Fig 2: Western blot (WB) analyses of OCSC markers in DSPP-MMP20 silenced OSC2 cells (a). Normalization of ALDH1, ABCG2, BMI1, Podoplanin (PDPN), CD44, CD133 and LGR4 protein levels was with ß-actin . Y- (vertical) axis of histograms represent expression level for each protein relative to ß-actin (b). OSC2 = parent (untreated) cells; shC = control (scramble sequence) cells; shD = DSPP silenced cells; shM = MMP20 silenced cells; shDM = combined DSPP-MMP20 silenced cells. *p < 0.05 compared with ShC. Experiments were performed in triplicate

Fig 3: HOTAIR regulated the DDP resistance, cell proliferation, invasion, and apoptosis of Saos2/DDP and MG-63/DDP cells by binding miR-106a-5p. HOTAIR overexpression vector was transfected into Saos2/DDP and MG-63/DDP cells alone or together with miR-106a-5p mimic; following transfection for 48 h, (A, B) the IC50 values of DDP, (C, D) and the protein levels of MDR1, ABCB1, ABCC1, ABCG2, MRP5, and LRP1 were detected by CCK-8 and western blotting. Cell proliferation (E, F), invasion (G, H), and apoptosis (I, J) were detected by CCK-8, transwell, and flow cytometry. n = 3, **P < 0.01. DDP: cisplatin.

Fig 4: Low-dose ATO downregulated expression of stemness-related genes and inhibited self-renewal and tumorigenic capacity of HCC CSCs. (A) Relative mRNA expression of stemness-related genes OCT4, NOTCH1, SOX2, ABCG2, and NANOG altered by ATO treatment in Huh7, Hep3B, and primary HCC cells. (B) Immunofluorescent staining of stemness-related proteins ABCG2, SOX2, OCT4, and CD133 in Huh7 cell spheres with or without ATO treatment (magnification: 200×). (C) ATO impaired sphere-forming ability of Huh7 and Hep3B cells (magnification: 200×). (D) Upon exposure to ATO, the number of clones diminished dramatically in Huh7 cells and Hep3B cells. (E) NOD/SCID mice were subcutaneously inoculated with CD133+ or CD133- Huh7 cells to explore the tumorigenic potential altered by ATO

Fig 5: UCP2 suppression induced ABCG2 expression via ROS/Nrf2 in hypoxia-triggered NSCLC chemoresistanceA. Western blot analysis of cells infected with lentiviruses expressing control or UCP2-targeted shRNAs in normoxia. B. Measurement of ROS levels in cells exposed to normoxia or hypoxia and treated with cisplatin (CP, 30 µM) or docetaxel (DTC, 10 µM). *, #P < 0.05 compared with normoxia and hypoxia groups, respectively. C. Western blot analysis of cells exposed to hypoxia and treated with vehicle or NAC (10 mM). D. CCK8 assays of the cytotoxicity of chemotherapeutic reagents in cells exposed to hypoxia and treated with vehicle or NAC. E. Western blot analysis of cells stably transfected with a control or UCP2-overexpressing construct after exposure to hypoxia. F. Assays for ROS levels in cells stably transfected with a control or UCP2-overexpressing construct after exposure to normoxia or hypoxia. G. Representative immunohistochemical staining using carcinoma tissues from chemotherapy-sensitive and -resistant patients. Scale bars, 100 µm. Data are represented as the mean ± SEM of n = 3 replicates or representative of 3 independent experiments. *P < 0.05.