Alkannin represses growth of pancreatic cancer cells based on the down regulation of miR‐199a

Alkannin displays tumor suppressive activity by initiating apoptosis. Here, we corroborated its role in pancreatic carcinoma (PANC-1) cells and addressed the molecular mechanism in which microRNA-199a (miR-199a) and Klotho might be implicated. PANC-1 and MIN6 cells were treated by alkannin and its role was evaluated in cellular viability. Next we assessed the ability of PANC-1 cells to proliferate, migrate, and invade as well as apoptosis process. Besides, proliferating cell nuclear antigen (PCNA), CyclinD1, p53, and caspases were quantified using Western blot. miR-199a was detected by qRT-PCR. miR-199a-silenced or -replenished cells were established to study its function role in Klotho in conjunction with alkannin. Further, Klotho-overexpressed or -silenced cells were constructed to investigate the alteration of mTOR and MEK/ERK pathways. Alkannin repressed the viability of PANC-1 cells instead of MIN6 cells. Alkannin counteracted the growth of PANC-1 cells through inhibiting proliferation, migration, and invasion and facilitating apoptosis, which was evidenced by the modulation on PCNA, CyclinD1, p53, and cleavage of caspases. The silence of miR-199a by alkannin was also involved in the antitumor process. Alkannin enhanced Klotho expression possibly through silencing miR-199a. Besides, mTOR and MEK/ERK signaling were counteracted by Klotho overexpression while facilitated by its silence. Alkannin inhibited the growth of PANC-1 cells via modulating miR-199a-Klotho node. During this process, mTOR and MEK/ERK pathways were blunted.