Fig. 5

CACNA1d was verified up-regulated in GC tissues and was selected as the potential target of tRF-Val-CAC-016. a The Venn diagram took the overlap of MAPK components and the predicted target genes of tRF-Val-CAC-016. b–c CACNA1d, PLA2G4A, and TNF in GSE65801, CACNA1d, and PLA2G4A in TCGA-STAD were significantly up-regulated. d–l CACNA1d, TNF, TGFBR1, PDGFC, GADD45B were significantly and negatively related to the prognosis of GC. m–n The tissue microarray (TMA) with 90 pairs of GC specimens, including detailed follow-up data. o The expression of CACNA1d was not significantly related to the prognosis of GC (p = 0.1805). p Ten representative IHC images of TMA were presented, including GC and NATS. q The protein levels of CACNA1d were highly expressed in nine GC tissues compared with corresponding NATs. r si-CACNA1d-1 was a better inhibitor for CACNA1d compared with si-CACNA1d-2 and si-CACNA1d-3. s pcDNA-CACNA1d could significantly enhance the expression of CACNA1d. t The tRF-Val-CAC-016 inhibitor was able to reverse the suppressive function of si-CACNA1d on GC cells to some extent. u The effect of pcDNA-CACNA1d on GC was partly relieved by tRF-Val-CAC-016 mimics. *P < 0.05, **P < 0.01, statistically significant