Fig 2: Co-localization of pluripotency markers with the proliferation marker MKI67 in neonatal marmoset ovary. (A) OCT4A-stained oogonia. Oogonia with weak OCT4A signals are highlighted by a red arrow. (B) The same tissue section shown in A stained for MKI67. (C) Merged stainings from A and B. (D) LIN28A-stained oogonia. (E) The same tissue section shown in D stained for MKI67. (F) Merged stainings from D and E.

Fig 3: The increasing expression of LKB1 inhibits proliferation of NRVMs. (A) The relative mRNA and protein expressions of LKB1 in the heart at different postnatal time point are shown. Relative mRNA levels of Lkb1 in P1, P7, and P28 mice hearts were assayed by qRT-PCR (n = 5) in A1; (A2) Relative protein expression of LKB1 in P1, P7, and P28 mice hearts were detected by western blots (n = 8); (A3) The quantitative grayscale density of western blots of A2; GAPDH was used for normalization; (B) Representative confocal microscopy of Ki67 and pH3 immunostaining at P7 and P28 hearts (Ki67+, pH3+ in red, and cTnT+ in green indicate proliferating cardiomyocytes). The Ki67 and pH3 positive cell percentages (from total >1000 cells) were calculated and shown in B2, scale bar = 50 µm. (C) Confocal microscopy of cell proliferation of NRVMs with LKB1 overexpression (Ki67+, pH3+, and Aurora B+ in red, and cTnT+ in green indicate proliferating cardiomyocytes), quantified in C2. 2000–5000 cells were randomly selected and quantified in each group, scale bar = 20 µm; (D) Cell cycle-associated gene expressions of NRVMs treated with vector or LKB1 overexpression plasmid were detected by qRT-PCR; (E) Representative images (E1) of cell cycle-related protein expression and quantification in E2, were analyzed by western blots (n = 6, GAPDH was used as internal control), *p < 0.05, **p < 0.01, ***p < 0.001. p: Postnatal day; NRVMs: Neonatal rat ventricular myocytes; LKB1: Liver kinase B1; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; qRT-PCR: Quantitative real-time PCR.

Fig 4: miR-495-3p inhibitor restores the effects of circ-BIRC6 knockdown on the proliferation of bladder cancer cells. (A) miR-495-3p expression was evaluated using reverse transcription-quantitative PCR after transfection with the miR-495-3p inhibitor. **P<0.01 vs. NC inhibitor. (B) Cell proliferation was assessed using a Cell Counting Kit-8 assay. (C) Colony formation assay. ***P<0.001 vs. sh-NC; ##P<0.01 vs. sh-circ-BIRC6#1 + NC inhibitor. (D) Ki-67 expression was assessed using immunofluorescence. Magnification, ×200. (E) Fluorescence intensity from part (D). ***P<0.001 vs. sh-NC; ##P<0.01 vs. sh-circ-BIRC6#1 + NC inhibitor. NC, negative control; sh, short hairpin RNA; circ-BIRC6, circular RNA baculoviral IAP repeat-containing 6; miR, microRNA.

Fig 5: Additive effect of PTX and SPA70 in PTX-resistant A549/TR xenograft tumor growth. BALB/c-Nude mice were treated with 5 mg/kg paclitaxel with or without SPA70 intraperitoneal injection three times per week. (A) The photograph of xenograft tumors in all groups. (B) The volume of the xenograft tumors from the combination group was remarkably smaller than the vehicle control and single compound groups. #, p < 0.05, compared with vehicle administration groups. (C) Mice body weight curves over drug administration time period. (D) H&E and IHC staining of tumor tissues revealed remarkably reduced expressions of P-gp, along with diminished PXR and Tip60 expression, decreased proliferation (Ki67), and increased cell apoptosis (cleaved caspase 3) in the combination treatment group. The photographs were taken by microscopy (200×).