Background: Melittin (MEL) has been reported to exhibit anti-cancer effects in vitro against several types of cancer. Long non-coding RNA (lncRNA) ADAMTS9-AS2 can be used as a tumor suppressor. However, there is insufficient data on the potential link between MEL and ADAMTS9-AS2 in hepatocellular carcinoma (HCC).
Methods: RT-qPCR, CCK-8, colony formation, scratch wound healing and transwell assays were used to detect the function of MEL or ADAMTS9-AS2 on HCC cells. Furthermore, Western blot analysis was applied to determine that whether an association existed in MEL or ADAMTS9-AS2 with the PI3K/AKT/mTOR signal pathway. In addition, RT-qPCR and Western blot analysis validated that whether MEL has a demethylation effect.
Results: All the experimental data showed that MEL or ADAMTS9-AS2 inhibited the proliferation, migration and invasion of MHCC97-H and HepG2 cells, which may relate to PI3K/AKT/mTOR signal pathway. Moreover, the result showed that MEL treatment inhibited the expression of DNA methyltransferase protein-1 (DNMT1), which acted as the role of demethylation, and then up-regulated the expression of ADAMTS9-AS2, affecting the development of HCC.
Conclusions: ADAMTS9-AS2 played a role in MEL-induced HCC inhibition. This study provided an interesting theoretical basis and further evidence for the potential application of MEL in the treatment of HCC.
Keywords: ADAMTS9-AS2; Autophagy; Invasion; Melittin; Migration; Proliferation.
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