Journal: Cell Death & Disease

Article Title: Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma

doi: 10.1038/s41419-026-08593-5

Figure Lengend Snippet: A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, Cyclin E1, CDK2, p-CDK2); combination treatment increased p27 and decreased Cyclin E1, CDK2, and p-CDK2 (representative of three independent experiments).

Article Snippet: The primary antibodies used were as follows: PI3K p110δ (A19742; ABclonal), pan-Akt (#4691; CST), phospho-Akt (Ser473, #4060; CST), PPARα (ab227074; Abcam), FoxO1 (#2880; CST), phospho-FoxO1 (Thr24, #9464; CST) and (Ser256, #9461; CST), FoxO3a (#12829; CST), FoxO4 (#9472; CST), Mcl-1 (#16225-1-AP; Proteintech), Bcl-2 (#12789-1-AP; Proteintech), Bim (A19702; ABclonal), Bax (#50599-2-Ig; Proteintech), Cleaved PARP(#5625; CST), P21(#2947; CST), p27 (#3686; CST), Cyclin E1 (#11935-1-AP; Proteintech), CDK2 (#10122-1-AP; Proteintech), phospho-CDK2 (#4539; CST), GLUT1(#73015; CST), PGK1(A12686; ABclonal), β-Tubulin (#10094-1-AP; Proteintech), Lamin B1 (#13435; CST), and β-Actin (#66009-1-Ig; Proteintech).

Techniques: DNA Synthesis, Staining, Western Blot

Journal: Molecular & Cellular Proteomics : MCP

Article Title: Multiomics Profiling Reveals Distinct Immunosuppression and Metabolic Dysregulation in Aggressive Subtypes of Thyroid Cancer

doi: 10.1016/j.mcpro.2026.101513

Figure Lengend Snippet: Identification of potential biomarkers in ATC/PDTC. A , volcano plot of DEPs in ATC/PDTC versus PTC with |log 2 FC| ≥ 1 and p < 0.05. B , correlation analysis of FCGR2A with NET formation markers PADI4 across groups. C , single-cell RNA-seq data ( GSE232237 ) showing FCGR2A expression predominantly in macrophages, with the highest expression in ATC. D , correlation analysis of FCGR2A expression with M0 macrophages, NK cells, and B cells examined by Spearman analysis. E , representative figures of IHC analysis validation of FCGR2A, UBE2C, and NUBPL expression in ATC (n = 11), PDTC (n = 7), and PTC (n = 10) tissues. The numbers at the upper left corner of each IHC image (0–3) indicate the immunoreactivity score for the representative case. The IHC scores were fully plotted in the bar plots assessed by pairwise student’s t tests. ns, not significant; ∗ p < 0.05; ∗∗∗ p < 0.001; and ∗∗∗∗ p < 0.0001. ATC, anaplastic thyroid carcinoma; FCGR2A, Fc fragment of IgG receptor IIa; IHC, immunohistochemistry; log 2 FC, log 2 fold change; NK, natural killer; PDTC, poorly differentiated thyroid carcinoma; PTC, papillary thyroid carcinoma; PADI4, peptidyl arginine deiminase 4; NUBPL, nucleotide-binding protein-like; UBE2C, ubiquitin-conjugating enzyme E2 C.

Article Snippet: Primary antibodies—including FCGR2A (RRID: AB_2246912 , Cat.15625-1-AP, Proteintech, 1:600 dilution), ubiquitin-conjugating enzyme E2 C (UBE2C) (RRID: AB_11232220 , Cat.66087-1-Ig, Proteintech, 1:500), and nucleotide-binding protein-like (NUBPL) (RRID: AB_2878402 , Cat.17393-1-AP, Proteintech, 1:200)—were diluted in antibody dilution buffer and applied to tissue sections.

Techniques: Single Cell, RNA Sequencing, Expressing, Biomarker Discovery, Immunohistochemistry, Binding Assay, Ubiquitin Proteomics

Journal: Virulence

Article Title: miR-17-5p inhibits classical swine fever virus replication by targeting the PKD2 -regulated AMPK/mTOR autophagy pathway

doi: 10.1080/21505594.2026.2629657

Figure Lengend Snippet: CSFV infection upregulates miR-17-5p expression.

