Fig 1: ZEB2-AS1 promotes the chemoresistance of ADR in AML cells through regulating INPP4B. (A–D) QRT-PCR and western blot assays showed that ZEB2-AS1 could regulate the expression of INPP4B. (E and F) IC50 of ADR was measured by MTT assay. (G and H) The apoptosis of AML cells was detected by flow cytometry analysis. (I and J) The apoptosis-related proteins Bcl-2, cleaved-caspase-3 and Bax were detected by western blot. *P < 0.05.
Fig 2: Regulation of apoptosis-related protein expression in H2O2-induced RPE cells by catalpol pretreatment. ARPE-19 cells were pretreated with or without catalpol (10, 20, and 40 µM) for 24 h and then treated with 400 µM H2O2 for 6 h. The bands and relative protein expressions of Bcl-2, Bax, Fas, cleaved caspase-3, cleaved caspase-8, cleaved caspase-9, and cleaved caspase-PARP were measured with Western blot assay. ß-actin was used as internal control. Data are presented as mean ± S.D. of three independent experiments (* p < 0.05 vs. control group, # p < 0.05 vs. H2O2 (400 µM)-treated group).
Fig 3: Hsa_circ_104348 regulated miR-187-3p to affect proliferation, migration, invasion, and apoptosis of HCC cells, and may have effect on Wnt/ß-catenin signaling pathway.Huh7 cells were co-transfected with sh-circRNA or sh-NC and miR-187-3p inhibitor or inhibitor NC: A and B Cell proliferation abilities were determined by CCK-8 assay (A) and colony formation assay (B). C and D Cell apoptosis was determined by EdU staining (C) and flow cytometry assay (D). The scale bars were 100 µm. E and F Cell migration and invasion abilities were checked by wound healing assay (E) and transwell assay (F). The scale bars were 50 µm. G The expression of E-cadherin, N-cadherin was determined by IF. The scale bars were 20 µm. H The expression of RTKN2, ß-catenin, PCNA, CyclinD1, c-Myc, Bcl-2, Bax, MMP-7, E-cadherin, N-cadherin was determined by western blot. Data were expressed as mean ± SD.
Fig 4: miR-326-mediated influences are partly reversed by the overexpression of TAZ in BC cells. MCF-7 and MDA-MB-468 cells were transfected with miR-NC, miR-326, miR-326 + pcDNA or miR-326 + TAZ. (A) Reverse transcription-quantitative PCR and (B) western blot assay were used to examine the mRNA and protein expression levels of TAZ, respectively, in BC cells. (C) Colony formation assay was performed to measure the proliferative capacity of BC cells, and the number of colonies in each group was detected. MTT assay was used to analyze the proliferative ability of (D) MCF-7 and (E) MDA-MB-468 cells. (F) Flow cytometry was conducted to assess the apoptosis of BC cells. Protein expression levels of Bcl-2, Bax and Cleaved caspase-3 were detected in (G) MCF-7 and (H) MDA-MB-468 cells by western blot assay. Transwell assays were conducted to assess the (I) migration and (J) invasion of BC cells. *P<0.05. Bcl-2, B cell leukemia/lymphoma 2; Bax, Bcl-2 associated X apoptosis regulator; BC, breast cancer; miR, microRNA; NC, negative control; TAZ, transcriptional co-activator with PDZ-binding motif; OD, optical density.
Fig 5: Circ_0000511 accelerates the proliferation, migration and invasion, and impedes the apoptosis of BC cells. MCF-7 and MDA-MB-468 cells were transfected with si-NC or si-circ_0000511. (A) Circ_0000511 expression was detected in BC cells by reverse transcription-quantitative PCR. (B) Colony formation assay was used to test the proliferative ability of BC cells. MTT assay was used to assess the proliferation of (C) MCF-7 and (D) MDA-MB-468 cells. (E) Apoptosis of BC cells was evaluated by flow cytometry. Western blot assay was used to detect the protein expression levels of Bcl-2, Bax and Cleaved caspase-3 in (F) MCF-7 and (G) MDA-MB-468 cells. Transwell assays were conducted to assess the (H) migratory and (I) invasive abilities of BC cells. *P<0.05 vs. si-NC. Bcl-2, B cell leukemia/lymphoma 2; Bax, Bcl-2 associated X apoptosis regulator; BC, breast cancer; circ_0000511, circular RNA 0000511; si, small interfering RNA; NC, negative control; OD, optical density.
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