Journal: iScience

Article Title: Decoding neuron-specific lineage to identify diagnostic biomarkers and therapeutic targets for ischemic stroke

doi: 10.1016/j.isci.2026.116257

Figure Lengend Snippet: Cherp serving an effective treatment target for IS (A) The neuron counts of cluster 3 and 5. (B) The Cherp expression in each cluster. (C) The WB image of Cherp expression after OGD/R process. (D) The IF images of Cherp expression after OGD/R process. Scale bars = 100 μm. (E) The efficiency validation of Cherp knocking down using shRNA. (F) The cell viability assay after Cherp knocking down. (G) LDH leakage assay after Cherp knocking down. (H) TUNEL assay after Cherp knocking down. Scale bars = 100 μm. (I) WB image of apoptosis-related markers after Cherp knocking down. (J) Morphology of cerebral edema in sham, MCAO and MCAO-shRNA intervention groups at 72 h post-surgery. (K) TTC staining of cerebral infarction in sham, MCAO and MCAO-shRNA intervention groups at 72 h post-surgery (Dashed area represents the infarcted brain region). (L) Statistics analysis of brain water content ( n = 5 mice/group). (M) Quantification of infarct area ( n = 5 mice/group). (N) The functional enrichment of Cherp high cells related pathways. (O) The intracellular calcium imaging after Cherp knocking down. Scale bars = 100 μm (P) Quantitative analysis of intracellular Ca 2+ fluorescence intensity in primary neurons under indicated conditions ( n = 3 independent experiments). Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 and ∗∗∗∗ p < 0.0001 as determined by Student’s t test.

Article Snippet: The shRNA sequences targeting Cherp were generated at Sangon Biotech.

Techniques: Expressing, Biomarker Discovery, shRNA, Viability Assay, TUNEL Assay, Staining, Functional Assay, Imaging, Fluorescence

Journal: Bone & Joint Research

Article Title: Naringin targets TGF-β1-mediated angiogenesis to enhance the osteogenic effect of induced membrane

doi: 10.1302/2046-3758.155.BJR-2025-0412.R1

Figure Lengend Snippet: The effect of naringin on the expression of transforming growth factor β (TGF-β)/SMAD pathway-related factors in induced membrane. a) The protein level of TGF-β1, phosphorylated SMAD (p-SMAD)2 and p-SMAD3 was detected by western blot. b) Immunohistochemistry result of TGF-β1, p-SMAD2 and p-SMAD3. N = 6/group. Each value was presented as the mean (SD). *p < 0.05, **p < 0.01, ***p < 0.001 vs the control group; #p < 0.05, ##p < 0.01, ###p < 0.001 vs the L-Naringin group.

Article Snippet: Three small interfering RNA sequences targeting TGF-β1 (si-TGF-β1 #1, si-TGF-β1 #2, si-TGF-β1 #3) and a negative control sequence (si-TGF-β1 NC) were synthesized separately by Sangon Biotech (China).

Techniques: Expressing, Membrane, Western Blot, Immunohistochemistry, Control

Journal: Bone & Joint Research

Article Title: Naringin targets TGF-β1-mediated angiogenesis to enhance the osteogenic effect of induced membrane

doi: 10.1302/2046-3758.155.BJR-2025-0412.R1

Figure Lengend Snippet: Characterization of endothelial progenitor cells (EPCs) and transfection efficacy of small interfering RNA targeting transforming growth factor-β1 (si-TGF-β1). a) was the immunofluorescence result of cluster of differentiation (CD)34 and vascular endothelial growth factor receptor 2 (VEGFR2). b) EPCs could simultaneously absorb DiI-labelled acetylated low-density lipoprotein (Dil-Ac-LDL) and fluorescein isothiocyanate-labeled Ulex europaeus agglutinin I (FITC-UEA-I). Scale bar: 100 μm. c) Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to validate the silencing effect of si-TGF-β1 #1, #2 and #3. N = 5/group. d) Western blot was used to validate the silencing effect of si-TGF-β1 #1, #2 and #3. N = 5/group. Each value was presented as the mean (SD). ***p < 0.001 vs the si-TGF-β1 negative control (NC) group; ##p < 0.01, ###p < 0.001 vs the si-TGF-β1 #2 group.

