Journal: Investigative Ophthalmology & Visual Science

Article Title: LPA1-Induced EMT of Retinal Pigment Epithelial Cells Promotes Subretinal Fibrosis via USP1-Mediated Deubiquitination and Stabilization of ZEB1

doi: 10.1167/iovs.67.10.34

Figure Lengend Snippet: LPA1 promotes EMT in RPE cells. ( A ) Relative LPA1 mRNA levels in ARPE-19 cells transfected with an empty vector or the LPA1 overexpression plasmid, as measured by RT-qPCR. ( B , C ) WB analysis verifying LPA1 overexpression in ARPE-19 cells. ( D , E ) Scratch wound healing assays in ARPE-19 cells performed under the indicated conditions, photographed at 0 and 24 hours. ( F , G ) Transwell migration assays in ARPE-19 cells under the indicated conditions. Scale bar : 50 µm. ( H – J ) Protein levels of E-cadherin, fibronectin 1, collagen I, α-SMA, and LPA1 in ARPE-19 cells under the designated conditions. ( K , L ) IF staining for α-SMA in the RPE–choroid complex from control and UCM-05194–treated mice in the laser-induced SRF model. Scale bar : 100 µm. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: One day after the initial laser treatment, mice in the indicated groups received intravitreal administration of UCM-05194 (HY-167862A; MedChemExpress, Monmouth Junction, NJ, USA), BMS-986278 (HY-139853; MedChemExpress), or aflibercept (EYLEA; Bayer, Leverkusen, Germany) at a volume of 1 μL per eye, corresponding to a final dose of 40 μg per eye.

Techniques: Transfection, Plasmid Preparation, Over Expression, Quantitative RT-PCR, Migration, Staining, Control

Journal: Neoplasia (New York, N.Y.)

Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability

doi: 10.1016/j.neo.2026.101314

Figure Lengend Snippet: ACLY activity regulates MDR1 expression in colorectal cancer. (A) Transcript levels of ACLY and MDR1 (ABCB1) in colorectal cancer (red) and normal colon tissues (grey) analyzed using GEPIA (TCGA/GTEx datasets). (B) Immunoblot analysis of MDR1 in SW480 and DLD1 cells treated with the ACLY inhibitor BMS-303141 (20 or 50 μM, 48 h). (C) Immunoblot analysis of ACLY and MDR1 in SW480 and DLD1 cells transduced with empty vector (pLV) or ACLY-overexpressing vector (pLV[Exp]-hACLY). (D) Immunoblot analysis of ACLY and MDR1 in control and ACLY-overexpressing cells treated with BMS-303141 (50 μM, 48 h). (E) Relative ABCB1 mRNA levels in control and ACLY-overexpressing cells, and in cells treated with BMS-303141. (F) Relative ACLY mRNA levels under the same conditions. Data are presented as mean ± SD (n = 3 unless otherwise indicated). Statistical significance was determined using unpaired two-tailed t-tests or one-way ANOVA with Tukey’s post hoc test. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: The ACLY inhibitor BMS-303141 (MedChemExpress; HY-16107) was dissolved in DMSO (10 mM stock) and used at 50 μM for 48 h. Vorinostat (MedChemExpress; HY-10221) was dissolved in DMSO and used at 0.5 μM (SW480) or 3.5 μM (DLD1) for 48 h. Sodium ascorbate (Sigma-Aldrich; A7632) was freshly prepared in sterile water (100 mM stock) and used at 5 mM for 6 h unless otherwise indicated.

Techniques: Activity Assay, Expressing, Western Blot, Transduction, Plasmid Preparation, Control, Two Tailed Test

Journal: Neoplasia (New York, N.Y.)

Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability

doi: 10.1016/j.neo.2026.101314

Figure Lengend Snippet: ACLY activity modulates histone acetylation and MDR1 expression. (A) Immunoblot analysis of MDR1 in SW480 and DLD1 cells treated with the histone deacetylase inhibitor vorinostat (VOR; 0.5 μM for SW480 and 3.5 μM for DLD1) or DMSO for 24 h. Representative blots and densitometric quantification relative to control are shown. (B) Immunoblot analysis of acetylated histone H3 (H3K9ac) and histone H4 (H4K16ac) in SW480 wild-type (WT) and ACLY-overexpressing (OE) cells treated with vehicle or the ACLY inhibitor BMS-303141 (50 μM, 48 h). (C) Immunoblot analysis of H3K9ac and H4K16ac in DLD1 cells under the same conditions. β-actin was used as a loading control. Data are presented as mean ± SD (n = 3). Statistical significance was determined using unpaired two-tailed t-tests. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: The ACLY inhibitor BMS-303141 (MedChemExpress; HY-16107) was dissolved in DMSO (10 mM stock) and used at 50 μM for 48 h. Vorinostat (MedChemExpress; HY-10221) was dissolved in DMSO and used at 0.5 μM (SW480) or 3.5 μM (DLD1) for 48 h. Sodium ascorbate (Sigma-Aldrich; A7632) was freshly prepared in sterile water (100 mM stock) and used at 5 mM for 6 h unless otherwise indicated.

Techniques: Activity Assay, Expressing, Western Blot, Histone Deacetylase Assay, Control, Two Tailed Test

Journal: Neoplasia (New York, N.Y.)

Article Title: Metabolic regulation of histone acetylation by ACLY supports MDR1 expression in colorectal cancer and highlights a targetable vulnerability

doi: 10.1016/j.neo.2026.101314

Figure Lengend Snippet: ACLY expression is associated with resistance-related transcriptional programs in colorectal cancer. (A) Correlation analysis between ACLY expression and a gene set associated with lipid metabolism (ACLY, ACSS2, ACSS1, FASN, SREBP1) and drug transport pathways (ABCB1, ABCC2, ABCG5, EpCAM, CD24) in colorectal cancer samples using GEPIA2 (TCGA dataset). (B) Schematic representation of a proposed model linking ACLY-dependent acetyl-CoA production to histone acetylation and transcriptional regulation in CRC cells. (C) Relative mRNA expression of EpCAM, ABCC2, and CD24 in SW480 and DLD1 cells overexpressing ACLY compared with empty vector controls. (D) Relative mRNA expression of EpCAM, ABCC2, and CD24 in SW480 and DLD1 cells treated with the ACLY inhibitor BMS-303141 (50 μM) compared with vehicle-treated controls. Gene expression levels were determined by qPCR and normalized to ACTB. Data are presented as mean ± SEM (n = 3). Statistical significance was determined using unpaired two-tailed t-tests. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: The ACLY inhibitor BMS-303141 (MedChemExpress; HY-16107) was dissolved in DMSO (10 mM stock) and used at 50 μM for 48 h. Vorinostat (MedChemExpress; HY-10221) was dissolved in DMSO and used at 0.5 μM (SW480) or 3.5 μM (DLD1) for 48 h. Sodium ascorbate (Sigma-Aldrich; A7632) was freshly prepared in sterile water (100 mM stock) and used at 5 mM for 6 h unless otherwise indicated.

Techniques: Expressing, Drug Transport Assay, Plasmid Preparation, Gene Expression, Two Tailed Test