Journal: Cancer letters

Article Title: WEE1 Stabilizes MYC to Promote Therapeutic Resistance in Esophageal Adenocarcinoma

doi: 10.1016/j.canlet.2026.218418

Figure Lengend Snippet: A. 21 positive hits (red), which synergized with MK-1775 in O19 cells during the first round of screening using an 892 FDA-approved drug screening library. B. Panobinostat (red arrow) was found to synergize with MK-1775 in FLO1 (blue) and SK-GT4 (red) cell lines during the second round of screening. C. Synergy Finder analysis results in FLO1, OE33, OE19, and SK-GT4 cell lines treated with MK-1775 and Panobinostat. *P<0.05, **P<0.01, ***P<0.001. D. Flow cytometric analysis of Annexin V & SYTOX red dual staining in OE33 cells treated with MK-1775/Panobinostat alone or a combination. E. Percentage of apoptotic cells from Fig D *P<0.05, **P<0.01, ***P<0.001. F. Western blot analysis of PARP, Cl-PARP, Caspase 3, Cl-Caspase 3, and β-ACTIN in OE33 cells treated with MK-1775/ Panobinostat alone or a combination. G. Flow cytometric analysis of Annexin V & SYTOX red dual staining in OE19 cells treated with MK-1775/Panobinostat alone or a combination. H. Percentage of apoptotic cells from Fig G *P<0.05, **P<0.01, ***P<0.001. I. Western blot analysis of PARP, Cl-PARP, Caspase 3, Cl-Caspase 3, and β-ACTIN in OE19 cells treated with MK-1775/ Panobinostat alone or a combination.

Article Snippet: Panobinostat (Selleckchem) was administered intraperitonially at a dose of 10 mg/kg, once a week for 4 weeks.

Techniques: Drug discovery, Staining, Western Blot

Journal: Cancer letters

Article Title: WEE1 Stabilizes MYC to Promote Therapeutic Resistance in Esophageal Adenocarcinoma

doi: 10.1016/j.canlet.2026.218418

Figure Lengend Snippet: A. Human EAC PDX-derived Organoids treated with MK-1775 / Panobinostat alone or in combination. B. Quantification of organoid diameter from A. C. Tumor growth curves in 4 experimental groups (Untreated control, MK-1775, Panobinostat, combination of MK-1775 & Panobinostat) at the end of the experiment. D. Western blot analysis of PARP, Cl-PARP, Caspase 3, CL-Caspase3, and β-ACTIN in Mouse Xenografts. E. Immunofluorescence staining for P-CDC2 Y15 (green), C-MYC (red), MRP1 (green), and Ki67 (red) in Mouse EAC PDXs, captured at 20X Magnification. F. Quantification data from E. *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001.

Article Snippet: Panobinostat (Selleckchem) was administered intraperitonially at a dose of 10 mg/kg, once a week for 4 weeks.

Techniques: In Vivo, Derivative Assay, Control, Western Blot, Immunofluorescence, Staining

Journal: bioRxiv

Article Title: A class act: HDAC1- Malat1 regulates MDSC apoptosis and cell cycling to decrease suppression of T cells

doi: 10.64898/2026.03.23.713743

Figure Lengend Snippet: (A) UMAP visualization of major cell clusters identified from single cell RNA sequencing (scRNA-seq) of NT2.5-LM breast-to-lung metastatic tumors after 3 weeks of treatment with: vehicle (V), Entinostat (E), anti-CTLA-4 + anti-PD-1 immune checkpoint inhibitors (PC), and Entinostat + anti-CTLA-4 + anti-PD-1 combination (EPC). Subclusters of MDSCs identified: G-MDSCs and M-MDSCs. (B) Iterative logistic regression analyses conducted on the major MDSC cluster comparing the Vehicle (V) and Entinostat + ICIs combination treatment (EPC). (C) Expression of Malat1 / MALAT1 in G- and M-MDSCs isolated from lung metastases of NT2.5-LM mice treated with vehicle vs. Entinostat for 3 weeks (left, n=2 from 5 pooled mice per treatment group), J774M murine MDSC-like cell line treated with Entinostat for 24 hours (middle, n=3), and human PBMC-derived MDSCs (hMDSCs) treated with Entinostat for 24 hours (right, n=3). (D) Median Fluorescence Intensity expression of Malat1 in CD45 + CD11b + MHC-II - F4/80 - Ly6G - Ly6C hi cells from lung metastases in 4T1 mice, treated with vehicle (V), Entinostat (E), and Entinostat + ICIs (EPC) for 3 weeks. (E) Expression of Malat1 in J774M cell line treated with various concentrations of various HDAC inhibitors, with corresponding targeted class and specific HDACs. One-way ANOVA for (C, E: all statistically significant with p<0.05, unless indicated as non-significant (ns)), Kruskal-Wallis test with Dunn’s correction for (D). * p<0.05, *** p< 0.001, **** p<0.0001. ENT = Entinostat; PAN = Panobinostat; BEL = Belinostat; VOR = Vorinostat; TSA = Trichostatin A; DOM = Domatinostat; CHL = Chlopynostat; PYR = Pyroxamide; SCA = Santacruzamate A; RGF = RGFP966; TMP = TMP269; SIS = SIS17.

