gene 1 inhibitor  (MedChemExpress)

Journal: EMBO Reports

Article Title: TGFβ-induced long non-coding RNA LINC00313 activates Wnt signaling and promotes cholangiocarcinoma

doi: 10.1038/s44319-024-00075-z

Figure Lengend Snippet: ( A ) TCF7 , LINC00313 and ACTL6A mRNA levels in HuCCT1 transfected with siACTL6A or siNC and in the presence or not of TGFβ. ( B ) Immunoblotting for TCF7, ACTL6A and β-actin, upon silencing ACTL6A, using the indicated siRNA concentrations. ( C ) TCF/LEF luciferase reporter assay in siACTL6A or siNC HuCCT1 cells treated with CHIR99021 or DMSO for 24 h. ( D – F ) qPCR analysis of ACTL6A ( D ), AXIN2 ( E ) and TCF7 ( F ) mRNAs in the same conditions as these of panel ( C ). ( G – I ) qPCR analysis of SULF2 ( G ), TCF7 ( H ) and ACTL6A ( I ) mRNA levels in pcDNA3 or LINC00313 over-expressing HuCCT1 transiently transfected with siACTL6A or siNC with or without TGFβ. ( J ) Immunoblotting for TCF7, ACTL6A and β-actin in the same conditions as these of panels G-I. ( K ) qPCR analysis of TCF7 , ACTL6A and LINC00313 RNA levels in HuCCT1 cells transiently transfected with siRNAs against LINC00313 or ACTL6A individually or simultaneously with both siRNAs and treated or not with TGFβ for 16 h. ( L ) RIP assay for endogenous Brg1 followed by qPCR for LINC00313 in HuCCT1 cells treated with TGFβ or BSA/HCl (vehicle control) for 16 h. ( M ) Proposed model for the molecular mechanism of LINC00313 . Data information: In panels ( A ), (D–I) and (K) qPCR data are presented as mean ± SD ( n = 3 biological replicates). In panel ( C ), luciferase assay data are presented as mean ± SD ( n = 6 biological replicates). In panel ( L ), RIP-qPCR data are presented as mean ± SD ( n = 3 technical replicates). * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001 (Student’s t -test). .

Article Snippet: The SMARCA2/4 bromodomain inhibitor PFI-3 (MedChemExpress, HY-12409) and the allosteric dual SMARCA2 and brahma-related gene 1 (BRG1)/SMARCA4 ATPase activity inhibitor BRM/BRG1 ATP Inhibitor-1 (MedChemExpress, HY-119374) were administrated to cells at 10 and 5 µM final concentrations, respectively.

Techniques: Transfection, Western Blot, Luciferase, Reporter Assay, Expressing, Control

Journal: Journal of Inflammation Research

Article Title: Mesenchymal Stem Cells Ameliorate DSS-Induced Experimental Colitis by Modulating the Gut Microbiota and MUC-1 Pathway

doi: 10.2147/JIR.S402592

Figure Lengend Snippet: Ferroptosis-related genes play a role in DSS-induced colitis and MSCs reverse the process of ferroptosis. ( A ) The qPCR detection of MUC-1 gene in colitis tissues. ( B ) The immunohistochemistry images of NC, DSS+PBS, and DSS+MSC groups in colon tissues (scale bar: 100µm). ( C ) The CCK-8 analysis of IEC-6 cell viability. The different concentration (10, 5, and 2.5µM) of GO-203 (MUC-1 inhibitor) was used to measure the cell viability at 48 h, GO-203 10, 5, and 2.5µM vs control. ( D ) The proliferation level of IEC-6 cells in the presence of GO-203 (5µM) at 24 h and 48 h measured by CCK-8 assay. ( E ) The cell viability of IEC-6 cells in the presence of GO-203 and co-culture with MSCs. ( F ) The Western blot analysis of MUC-1 expression after transfected with overexpressing MUC-1 lentivirus in IEC-6 cells. ( G ) The proliferation level of IEC-6 cells transfected with overexpressing MUC-1 lentivirus in 24 h, 48 h, and 72 h. ( H ) The IEC-6 cell viability after treated with erastin and RSL3 with the comparison of control and overexpressed MUC-1 group. ( I ) qRT-PCR analysis of MUC-1, SLC7A11 , and GPX4 after treated with GO-203 (5µM) for 48 h in IEC-6 cells. ( J ) qRT-PCR analysis of SLC7A11 and GPX4 after overexpressed MUC-1 in IEC-6 cells. ( K ) qRT-PCR analysis of SLC7A11 and GPX4 in the presence of erastin in the control and overexpressed MUC-1 group. ( L ) qRT-PCR analysis of SLC7A11, GPX4 , and ACSL4 in the presence of RSL3 in the control and overexpressed MUC-1 group. Data are presented as mean ± SD. ***P < 0.001, **P < 0.01, *P < 0.05.

Article Snippet: The MUC-1 gene inhibitor GO-203 (MCE) was added to IEC-6 cells with different concentrations (10, 5, and 2.5μM).

Techniques: Immunohistochemistry, CCK-8 Assay, Concentration Assay, Control, Co-Culture Assay, Western Blot, Expressing, Transfection, Comparison, Quantitative RT-PCR