Article Snippet: Anti CSFV E2 mouse mAb , Biorbyt , Or318086.

Techniques: Infection, Expressing

Journal: Virulence

Article Title: miR-17-5p inhibits classical swine fever virus replication by targeting the PKD2 -regulated AMPK/mTOR autophagy pathway

doi: 10.1080/21505594.2026.2629657

Figure Lengend Snippet: miR-17-5p inhibits CSFV replication PK-15 cells.

Article Snippet: Anti CSFV E2 mouse mAb , Biorbyt , Or318086.

Techniques:

Journal: Virulence

Article Title: miR-17-5p inhibits classical swine fever virus replication by targeting the PKD2 -regulated AMPK/mTOR autophagy pathway

doi: 10.1080/21505594.2026.2629657

Figure Lengend Snippet: PKD2 is a host target of miR-17-5p involved in the regulation of CSFV replication. (A) venn diagram showing predicted miR-17-5p target genes identified by by TargetScan (1,385 genes) and miRDB (1,333 genes), with 936 overlapping targets. (B) PK-15 cells were transfected with 100 nM miR-17-5p mimics or negative control (miR-NC) for 12h. mRNA levels of candidate target genes were measured by RT-qPCR. (C, D) PK-15 cells were transfected for 12 h with overexpression plasmids for PKD2 (OE- PKD2 ), MED12L (OE- MED12L ), FGD4 (OE- FGD4 ), or control vector, followed by CSFV infection at MOI=1 for 24 h. CSFV RNA and protein levels were analyzed by RT-qPCR (C) and Western blot, (D),respectively, and band intensities were quantified using image J. (E) for viral titer analysis, PK-15 cells were transfected with PKD2 (OE-PKD2), MED12L (OE-MED12L), or FGD4 (OE-FGD4), followed by CSFV inoculation using ten-fold serial dilutions. After 3 days, viral titers were determined using the TCID 50 assay and expressed as Log 10 TCID 50 /0.1mL. (F, G) PK-15 cells were transfected with increasing concentrations of miR-17-5p mimics (0–150 nM) for 12 h. Expression of PKD2 at the mRNA and protein levels was evaluated by RT-qPCR (F) and Western blot (G), respectively,the relative intensity of each band was quantified through image J. Data are presented as mean ± standard deviation (SD) from three independent experiments. Statistical significance was determined using Student’s t-test and one-way ANOVA. ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Article Snippet: Anti CSFV E2 mouse mAb , Biorbyt , Or318086.

Techniques: Transfection, Negative Control, Quantitative RT-PCR, Over Expression, Control, Plasmid Preparation, Infection, Western Blot, Expressing, Standard Deviation

Journal: Virulence

Article Title: miR-17-5p inhibits classical swine fever virus replication by targeting the PKD2 -regulated AMPK/mTOR autophagy pathway

doi: 10.1080/21505594.2026.2629657

Figure Lengend Snippet: Down-regulation of PKD2 inhibits CSFV replication. (A) PK-15 cells were transfected with siNC, si PKD2 -1, or si PKD2 -2, followed by infection with CSFV at an MOI of 1 after 12 h. Intracellular levels of PKD2 mRNA and CSFV RNA were quantified by RT-qPCR at 0, 24, and 48 hr post-infection. (B) for viral titer analysis, PK-15 cells were transfected with siNC, siPKD2-1, or siPKD2-2, followed by CSFV inoculation using ten-fold serial dilutions. After 3 days, viral titers were determined using the TCID 50 assay and expressed as Log 10 TCID 50 /0.1mL.(C) Western blot analysis was performed to assess the expression levels of PKD2 and CSFV E2 at the corresponding time points, and band intensities were quantified using image J. (D) PK-15 cells were transfected with a miR-17-5p mimics or co-transfected with the miR-17-5p mimics and a PKD2 overexpression plasmid (OE- PKD2 ), followed by CSFV infection (MOI = 1) after 12 h. Intracellular CSFV E2 protein levels were analyzed by Western blot, and band intensities were quantified using image J. (E) PK-15 cells were transfected with a miR-17-5p inhibitor or co-transfected with the inhibitor and si PKD2 -2, followed by CSFV infection (MOI=1) after 12 h. CSFV E2 protein expression was examined by Western blot (upper panel), and the relative grayscale intensities were quantified by image J (lower panel). Data are presented as mean ± standard deviation (SD) from three independent experiments. Error bars represent SD. Asterisks denote statistical significance compared with the siNC group (A, B) or Mock group (C, D): ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 (Student’s t-test and one-way ANOVA). Representative blot images from three independent experiments are shown.