Article Snippet: Chemical inhibitors used in this study: Entinostat (Syndax Pharmaceuticals), Panobinostat (MedChemExpress, cat. #HY-10224), Belinostat (MedChemExpress, cat. #HY-10225), Vorinostat (MedChemExpress, cat. #HY-10221), Trichostatin A (MedChemExpress, cat. #HY-15144), Domatinostat (MedChemExpress, cat. #HY-16012A), Chlopynostat (MedChemExpress, cat. #HY-161464), Pyroxamide (MedChemExpress, cat. #HY-13216), Santacruzamate A (MedChemExpress, cat. #HY-N0931), RGFP966 (MedChemExpress, cat. #HY-13909), TMP269 (MedChemExpress, cat. #HY-18360), SIS17 (MedChemExpress, cat. #HY-128918), Stattic (MedChemExpress, cat. #HY-13818), Abemaciclib (MedChemExpress, cat. #HY-16297A), Palbociclib (MedChemExpress, cat. #50767).

Techniques: Single Cell, RNA Sequencing, Expressing, Isolation, Derivative Assay, Fluorescence

Journal: bioRxiv

Article Title: A class act: HDAC1- Malat1 regulates MDSC apoptosis and cell cycling to decrease suppression of T cells

doi: 10.64898/2026.03.23.713743

Figure Lengend Snippet: (A) Western blots of Tyr705 phosphorylated-STAT3 (pSTAT3), STAT3, and Beta-actin in G-MDSCs isolated from NT2.5-LM metastatic lung tumors. G-MDSCs were isolated with Ly-6G+ magnetic beads from single cell suspensions of dissociated metastatic lung tumors and stimulated with LPS (2 hours, 1 ug/mL). NT2.5-LM tumor-bearing mice were treated with vehicle vs. Entinostat (5 mg/kg, 5x/wk) for 3 weeks. Each lane represents one mouse (n=5 per treatment group). 50 ug of total protein lysate loaded in each lane. Band density quantified with Image J and adjusted density normalized to Beta-actin (right), outlier mouse #2 in Vehicle removed with ROUT at threshold Q=1%. Two-way ANOVA, * p<0.05. (B) Western blot of pSTAT3, STAT3, and Beta-actin in J774M cells after 24 hours of Entinostat treatment and IFN-γ stimulation (30 min, 20 ng/mL). 20 ug of total protein lysate loaded in each lane. (C) Western blot of pSTAT3, STAT3, and Beta-actin in hMDSCs after 24 hours of Entinostat treatment. 50 ug of total protein lysate loaded in each lane. (D) Representative flow plots (left) and quantification (right, n=3) of J774M STAT3-responsive GFP reporter after 18 hours of pre-treatment with various concentrations of various HDAC inhibitors and IFN-γ stimulation for 5-7 hours (20 ng/mL), indicative of percentage of STAT3 activation. One-way ANOVA for (D: all statistically significant with p<0.05, unless indicated as non-significant (ns)). ENT = Entinostat; PAN = Panobinostat; BEL = Belinostat; VOR = Vorinostat; TSA = Trichostatin A; DOM = Domatinostat; CHL = Chlopynostat; PYR = Pyroxamide; SCA = Santacruzamate A; RGF = RGFP966; TMP = TMP269; SIS = SIS17.

