Journal: Clinical Epigenetics

Article Title: Decitabine regulates the resistance of HCC to sorafenib through demethylation

doi: 10.1186/s13148-025-01925-w

Figure Lengend Snippet: Effect of sorafenib on Hep3B after combination with DAC. A , B Effect of varying concentrations of DAC on the proliferation of Hep3B and HepG2 cells. C , D Effect of different concentrations of sorafenib on Hep3B and HepG2 proliferation. E , F Combined effects of sorafenib and DAC on the proliferation of Hep3B and HepG2 cells. G Apoptosis of Hep3B cells following treatment with various drugs. H – J Sorafenib uptake measured by LC–MS/MS in HEK-293 cells stably expressing OATP1B3 ( H ), Hep3B cells overexpressing OATP1B3 ( I ), and HepG2 cells overexpressing OATP1B3 ( J ). K , L Sorafenib uptake in Hep3B and HepG2 cells detected by LC–MS/MS, with rifampicin (Rif) as an OATP1B3 inhibitor. M , N Cell viability of Hep3B and HepG2 measured by MTS assay ( n = 3). * p < 0.05, ** p < 0.005 (× 100)

Article Snippet: The following day, culture medium was replaced with fresh medium containing 0, 1, 3, or 10 μM DAC (#HY-A0004, MCE) or sorafenib (#HY-10201, MCE).

Techniques: Liquid Chromatography with Mass Spectroscopy, Stable Transfection, Expressing, MTS Assay

Journal: Clinical Epigenetics

Article Title: Decitabine regulates the resistance of HCC to sorafenib through demethylation

doi: 10.1186/s13148-025-01925-w

Figure Lengend Snippet: Combining DAC with sorafenib induces ferroptosis. A , B Effects of different drug treatments on the proliferation of Hep3B and HepG2 cells. C – F Lipid peroxidation in Hep3B ( C , E ) and HepG2 ( D , F ) was measured using C11 BODIPY 581/591; fluorescence intensity was assessed by fluorescence microscopy and flow cytometry, respectively ( n = 3). G Intracellular MDA content in different groups was assayed with an MDA kit in Hep3B and HepG2 cells ( n = 3)

Article Snippet: The following day, culture medium was replaced with fresh medium containing 0, 1, 3, or 10 μM DAC (#HY-A0004, MCE) or sorafenib (#HY-10201, MCE).

Techniques: Fluorescence, Microscopy, Flow Cytometry

Journal: Clinical Epigenetics

Article Title: Decitabine regulates the resistance of HCC to sorafenib through demethylation

doi: 10.1186/s13148-025-01925-w

Figure Lengend Snippet: DAC enhanced the inhibitory effect of sorafenib on tumor growth in vivo. A Body weight changes in tumor-bearing BALB/c nude mice. B Tumor volume growth curves. C Relative tumor growth rate. D Time-dependent tumor volume. E , F Final tumor size measurements. G IHC staining showing OATP1B3 expression (× 40). H , I OATP1B3 protein expression ( n = 3). (J) SLCO1B3 mRNA expression ( n = 3)

Article Snippet: The following day, culture medium was replaced with fresh medium containing 0, 1, 3, or 10 μM DAC (#HY-A0004, MCE) or sorafenib (#HY-10201, MCE).

Techniques: In Vivo, Immunohistochemistry, Expressing

Journal: Clinical Epigenetics

Article Title: Decitabine regulates the resistance of HCC to sorafenib through demethylation

doi: 10.1186/s13148-025-01925-w

Figure Lengend Snippet: Mechanism of action diagram. Left: DNMT1 down-regulates the expression of OATP1B3 by mediating DNA methylation of OATP1B3 in HCC cells. Eventually, it leads to HCC cells resistance. Right: DAC reversed HCC drug resistance by inhibiting SLCO1B3 DNA methylation, increasing OATP1B3 expression, and promoting the accumulation of sorafenib in HCC cells

Article Snippet: The following day, culture medium was replaced with fresh medium containing 0, 1, 3, or 10 μM DAC (#HY-A0004, MCE) or sorafenib (#HY-10201, MCE).

Techniques: Expressing, DNA Methylation Assay

Journal: Life Science Alliance

Article Title: The type of DNA damage response after decitabine treatment depends on the level of DNMT activity

doi: 10.26508/lsa.202302437

Figure Lengend Snippet: List of chemicals used in this study.