Article Snippet: Anti CSFV E2 mouse mAb , Biorbyt , Or318086.

Techniques: Transfection, Infection, Quantitative RT-PCR, Western Blot, Expressing, Over Expression, Plasmid Preparation, Standard Deviation

Journal: Virulence

Article Title: miR-17-5p inhibits classical swine fever virus replication by targeting the PKD2 -regulated AMPK/mTOR autophagy pathway

doi: 10.1080/21505594.2026.2629657

Figure Lengend Snippet: PKD2 regulates autophagic flux via the AMPK/mTOR pathway to promote CSFV proliferation. (A) PK-15 cells were infected with CSFV (MOI = 1), and the expression of autophagy-related markers (LC3I, LC3II, and p62) and CSFV E2 protein was quantified by Western blotting at 48 hours post-infection. (B) quantitative analysis of band intensity was performed using image J software to evaluate autophagy changes induced by CSFV infection. (C) PK-15 cells were transfected with siPKD2-2 for 12 hours. Western blotting was performed to detect the expression of total AMPK, phosphorylated AMPK (Thr172), total mTOR, and phosphorylated mTOR (Ser2448). (D) densitometric quantification of protein bands was carried out using image J software to assess alterations in pathway activity after PKD2 silencing. (E) PK-15 cells were treated with either an AMPK inhibitor (Compound C, 10 μM, 6 hours) or an mTOR inhibitor (Sapanisertib, 100 nM, 6 hours). Cells were then infected with CSFV (MOI = 1), and samples were harvested 24 h post-infection for protein analysis. Western blotting was performed to detect autophagy-related markers (LC3I, LC3II, and p62), key components of the AMPK/mTOR signaling pathway (total and phosphorylated AMPK [Thr172], total and phosphorylated mTOR [Ser2448]), and CSFV E2 protein expression. (F-H) quantitative densitometric analysis of protein bands was conducted using image J software to evaluate alterations in pathway activity and autophagic flux. (I) for viral titer analysis, PK-15 cells were treated with either an AMPK inhibitor (Compound C, 10 μM, 6 hours) or an mTOR inhibitor (Sapanisertib, 100 nM, 6 hours), followed by CSFV inoculation using ten-fold serial dilutions. After 3 days, viral titers were determined using the TCID 50 assay and expressed as Log 10 TCID 50 /0.1mL. Data are presented as mean ± standard deviation (SD), with error bars representing SD from three independent biological replicates. Statistical significance was determined using Student’s t-test and one-way ANOVA. Asterisks denote significant differences compared to control: ns, not significant; * p <0.05; ** p < 0.01; *** p < 0.001. **** p < 0.0001. Representative blots are shown from three independent experiments.

Article Snippet: Anti CSFV E2 mouse mAb , Biorbyt , Or318086.

Techniques: Infection, Expressing, Western Blot, Software, Transfection, Activity Assay, Standard Deviation, Control

Journal: Virulence

Article Title: miR-17-5p inhibits classical swine fever virus replication by targeting the PKD2 -regulated AMPK/mTOR autophagy pathway

doi: 10.1080/21505594.2026.2629657

Figure Lengend Snippet: Schematic model illustrating the interaction between CSFV and host miR-17-5p . In PK-15 cells, CSFV infection induces upregulation of host miR-17-5p expression. Under normal conditions, PKD2 promotes autophagic flux via activation of the AMPK/mTOR signaling pathway, thereby facilitating CSFV replication. However, miR-17-5p directly targets the 3’-UTR of PKD2 mRNA, leading to the suppression of PKD2 expression. This miR-17-5p -mediated downregulation of PKD2 attenuates autophagy, thereby limiting CSFV proliferation. These findings suggest a host defense mechanism in which miR-17-5p negatively regulates CSFV replication by targeting the pro-autophagic factor PKD2 .

Article Snippet: Anti CSFV E2 mouse mAb , Biorbyt , Or318086.

Techniques: Infection, Expressing, Activation Assay