Article Snippet: Chemical inhibitors used in this study: Entinostat (Syndax Pharmaceuticals), Panobinostat (MedChemExpress, cat. #HY-10224), Belinostat (MedChemExpress, cat. #HY-10225), Vorinostat (MedChemExpress, cat. #HY-10221), Trichostatin A (MedChemExpress, cat. #HY-15144), Domatinostat (MedChemExpress, cat. #HY-16012A), Chlopynostat (MedChemExpress, cat. #HY-161464), Pyroxamide (MedChemExpress, cat. #HY-13216), Santacruzamate A (MedChemExpress, cat. #HY-N0931), RGFP966 (MedChemExpress, cat. #HY-13909), TMP269 (MedChemExpress, cat. #HY-18360), SIS17 (MedChemExpress, cat. #HY-128918), Stattic (MedChemExpress, cat. #HY-13818), Abemaciclib (MedChemExpress, cat. #HY-16297A), Palbociclib (MedChemExpress, cat. #50767).

Techniques: Western Blot, Isolation, Magnetic Beads, Single Cell, Activation Assay

Journal: bioRxiv

Article Title: A class act: HDAC1- Malat1 regulates MDSC apoptosis and cell cycling to decrease suppression of T cells

doi: 10.64898/2026.03.23.713743

Figure Lengend Snippet: (A) Representative brightfield images of J774M cells after 72 hours of Entinostat and Stattic treatment. Scale bars = 300 um. (B) Representative flow cytometry plots and (C) percentage of apoptotic (Annexin V+, Propidium Iodide -) J774M cells after 72 hours of Entinostat and Stattic treatment (n=3). (D) Representative flow cytometry plots and (E) percentage of apoptotic hMDSCs after 48 hours of Entinostat and Stattic treatment (n=3). (F) Expression of anti-apoptotic genes ( Bcl2a1a, Bcl2a1b, Bcl2l1 ; green) and pro-apoptotic genes ( Bcl6, Bid, Bax ; red) in J774M cells after 24 hours of Entinostat treatment (n=3). (G) Western blot of pro-apoptotic BCL-xL, anti-apoptotic BID, and Beta-actin in J774M cells after 24 hours of Entinostat treatment and IFN-γ stimulation (30 min, 20 ng/mL). 20 ug of total protein lysate loaded in each lane. (H) Representative phase + NucView488 (top) and NucView488 only (bottom) live cell images at 20x magnification of J774M cells after 48 hours of various HDAC inhibitor treatments, indicative of active caspase 3/7. Scale bars = 200 um. (I) Total Integrated Intensity (TII) live cell imaging timecourse quantification of NucView488 fluorescence in J774M cells after 48 hours of various concentrations of Entinostat treatment and (J) various HDAC inhibitor treatments, indicative of active caspase 3/7 (n=3), with TII calculated from 9 images for each replicate. Statistical significance indicated for 48-hour timepoint by One-way ANOVA. ns = not significant, * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001. ENT = Entinostat; PAN = Panobinostat; BEL = Belinostat; VOR = Vorinostat; CHL = Chlopynostat; SCA = Santacruzamate A; RGF = RGFP966; TMP = TMP269.

Article Snippet: Chemical inhibitors used in this study: Entinostat (Syndax Pharmaceuticals), Panobinostat (MedChemExpress, cat. #HY-10224), Belinostat (MedChemExpress, cat. #HY-10225), Vorinostat (MedChemExpress, cat. #HY-10221), Trichostatin A (MedChemExpress, cat. #HY-15144), Domatinostat (MedChemExpress, cat. #HY-16012A), Chlopynostat (MedChemExpress, cat. #HY-161464), Pyroxamide (MedChemExpress, cat. #HY-13216), Santacruzamate A (MedChemExpress, cat. #HY-N0931), RGFP966 (MedChemExpress, cat. #HY-13909), TMP269 (MedChemExpress, cat. #HY-18360), SIS17 (MedChemExpress, cat. #HY-128918), Stattic (MedChemExpress, cat. #HY-13818), Abemaciclib (MedChemExpress, cat. #HY-16297A), Palbociclib (MedChemExpress, cat. #50767).

Techniques: Flow Cytometry, Expressing, Western Blot, Live Cell Imaging, Fluorescence

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend 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.

Article Snippet: U2932 cells were treated with HDACi: panobinostat (MedchemExpress, #HY-10224; 30 nM), belinostat (MedchemExpress, #HY-10225; 2.5 μM), entinostat (MedchemExpress, #HY-12163; 10 μM, romidepsin (Sigma-Aldrich, #SML1175; 10 nM), and vorinostat (Selleckchem, #S1047; 2.5 μM) for 24 h followed by PBS, γPNA1, and ScR-γPNA2 at 3 μM for 48 h cotreatment.