Article Snippet: 5-Aza-2′-deoxycytidine , Biosynth , 2353-33-5 , ID74843.

Techniques: Binding Assay, Bicinchoninic Acid Protein Assay, Saline, Protease Inhibitor, Staining

Journal: Cell reports

Article Title: Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy

doi: 10.1016/j.celrep.2023.113016

Figure Lengend Snippet: Human SCLC cells H82 and H146 were transfected with DNMT1 siRNA (siDNMT1) or scrambled siRNA (siCtrl). (A) DNMT1 knockdown. DNMT1 protein was measured by western blot 72 h after transfection. (B) Cell growth inhibition. Cell counts by automated counter 72 h after transfection. Mean ± SD of four independent experiments. (C) Apoptosis not activated. Apoptosis was measured by Annexin V staining and flow cytometry analysis 24 h after transfection. Fluorizoline (10 μM) was used as a positive control for apoptosis. Mean ± SD of three independent experiments. (D) Activation of pulmonary NE-lineage signature genes. Gastrin-related peptide (GRP), neuronatin (NNAT), chromogranin B (CHGB), and secretogranin II (SCG2), also known as chromogranin C (CHGC), were increased by DNMT1 knockdown. Quantitative reverse polymerase chain reaction (qPCR) 72 h after transfection. Internal control was β-ACTIN; relative gene expression was calculated by the Livak-Schmittgen method. Mean ± SD of three independent experiments. ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05, p > 0.05. t test two-sided vs. siCtrl. (E) Cell morphology. Giemsa-stained cell imaged by Leica Upright Microscope-Orion. Magnification ×400; scale bar, 10 μm. (F) DNMT1 depletion using decitabine (Dec) or 5-azacytidine (5Aza) decreased SCLC proliferation. SCLC cells H82 and H146 were treated with DMSO vehicle control, Dec 0.5 μM, or 5Aza 1 μM added once at time 0 h. Cell counts by automated counter. (G) The cytoreduction was not by apoptosis. Apoptosis was measured by Annexin V staining and flow cytometry at 24 h. Positive control fluorizoline (10 μM). (H) Dec and 5Aza treatment decreased DNMT1 and MYC and increased p27/CKDN1B (mediator of cell-cycle exits by terminal lineage differentiation). Western blot. (I) Dec and 5Aza treatment increased expression of pulmonary NE-lineage signature genes. Measured at 72 h in H82 cells and 96 h in H146 cells, as per (D). Experiment in triplicate. Statistics are as per (D) treated vs. vehicle. (J) Cell morphology. Giemsa-stained cytospin preparations of cells harvested after 72–96 h. Leica Upright Microscope-Orion; magnification ×400; scale bar, 10 μm.

Article Snippet: Decitabine , BOC Sciences , Cat# 2353-33-5.

Techniques: Transfection, Knockdown, Western Blot, Inhibition, Staining, Flow Cytometry, Positive Control, Activation Assay, Polymerase Chain Reaction, Control, Gene Expression, Microscopy, Expressing

Journal: Cell reports

Article Title: Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy

doi: 10.1016/j.celrep.2023.113016

Figure Lengend Snippet:

Article Snippet: Decitabine , BOC Sciences , Cat# 2353-33-5.

Techniques: Control, Recombinant, SYBR Green Assay, Bicinchoninic Acid Protein Assay, Giemsa Stain, cDNA Synthesis, Software

Journal: Journal of Hematology & Oncology

Article Title: Recent developments in immunotherapy of acute myeloid leukemia

doi: 10.1186/s13045-017-0505-0

Figure Lengend Snippet: Current clinical trials using antibody-drug conjugates for immunotherapy of AML

Article Snippet: NCT01902329 , A phase 1 trial of SGN-CD33A in patients with CD33-positive acute myeloid leukemia , CD33 , SGN-CD33A , Azacitidine or decitabine , I , Relapsed AML or newly diagnosed AML if not a candidate for intensive chemotherapy; CD33 expression , Toxicity , 195 , Seattle Genetics , USA , 2013 , 2017 , Active, not recruiting.

Techniques: Clinical Proteomics, Expressing