u2932 cells (MedChemExpress)
Structured Review

U2932 Cells, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 93 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/u2932+cells/pmc12796863-242-0-7?v=MedChemExpress
Average 95 stars, based on 93 article reviews
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1) Product Images from "Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy"
Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy
Journal: Molecular Therapy. Nucleic Acids
doi: 10.1016/j.omtn.2025.102804
Figure Legend Snippet: Design of anti-transcription γPNA and combination treatments to target the c-Myc oncogene (A) Schematic representation of gamma peptide nucleic (γPNA)-mediated inhibition of human c-Myc transcription and target site (NCBI database RefSeq: NG_007161.2 ). (B) Design of γPNA conjugated with nuclear localization signal (NLS) to target the indicated sites. ScR-γPNA2 is the scramble control. (C) Graphic representation of combination treatments with anti-transcription, γPNA1. The combination treatments include histone deacetylase inhibitors (HDACis), MYC/MAX inhibitors, small interfering RNA (siRNA), and small molecules targeting other pathways. (D) Polymerase chain reaction (PCR)-based amplicon assay to confirm binding of γPNA1 to the target site in U2932 cells. Amplicon assay after treatment of γPNA1 and ScR-γPNA2 with HDACi. (E) The graph represents quantification of γPNA1 and ScR-γPNA2 amplicon in combination with HDACi. (F) The graph represents the quantification of amplicon assay from class I HDACi with γPNA1. Results are presented as mean ± SEM. One-way ANOVA was used to determine the statistically significant difference between groups.
Techniques Used: Inhibition, Control, Histone Deacetylase Assay, Small Interfering RNA, Polymerase Chain Reaction, Amplification, Binding Assay
Figure Legend Snippet: Anti-transcription activity of γPNA1 with HDACi in lymphoma cells Relative fold change of c-Myc levels in U2932 cells measured by real-time PCR on day 2 after treatment with (A) γPNA1 and (B) ScR-γPNA2 in combination with romidepsin, entinostat, vorinostat, panobinostat, and belinostat. Results are presented as mean ± SEM and two-way ANOVA was used to determine the statistically significant difference between groups. Western blot analysis representing the change in c-MYC protein on day 2 after treatment with γPNA1 and ScR-γPNA2 in combination with (C) romidepsin, (D) entinostat, (E) vorinostat, (F) panobinostat, and (G) belinostat. ∗∗(C–F) Cyclophilin B was used as an endogenous control, and the same blots are presented in C–S3G. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, and the p value between groups was determined using one-way ANOVA.
Techniques Used: Activity Assay, Real-time Polymerase Chain Reaction, Western Blot, Control
Figure Legend Snippet: Cell viability of Histone deacetylase inhibitors in combination with γPNA1 (A) Cell viability of U2932 cells treated with increasing doses of HDACi (romidepsin, entinostat, vorinostat, panobinostat, and belinostat) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 48 h. Results are presented as mean ± SEM. (B) The IC 50 ± SEM values of HDACi and combination treatment of HDACi with γPNA1 in U2932 cells. (C) Cell viability of Raji cells treated with increasing doses of HDACi (romidepsin, entinostat, vorinostat, panobinostat, and belinostat) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 48 h. Results are presented as mean ± SEM. (D) The IC 50 ± SEM values of HDACi and combination treatment of HDACi with γPNA1 in Raji cells.
Techniques Used: Histone Deacetylase Assay
Figure Legend Snippet: MYC/MAX inhibitors in combination with anti-transcription γPNA1 Cell viability of (A) U2932 and (B) Raji cells treated with increasing doses of MYC/MAX inhibitors (Myci975, EN4, 10058-F4, and sAJM589) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 72 h. Results are presented as mean ± SEM. The IC 50 (95% CI) values of MYC/MAX inhibitors alone and combination treatment of MYC/MAX with γPNA1 in (C) U2932 and (D) Raji cells. (E) Cell viability of γPNA1-treated U2932 and Raji cells at 8 μM concentration. Western blot analysis representing the change in c-MYC protein 72 h after treatment with γPNA1 and ScR-γPNA2 in combination with (F) Myci975, (G) EN4, (H) 10058-F4, and (I) sAJM589. ∗∗(F–I) Cyclophilin B was used as an endogenous control, and the same blots are presented in A–S7D. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, p value for one-way ANOVA.
Techniques Used: Concentration Assay, Western Blot, Control
Figure Legend Snippet: Efficacy of small molecules targeting other pathways with anti-transcription γPNA1 (A) Cell viability of U2932 and Raji cells treated with increasing doses JQ1 (BRD4 inhibitor) alone and with γPNA1 and ScR-γPNA2 for 48 h. (B) Cell viability of U2932 and Raji cells treated with increasing doses of sapnisertid (mTOR inhibitor) alone and with γPNA1 and ScR-γPNA2 for 48 h. (C) Cell viability of MDA-MB-231 cells treated with increasing doses of dinaciclib (CDK inhibitor) alone and with γPNA1 and ScR-γPNA2 for 48 h. (D) The IC 50 (95% CI) values of small molecule inhibitors alone and in combination with γPNA1. (A–C) Results are presented as mean ± SEM.
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