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. 2022 Jun 8;12:759864. doi: 10.3389/fonc.2022.759864

Figure 8.

Figure 8

Knockdown of miR-4800-3p inhibits the growth and EMT of implanted tumors promoted by Huh7-derived exosomes in vivo. (A–C) Knockdown of miR-4800-3p suppressed tumor growth promoted by Huh7-derived exosomes. (D) The expression of miR-4800-3p was measured by qPCR assay. (E) The expression of E-cadherin, ZO-1, N-cadherin, STK25, p-YAP, YAP, TAZ, and PCNA was detected by Western blot analysis. (F) Schematic diagram of how exosomal miR-4800-3p is derived from high-metastatic HCC cells to promote the progression of HCC by mediating the Hippo signaling pathway by targeting STK25. Exosomal miR-4800-3p derived from high-metastatic HCC cells converted low-metastatic HCC cells to more aggressive HCC cells by mediating YAP/TAZ activation by targeting STK25 to promote stemness, proliferation, migration, invasion, and EMT in HCC. *p < 0.05, **p < 0.01 vs. control; ## p < 0.01 vs. Exo; & p < 0.05, && p < 0.01 vs. antagomir.