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. 2022 Apr 14;12:804689. doi: 10.3389/fcimb.2022.804689

Figure 4.

Figure 4

ETBF induces tumor growth by downregulating miR-155-5p, miR-200a-3p, and miR-149-3p. BFAL1 was upregulated in ETBF-infected CRC cells and subsequently decreased the levels of miR-155-5p and miR-200a-3p, which attenuated their suppressive function on target RHEB mRNA expression. The downregulated RHEB consequently activates the RHEB/mTOR pathway, thereby mediating ETBF-induced tumor growth. miR-149-3p is also significantly downregulated in ETBF-infected CRC cells. Regulation of miR-149-3p was attributed to METTL14-dependent m6A modification via modifying pri-miRNA splicing. In ETBF-infected CRC cells, METTL14 was downregulated so that the level of miR-149-3p was reduced, which further upregulated target PHF5A. The overexpression of PHF5A upregulated the target mRNA level of KAT2A in CRC cells, which can upregulate SOD2 via directly binding to the promoter region of SOD2. More importantly, the overexpression of SOD2 is relevant to poor clinical outcomes in gastric cancer, and SOD2 may promote intestinal inflammation and tumorigenesis.