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. 2021 Aug 23;11:733763. doi: 10.3389/fonc.2021.733763

Figure 4.

Figure 4

tRF-Glu-TTC-027 declined the biological function of gastric cancer in vitro. (A, B) The CCK-8 assay indicated that tRF-Glu-TTC-027 and p38 MAPK pathway inhibitor (p38 MAPK-IN) could effectively decline the proliferation of NCI-N87 and HGC-27. (C–E) tRF-Glu-TTC-027 was capable of suppressing the migration and invasion capacities of NCI-N87 and HGC-27 cell lines. (F, G) Through the observation and calculation of the cell gap closure, we demonstrated that tRF-Glu-TTC-027 was capable of fully inhibiting the migration ability of GC cells in the wound healing assays. (H, I) EdU assays showed that tRF-Glu-TTC-027 and p38 MAPK-IN formed fewer DNA replication levels than the control group. (J–L) The impact of tRF-Glu-TTC-027 and p38 MAPK-IN on GC cell cycle profile using flow cytometry. (M, N) The obvious change in the number of cell clones in the colony formation assays fully confirmed the inhibitory effect of tRF-Glu-TTC-027 and p38 MAPK-IN on GC. (*P < 0.05, Student’s t-test. Scale bar = 100 µm).