Journal: Nature Communications

Article Title: Rapid acceleration of KRAS- mutant pancreatic carcinogenesis via remodeling of tumor immune microenvironment by PPARδ

doi: 10.1038/s41467-022-30392-7

Figure Lengend Snippet: a – c Pancreatic tissues from KC or KC/Pd mice fed the HFD or Ctrl diet; and KC/Pd mice fed the GW or Ctrl diet for 3 days ( n = 3–4 biologically independent samples). Venn diagram of differentially expressed chemokines ( a ). Quantitative results of Ccl2 protein levels for KC/Pd mice on the GW diet ( b ) and KC or KC/Pd mice on the HFD ( c ). d Representative images of Ccl2 RNAscope in situ hybridization for normal pancreatic tissues of KC/Pd mice fed the GW or Ctrl diet for 3 days ( n = 3 biologically independent samples). e Venn diagram of differentially expressed chemokines for mouse tdTomato RFP–sorted pancreatic epithelial cells of KC/tdPd mice on GW or control diet for 3 days and for the cell culture media from mouse NB490 KPC cells with WT or Ppard KO. f , g Quantitative results of Ccl2 protein levels for tdTomato-RFP + cells ( f , n = 4 biologically independent samples) and for the cell culture media from mouse NB490 KPC cells from 4 independent experiments ( g ). h , i Ccl2 mRNA expression levels in tdTomato-RFP + pancreatic epithelial cells ( h , n = 4 biologically independent samples) and in mouse NB490 KPC cells from 4 independent experiments ( i ). j Ccl2 mRNA expression levels in mouse KC and KC/Pd PDAC cells with or without GW treatment from 4 independent experiments. k , l PPARδ ( k ) and CCL2 ( l ) mRNA expression levels in human PDAC cells transfected with PPARδ siRNAs (siPPARD) or control siRNA (Ctrl) from 3 independent experiments. m The PPARδ binding to the four predicted PPARδ binding sites (pPDBS) in the mCcl2 promoter in mouse KC PDAC cells stably transduced with mouse DDK-tagged PPARδ expressing lentivirus and treated with 1 µM GW or solvent (DMSO) from 3 independent experiments. Data are mean ± SEM. For ( b ), ( f ), ( h ), unpaired two-tailed Student’s t test, for ( c ), ( k – m ), multiple t -tests, for ( g ), ( i ), one-way ANOVA with Bonferroni correction, and for ( j ), two-way ANOVA with Bonferroni correction. * P < .05, ** P < .01, *** P < .001, and **** P < .0001. Source data are provided as a Source Data file.

Article Snippet: Briefly, lentivirus plasmids for human PPARD ORF (#RC214735L3, OriGene), mouse PPARD ORF (#MR207001L3, OriGene) in pLenti-C-myc-DDK-P2A-Puro, and control plasmid pLenti-C-Myc-DDK-P2A-Puro (#PS100092, OriGene) were packaged into lentivirus particles at MD Anderson’s shRNA and ORFeome Core Facility.

Techniques: RNAscope, In Situ Hybridization, Control, Cell Culture, Expressing, Transfection, Binding Assay, Stable Transfection, Transduction, Solvent, Two Tailed Test

Journal: Frontiers in Oncology

Article Title: Suppression of EGFR/PKC-δ/NF-κB Signaling Associated With Imipramine-Inhibited Progression of Non-Small Cell Lung Cancer

doi: 10.3389/fonc.2021.735183

Figure Lengend Snippet: The inhibition of EGFR/PKC-δ/NF-κB proteins phosphorylation and induction of apoptosis-related proteins by imipramine in CL1-5-F4/ NF-κB-luc2 bearing tumor. (A–C) The protein expression from IHC of EGFR (Try 1068), PKC-δ (Thr507), NF-κB (Ser536), cleaved caspase-3, -8, -9, MMP-9, XIAP, MCL-1 and their quantification bar chart are presented. (D, E) The tumor ex vivo Western blotting from each mice of cleaved caspase-3, -8, -9 and PARP-1 is presented. ( ** p < 0.01 vs . vehicle; scale bar =100 μm).

Article Snippet: Primary antibodies against Matrix metalloproteinase-9 (MMP-9) (AB19016, Millipore), vascular endothelial growth factor (VEGF) (ab1316, Abcam, Cambridge, UK), EGFR (Try 1068) (#2234, Cell signaling, Danvers, MA, USA), EGFR (E-AB-63555, Elabscience, Houston, TX, USA), PKC-δ (Thr507) (E-AB-20968, Elabscience), PKC-δ (E-AB-14675, Elabscience), NF-κB p65 (Ser536) (E-AB-70335, Elabscience), NF-κB p65 (E-AB-22066, Elabscience), cell leukemia-1 (MCL-1) (BV-438, BioVision), cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein (cFLIP) (D16A8, Cell signaling), X-linked inhibitor of apoptosis protein (XIAP) (PA5-29253, Thermo Fisher Scientific), Fas (E-AB-40063, Elabscience), Fas ligand (FasL) (E-AB-31410, Elabscience), cleaved caspase-3 (E-AB-30004, Elabscience), cleaved caspase-8 (E-AB-22107, Elabscience), cleaved caspase-9 (#9505, Cell Signaling Technology), PARP-1 (#9532, Cell Signaling Technology) and β-actin (sc-47778, Santa Cruz Biotechnology, Dallas, Texas, Waltam, MA, USA) for Western blotting were purchased from different companies as listed.

Techniques: Inhibition, Phospho-proteomics, Expressing, Ex Vivo, Western Blot

Journal: Science Advances

Article Title: Harnessing skin-resident γδ T cells for immunotherapy in cutaneous squamous cell carcinoma

doi: 10.1126/sciadv.aec7215

Figure Lengend Snippet: Human cutaneous γδ T cells, isolated from skin biopsies of HDs and adoptively transferred into recipient mice, infiltrated the human cSCC xenograft from the circulation, homed into the tumor tissue, and were maintained within the tumor. γδ T cells can proliferate following TCR activation and stimulation with IL-1α and IL-18, which are also produced by the tumor tissue. cSCC-infiltrating γδ T cells displayed an activated and cytotoxic phenotype, and infiltration can lead to reduced tumor growth. Figure created in BioRender. I. Gratz (2026) https://BioRender.com/m9vgwti .

Article Snippet: Subsequently, in vitro expanded γδ T cells were isolated by magnetic cell sorting via positive selection, using biotin labeled anti-human TCRγδ antibody (Miltenyi Biotec, catalog no. 130-113-502, AB_2733575) to obtain highly purified γδ T cells (>90%).

Techniques: Isolation, Activation Assay, Produced