Fig 2: ANXA1 regulates cell migration through epithelial-mesenchymal transition. (A) GSEA analysis demonstrated a positive correlation between ANXA1 enrichment and epithelial-mesenchymal transition in PTC. NES: normalized enrichment score. (B) Western blot analysis showing the expression of E-cadherin, ZO-1, N-cadherin and Vimentin was changed after inhibition or overexpression of ANXA1 in PTC cells. GAPDH was used as a loading control. (C) The mRNA expression of EMT-related genes was detected by RT-PCR from three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001.

Fig 3: Effect of CSE exposure (24 h) on endothelial expression and distribution of ZO-1, Occludin and actin filaments. (A) Down-regulation of ZO-1 expression and disruption and cell-cell junctions were progressively more significant following exposure to 3R4F, NF and ultralow nicotine CSEs. Down-regulation and disruption at cell-cell contacts of occludin were also observed (B). Immunofluorescence analyses were confirmed by WB of corresponding membrane fractions (C). Loss of BBB integrity was further assessed by permeability measurements to dextran molecules ranging from 3 to 70 kDa (D) n = 3 biological replicates, *p < 0.05, **p < 0.01, ***p < 0.001 compared to controls.

Fig 4: αPD-L1 reverses TNBC malignant evolution in the co-culture of TNBC cells and TAMs. (A and B) MDA-MB-231 and Hs578T cell migration capacity was assessed using wound healing and Transwell assays when the cells were treated with or without αPD-L1 in a co-culture system (magnification, ×200). (C) Protein expression levels of VEGF, MMP2 and MMP9 in MDA-MB-231 and Hs578T cells, with or without αPD-L1 in a co-culture system, were determined using western blot analysis. (D) Protein expression levels of the EMT markers, E-cadherin, ZO-1, N-cadherin, vimentin, Slug and Twist, in MDA-MB-231 and Hs578T cells, with or without αPD-L1 in a co-culture system, were determined using western blot analysis. (E) Protein expression levels of the stemness markers, CD44, Oct4, Nanog, Bmi1 and Sox2 in MDA-MB-231 and Hs578T cells, with or without αPD-L1 in a co-culture system were determined using western blot analysis. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. αPD-L1, programmed death-ligand 1 inhibitor; TNBC, triple-negative breast cancer; TAM/M2, tumor-associated macrophages/M2-type; VEGF, vascular endothelial growth factor; EMT, epithelial-mesenchymal transition; ZO-1, zonula occludens-1.

Fig 5: 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.