Techniques: Inhibition, Control, Histone Deacetylase Assay, Small Interfering RNA, Polymerase Chain Reaction, Amplification, Binding Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend 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.

Article Snippet: U2932 cells were treated with HDACi: panobinostat (MedchemExpress, #HY-10224; 30 nM), belinostat (MedchemExpress, #HY-10225; 2.5 μM), entinostat (MedchemExpress, #HY-12163; 10 μM, romidepsin (Sigma-Aldrich, #SML1175; 10 nM), and vorinostat (Selleckchem, #S1047; 2.5 μM) for 24 h followed by PBS, γPNA1, and ScR-γPNA2 at 3 μM for 48 h cotreatment.

Techniques: Activity Assay, Real-time Polymerase Chain Reaction, Western Blot, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend 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.

Article Snippet: U2932 cells were treated with HDACi: panobinostat (MedchemExpress, #HY-10224; 30 nM), belinostat (MedchemExpress, #HY-10225; 2.5 μM), entinostat (MedchemExpress, #HY-12163; 10 μM, romidepsin (Sigma-Aldrich, #SML1175; 10 nM), and vorinostat (Selleckchem, #S1047; 2.5 μM) for 24 h followed by PBS, γPNA1, and ScR-γPNA2 at 3 μM for 48 h cotreatment.

Techniques: Histone Deacetylase Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend 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.

Article Snippet: U2932 cells were treated with HDACi: panobinostat (MedchemExpress, #HY-10224; 30 nM), belinostat (MedchemExpress, #HY-10225; 2.5 μM), entinostat (MedchemExpress, #HY-12163; 10 μM, romidepsin (Sigma-Aldrich, #SML1175; 10 nM), and vorinostat (Selleckchem, #S1047; 2.5 μM) for 24 h followed by PBS, γPNA1, and ScR-γPNA2 at 3 μM for 48 h cotreatment.

Techniques: Concentration Assay, Western Blot, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend 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.

Article Snippet: U2932 cells were treated with HDACi: panobinostat (MedchemExpress, #HY-10224; 30 nM), belinostat (MedchemExpress, #HY-10225; 2.5 μM), entinostat (MedchemExpress, #HY-12163; 10 μM, romidepsin (Sigma-Aldrich, #SML1175; 10 nM), and vorinostat (Selleckchem, #S1047; 2.5 μM) for 24 h followed by PBS, γPNA1, and ScR-γPNA2 at 3 μM for 48 h cotreatment.

Techniques:

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend 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.

Article Snippet: U2932 cells were treated with HDACi: panobinostat (MedchemExpress, #HY-10224; 30 nM), belinostat (MedchemExpress, #HY-10225; 2.5 μM), entinostat (MedchemExpress, #HY-12163; 10 μM, romidepsin (Sigma-Aldrich, #SML1175; 10 nM), and vorinostat (Selleckchem, #S1047; 2.5 μM) for 24 h followed by PBS, γPNA1, and ScR-γPNA2 at 3 μM for 48 h cotreatment.

Techniques: Inhibition, Control, Histone Deacetylase Assay, Small Interfering RNA, Polymerase Chain Reaction, Amplification, Binding Assay

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend 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.

Article Snippet: U2932 cells were treated with HDACi: panobinostat (MedchemExpress, #HY-10224; 30 nM), belinostat (MedchemExpress, #HY-10225; 2.5 μM), entinostat (MedchemExpress, #HY-12163; 10 μM, romidepsin (Sigma-Aldrich, #SML1175; 10 nM), and vorinostat (Selleckchem, #S1047; 2.5 μM) for 24 h followed by PBS, γPNA1, and ScR-γPNA2 at 3 μM for 48 h cotreatment.

Techniques: Activity Assay, Real-time Polymerase Chain Reaction, Western Blot, Control

Journal: Molecular Therapy. Nucleic Acids

Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

doi: 10.1016/j.omtn.2025.102804

Figure Lengend 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.

Article Snippet: U2932 cells were treated with HDACi: panobinostat (MedchemExpress, #HY-10224; 30 nM), belinostat (MedchemExpress, #HY-10225; 2.5 μM), entinostat (MedchemExpress, #HY-12163; 10 μM, romidepsin (Sigma-Aldrich, #SML1175; 10 nM), and vorinostat (Selleckchem, #S1047; 2.5 μM) for 24 h followed by PBS, γPNA1, and ScR-γPNA2 at 3 μM for 48 h cotreatment.

Techniques: Histone Deacetylase Assay