Solamargine, a derivative from the steroidal
solasodine in Solanum species, has exhibited anticancer activities in numerous types of
cancer; however, its role in
gastric cancer (GC) remains unknown. In the present study, it was demonstrated that
Solamargine suppressed the viability of five
gastric cancer cell lines in a dose‑dependent manner and induced notable alterations in morphology. Treatment with
Solamargine promoted cell apoptosis (P<0.01).
Solamargine increased the expression of
long noncoding RNA (lnc) p53 induced transcript and lnc nuclear paraspeckle assembly transcript 1 (NEAT1)_2 (P<0.01) in GC by reducing the phosphorylation of extracellular signal‑regulated
kinase (Erk)1/2 mitogen‑activated
protein kinase (MAPK). To gain insight into the potential mechanism, an Erk1/2 inhibitor (
U0126) was applied. The results revealed that lncNEAT1_2 expression levels increased, which was consistent with the effects of
Solamargine. Downregulation of lncNEAT1_2 in GC cells revealed no effect on the expression levels of total Erk1/2 and, and counteracted the effect of
Solamargine.
Solamargine was observed to increase the expression of lncNEAT1_2 via the Erk1/2 MAPK signaling pathway. Of note, the knockdown of lncNEAT1_2 reduced the inhibitory effect of
Solamargine (P<0.05). Additionally, experiments in vivo and in primary GC cells from patients demonstrated that
Solamargine significantly suppressed
tumor growth (P<0.05). In vivo analysis of a xenograft mouse model further supported that
Solamargine could induce the apoptosis of
cancer cells in
tumor tissue as observed by a terminal deoxynucleotidyl transferase‑mediated dUTP‑biotin nick end labeling and H&E staining (P<0.05). Experiments in primary GC cells from patients verified the anti‑tumor effect of
Solamargine. In summary, the findings of the present study indicated that
Solamargine inhibited the progression of GC by regulating lncNeat1_2 via the MAPK pathway.