Journal: Journal of Hematology & Oncology

Article Title: UVI5008: the first reversible, non-covalent Bruton’s tyrosine kinase epi-inhibitor for B-cell malignancies

doi: 10.1186/s13045-026-01784-9

Figure Lengend Snippet: UVI5008 exhibits BTK inhibitory activity in CLL cells. (A) Cytotoxicity of UVI5008 and ibrutinib (5 µM, 24 h) in Mec-1, Mino, and Granta-519 cells assessed by trypan blue (left) and MTT assay (right). (B) FACS analysis of cell viability (PI, top) and cell cycle (bottom) after treatment. (C) BTK mRNA levels (left) and Western blot of BTK, p-BTK, AKT, and p-AKT (right) after treatment. GAPDH was used for normalization (* and # indicate the same loading control for the corresponding cell line). DMSO was used as the control condition (CTR). (D) ChIP-qPCR in Mec-1 cells after UVI5008 (5 µM, 24 h) showing changes in H3K9/14ac, H3K27me3, and p-Ser5 RNA Pol II at BTK promoter . (E) Venn diagram (upper) and heatmap (lower) of differentially expressed kinases shared across all three cell lines after UVI5008 treatment. Data are presented as mean ± SEM, and statistical significance was assessed using a paired t -test ± SEM; T-test: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

Article Snippet: Samples with a RIN ≥ 7 were processed to generate libraries for mRNA sequencing following the Illumina® TruSeq Stranded mRNA Sample Preparation Guide, starting from a defined concentration of 500 ng of material per sample.

Techniques: Activity Assay, MTT Assay, Western Blot, Control, ChIP-qPCR

Journal: Journal of Hematology & Oncology

Article Title: UVI5008: the first reversible, non-covalent Bruton’s tyrosine kinase epi-inhibitor for B-cell malignancies

doi: 10.1186/s13045-026-01784-9

Figure Lengend Snippet: UVI5008 effects in CLL patient samples and Eμ-TCL1 mouse model. (A) PI cell viability staining of Mec-1, Mino, and Granta-519 cells after 24 h treatment with UVI5008 or ibrutinib (5 µM). (B) Pie chart showing patient stratification by treatment response (≥ twofold increase in cell death). (C) Cell cycle analysis by FACS after 24 h treatment with UVI5008 or ibrutinib (5 µM). (D) BTK mRNA (median of 50 CLL patients, left) and Western blot of BTK, p-BTK, AKT, and p-AKT (right) following 24 h treatment with UVI5008 or ibrutinib (5 µM). (E) WB on analysis on a cohort of 16 patients to assess BTK, AKT, pBTK, and pAKT expression after 24 h treatment with UVI5008 or ibrutinib (5 µM). DMSO was used as the control condition (CTR). Data are presented as mean ± SEM, and statistical significance was assessed using a paired t -test *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

Article Snippet: Samples with a RIN ≥ 7 were processed to generate libraries for mRNA sequencing following the Illumina® TruSeq Stranded mRNA Sample Preparation Guide, starting from a defined concentration of 500 ng of material per sample.

Techniques: Staining, Clinical Proteomics, Cell Cycle Assay, Western Blot, Expressing, Control

Journal: Cell Biology and Toxicology

Article Title: CD36 inhibition reduces non-small-cell lung cancer development through AKT-mTOR pathway

doi: 10.1007/s10565-024-09848-7

Figure Lengend Snippet: CD36 expression is positively correlated with cell proliferation and migration in vitro . A–F A549 cells were transfected with pCMV or pCMV-CD36 plasmid, and NCI-H520 cells were transfected with CasRX or CasRX-CD36 plasmid for 12 h in serum-free medium and then cultured in complete medium for another 24 h. Cells were collected for determination of cell viability ( A ), cell cycle ( B , C ), migration ( D ), and apoptosis ( E ) by MTT assay, FACS, wound healing test, and Annexin V-FITC/PI staining, respectively. Protein expression of CD36, CDH1, PCNA, vimentin, Bcl-2, and BAX was determined by Western blot with density quantitative analysis ( F ). G , H NCI-H520 cells were transfected with CasRX or CasRX-CD36 plasmid for 12 h and then cultured in complete medium for 24 h, followed by FFAs (150 µM) treatment for 24 h. Cells were collected for determination of cell viability ( G ) and apoptosis ( H ). Mean ± SEM; * p < 0.05; ** p < 0.01; *** p < 0.001; A , G : n = 6; B – F , H : n = 3

Article Snippet: CasRx gRNA cloning backbone (pXR003, #109053, Addgene) was digested with BbsI and then ligated with annealed oligo duplex using T4 ligase.

