To explore the effects of woginostatin (WOG) on the biological behaviors of gastric cancer cells through long non-coding RNA small nucleolar RNA host gene 16 (LncRNA SNHG16)/microRNA (miR)-302a-3p/E2F transcription factor 1 (E2F1).

In cell experiment, human gastric cancer cells (MGC-803) were divided into cell control group (normal culture), cell experimental-H group (100 μmol·L^-1 WOG treated cells), oe-NC group (transfected oe-NC), oe-LncSNHG16 group (transfected oe-LncSNHG16), mimic-NC group (transfected mimic-NC), miR-302a-3p mimic group (transfected miR-302a-3p mimic), WOG + oe-NC group (transfected oe-NC based on 100 μmol·L^-1 WOG treated cells), WOG + oe-LncSNHG16 group (transfected oe-LncSNHG16 based on 100 μmol·L^-1 WOG treated cells), WOG +oe-LncSNHG16+miR-302a-3p mimic group (transfection of oe-LncSNHG16 and miR-302a-3p mimic on the basis of 100 μmol·L^-1WOG treatment group). In animal experiment, the subcutaneous transplanted tumor model of gastric cancer was established in BALB/C male nude mice. The nude mice were randomly divided into animal experimental-L, -M and -H dose groups (15, 30 and 60 mg·kg^-1 WOG gavage), and the animal control group was gavaged with equal volume of physiological saline, with 10 mice in each group. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression levels of LncRNA SNHG16, miR-302a-3p and E2F1. The cell viability was detected using the cell counting kit 8 (CCK-8). The cell proliferation, invasion and apoptosis were detected using 5-ethynyl-2′-deoxyuridine (Edu), Transwell and in situ terminal transferase labeling technique (TUNEL).

In cell experiment, the relative expression levels of LncRNASNHG16 in cell control group, cell experimental-H group, mimic-NC group, miR-302a-3p mimic group, oe-NC group and oe- LncSNHG16 group were 1.00±0.13, 0.47±0.05, 1.00±0.10, 0.81±0.12, 1.02±0.09 and 3.76±0.41, respectively; the relative expression levels of miR-302a-3p were 1.00±0.11, 3.60±0.39, 1.00±0.09, 3.74±0.32, 0.97±0.10 and 0.27±0.03, respectively; the relative expression levels of E2F1 mRNA were 1.00±0.14, 0.23±0.02, 1.00±0.10, 0.33±0.03, 0.95±0.08 and 2.18±0.25, respectively. Compared the cell experimental-H group with cell control group, compared miR-302a-3p mimic group with mimic-NC group and compared oe-LncSNHG16 group with oe-NC group, the above indicators were all statistically significantly different (P<0.01, P<0.001). The proliferation rates of cell control group, cell experimental-H group, WOG + oe-LncSNHG16 group and WOG + oe-LncSNHG16 + miR-302a-3p mimic group were (95.04±10.14)%, (36.36±4.75)%, (97.64±11.04)% and (31.87±3.56)%, respectively; the number of invasive cells were (147.36±15.01), (43.31±6.25), (153.45±15.22) and (37.35±5.04), respectively; the apoptosis rates were (7.83±0.83)%, (35.77±4.38)%, (8.44±0.88)% and (29.35±3.09)%, respectively. There were statistically significant differences in the above indexes between the cell experimental-H group and the cell control group, between the WOG + oe-LncSNHG16 group and the cell experimental-H group, and between the WOG + oe-LncSNHG16 group and the WOG + oe-LncSNHG16 + miR-302a-3p mimic group (all P<0.001). In animal experiment, the tumor volume of animal control group and animal experimental-L,-M,-H groups were (2 554.50±280.41), (2 194.10±234.22), (1 512.40±166.75) and (1 146.20±124.32) mm³, respectively; the tumor mass was (2.13±0.28), (1.84±0.23), (1.65±0.21) and (1.32±0.14) g, respectively. There were statistically significant differences in the above indicators between experimental-L, -M, -H groups and animal control group (P<0.05, P<0.01, P<0.001).

WOG can inhibit the proliferation and invasion of gastric cancer cells and promote their apoptosis. This may be related to the regulation of the LncRNA SNHG16/miR-302a-3p/E2F1 axis, which blocks the cell cycle.