Fig 2: IL-22 administration activates autophagy in livers.a HepG2 cells were processed for transmission electron microscopy (n = 3) (left) with quantitative analysis (right). Red arrows indicate the number and location of autophagosomes. b The protein levels of P62, LC3II/I, and Cleaved Caspase 3 in livers of mice (left) and the quantity of the protein levels (right). * indicates the significant difference compared with Control group, p < 0.05, # indicates the significant difference compared with LPS group, p < 0.05.

Fig 3: BET bromodomain inhibition increases the sensitivity of the small intestine to chemotoxic stress.(A) Representative H&E images, immunohistochemistry for active caspase-3, and immunofluorescence for Ki67 of the small intestine of mice after treatment with vehicle control, BETi, gemcitabine (Gem), or BETi + Gem are shown. (B) The villus height (avg. ± std. dev.) measured from 3 control and BETi treated mice are shown. (C) The apoptotic index (avg. ± std. dev.) from each group is shown. Significant increases (p < 0.01) in apoptosis relative to control mice are noted by an asterisks. (D) The proliferative index (avg. ± std. dev.) from each group is shown. Significant increases (p < 0.01) in proliferation relative to control mice are noted by an asterisks. (E) Difference in the height of the crypts from mice treated with BETi, Gem, and BETi + Gem relative to mice treated with vehicle control. The average (±std. dev.) of three mice are shown. Asterisk indicate p < 0.007.

Fig 4: Inhibition of both PLK1 and EGFR is more effective than inhibition of either target alone in ER NSCLC xenograft models. Mice bearing PC9-ER9 xenograft tumors with volumes of 150 mm3 were treated with volasertib and/or erlotinib or with vehicle controls(A) Tumor volume was measured twice weekly and significantly decreased after combination treatment. After 3 weeks of treatment, the mice were humanely killed. Resected tumors were subjected to immunohistochemical analysis for Ki67 (C) and caspase 3 (B) protein expression, which was scored and quantitated.

Fig 5: Salidroside affects CML cell proliferation, apoptosis and cell cycle-related protein expression by downregulating miR-140-5p. (A) K562 and KCL22 cells were treated with 80 µM salidroside for 24 h. RT-qPCR was then utilized to examine the expression levels of miR-140-5p. **P<0.01 and ***P<0.001 vs. control. (B) K562 and KCL22 cells were transfected with miR-140-5p inhibitor or inhibitor NC. RT-qPCR was utilized to examine the expression levels of miR-140-5p. ***P<0.001 vs. inhibitor NC. (C and D) After transfection with miR-140-5p inhibitor or NC for 48 h, K562 and KCL22 cells were stimulated with 80 µM salidroside for 24 h. CCK-8 assay was performed to assess cell viability. (E and F) The protein expression levels of Cyclin D1 and p21 were measured by western blotting. (G and H) Apoptosis was measured by flow cytometry. (I and J) The protein expression levels of Bcl-2, Bax, pro-caspase-3 and cleaved caspase-3 were determined by western blotting; Results for Bcl-2 and Bax were plotted as fold-ratios relative to β-actin. Results for cleaved caspase-3 were plotted as fold-ratios relative to pro-caspase-3. ***P<0.001 vs. control; #P<0.05, ##P<0.01 and ###P<0.001 vs. Sal + inhibitor NC. CML, chronic myeloid leukemia; RT-qPCR, reverse transcription-quantitative PCR; NC, negative control.