric cancer. Required
apatinib resistance greatly limits its efficacy in patients. Thus, the aim of the present study was to investigate the potential role of miR-106a-3p in
gastric cancer cells with
apatinib-resistance. MATERIAL AND METHODS The expression of miR-106a-3p was quantified by real-time quantitative polymerase chain reaction (RT-qPCR). Cell Counting Kit-8 (CCK-8) assay was performed to analyze the sensitivity of
gastric cancer cells to
apatinib. The expression of relevant drug-resistant
proteins was detected by western blot. We searched Targetscan6.2 to find out the target gene of miR-106a-3p.
Luciferase reporter assay was used to analyze whether miR-106a-3p bound to relevant gene of SOCS family. The SOCS2, SOCS4, and SOCS5 were qualified by western blot, and their
mRNA levels were detected by RT-qPCR. Further, JAK2, STAT3, and their phosphorylation levels were detected by western blot. RESULTS The results showed that the expression of miR-106a-3p was increased in apatinib‑resistant
gastric cancer, while miR-106a-3p inhibitor reduced the drug-resistance of SGC-7901-AP cells to
apatinib. Dual
luciferase reporter gene assay suggested that SOCS2, SOCS4, and SOCS5 were target genes of miR-106a-3p. The relevant SOCS genes silencing reversed the effects of miR-106a-3p inhibitor on decreasing the
apatinib resistance of SGC-7901-AP cells, while the phosphorylation level of JAK and STAT reduced by miR-106a-3p inhibitor were increased. CONCLUSIONS miR-106a-3p induces
apatinib resistance and activates JAK2/STAT3 by targeting SOCS system in
gastric cancer. miR-106a-3p/SOCS plays a potent role in
gastric cancer cell resistance to
apatinib.