Techniques: Expressing, Migration, In Vitro, Transfection, Plasmid Preparation, Cell Culture, MTT Assay, Staining, Western Blot

Journal: Cell Biology and Toxicology

Article Title: CD36 inhibition reduces non-small-cell lung cancer development through AKT-mTOR pathway

doi: 10.1007/s10565-024-09848-7

Figure Lengend Snippet: The effects of pitavastatin on cell proliferation, migration, and apoptosis are related to CD36 expression. A549 cells were transfected with pCMV or pCMV-CD36 plasmid, and NCI-H520 cells were transfected with CasRX or CasRX-CD36 plasmid for 12 h and then cultured in complete medium for 24 h, followed by received pitavastatin (5 µM) treatment for 24 h. Cells were collected for determination of cell viability ( A ), cell cycle ( B , C ), migration ( D ), and apoptosis ( E ). Protein expression of CD36, PCNA, Bcl-2, and BAX was determined by Western blot with density quantitative analysis ( F , G ). Mean ± SEM; * p < 0.05; ** p < 0.01; *** p < 0.001; A : n = 6; B – F : n = 3; Pita, pitavastatin

Article Snippet: CasRx gRNA cloning backbone (pXR003, #109053, Addgene) was digested with BbsI and then ligated with annealed oligo duplex using T4 ligase.

Techniques: Migration, Expressing, Transfection, Plasmid Preparation, Cell Culture, Western Blot

Journal: Cell Biology and Toxicology

Article Title: CD36 inhibition reduces non-small-cell lung cancer development through AKT-mTOR pathway

doi: 10.1007/s10565-024-09848-7

Figure Lengend Snippet: The reduction effects of pitavastatin on tumor progression are regulated by CD36/AKT/mTOR pathway. A–E A549 ( A ) and NCI-H520 ( B ) cells were treated with 150 µM FFAs or 5 µM pitavastatin plus FFAs for 24 h. A549 cells were transfected with pCMV or pCMV-CD36 plasmid for 12 h ( C ); NCI-H520 cells were transfected with CasRX or CasRX-CD36 plasmid ( D , E ) for 12 h and then cultured in complete medium for 24 h, followed by treatment with 5 µM pitavastatin ( C , D ) or 150 µM FFAs ( E ) for 24 h. Protein expression of p-AKT, AKT, p-mTOR, and mTOR was detected by Western blot. F , G Tumor paraffin sections collected from Fig. A ( F ) or Fig. A ( G ) were performed IHC staining to detect the expression of p-AKT and p-mTOR with MD quantified by ImageJ software. H–L A549 cells were transfected with pCMV or pCMV-CD36 plasmid for 12 h and then cultured in complete medium for 24 h, followed by received LY294002 (10 µM) treatment for 24 h. Cells were collected for determination of cell viability ( H ) and apoptosis ( I , J ). Protein expression of CD36, vimentin, PCNA, BAX, p-AKT, AKT, p-mTOR, and mTOR was determined by Western blot ( K , L ). Mean ± SEM; * p < 0.05; ** p < 0.01; *** p < 0.001; A – E , I – L : n = 3; F , G : n = 5; H : n = 6; Pita, pitavastatin; LY, LY294002

Article Snippet: CasRx gRNA cloning backbone (pXR003, #109053, Addgene) was digested with BbsI and then ligated with annealed oligo duplex using T4 ligase.

Techniques: Transfection, Plasmid Preparation, Cell Culture, Expressing, Western Blot, Immunohistochemistry, Software