Article Snippet: Three small interfering RNA sequences targeting TGF-β1 (si-TGF-β1 #1, si-TGF-β1 #2, si-TGF-β1 #3) and a negative control sequence (si-TGF-β1 NC) were synthesized separately by Sangon Biotech (China).

Techniques: Transfection, Small Interfering RNA, Immunofluorescence, Labeling, Reverse Transcription, Polymerase Chain Reaction, Quantitative RT-PCR, Western Blot, Negative Control

Journal: Bone & Joint Research

Article Title: Naringin targets TGF-β1-mediated angiogenesis to enhance the osteogenic effect of induced membrane

doi: 10.1302/2046-3758.155.BJR-2025-0412.R1

Figure Lengend Snippet: The effect of naringin on the proliferation and viability of endothelial progenitor cells (EPCs). a) 5-ethynyl-2'-deoxyuridine (EdU) staining method was used to detect the effect of naringin on the viability of EPCs at different stages (24, 48, and 72 hours). Scale bar: 100 μm. N = 5/group. b) Cell Counting Kit-8 (CCK-8, Beyotime, China) method was used to detect the effect of naringin on the viability of EPCs at different stages (24, 48, and 72 hours). N = 5/group. Each value was presented as the mean (SD). *p < 0.05, ** p< 0.01, ***p < 0.001 vs the control group; #p < 0.05, ##p < 0.01 vs the small interfering RNA targeting transforming growth factor-β1 (si-TGF-β1) group.

Article Snippet: Three small interfering RNA sequences targeting TGF-β1 (si-TGF-β1 #1, si-TGF-β1 #2, si-TGF-β1 #3) and a negative control sequence (si-TGF-β1 NC) were synthesized separately by Sangon Biotech (China).

Techniques: Staining, Cell Counting, CCK-8 Assay, Control, Small Interfering RNA

Journal: Bone & Joint Research

Article Title: Naringin targets TGF-β1-mediated angiogenesis to enhance the osteogenic effect of induced membrane

doi: 10.1302/2046-3758.155.BJR-2025-0412.R1

Figure Lengend Snippet: The effect of naringin on the migration, invasion and tube formation of endothelial progenitor cells (EPCs). a) Scratch wound was used to detect the invasion area of EPCs within 24 hours. Scale bar: 200 μm. b) Transwell assay was used to detect the number of migrated EPCs at 24 hours. Scale bar: 100 μm. c) The tube formation experiment detected the total tube length of EPCs. Scale bar: 100 μm. N = 5/group. Each value was presented as the mean (SD). **p < 0.01, ***p < 0.001 vs the control group; ###p < 0.001 vs the small interfering RNA targeting transforming growth factor-β1 (si-TGF-β1) group.

Article Snippet: Three small interfering RNA sequences targeting TGF-β1 (si-TGF-β1 #1, si-TGF-β1 #2, si-TGF-β1 #3) and a negative control sequence (si-TGF-β1 NC) were synthesized separately by Sangon Biotech (China).

Techniques: Migration, Transwell Assay, Control, Small Interfering RNA

Journal: Bone & Joint Research

Article Title: Naringin targets TGF-β1-mediated angiogenesis to enhance the osteogenic effect of induced membrane

doi: 10.1302/2046-3758.155.BJR-2025-0412.R1

Figure Lengend Snippet: The effect of naringin on angiogenic-osteogenic and transforming growth factor β (TGF-β)/SMAD pathway-related factors of endothelial progenitor cells (EPCs). a) The concentrations of platelet derived growth factor BB (PDGF-BB), vascular endothelial growth factor (VEGF), and slit guidance ligand 3 (SLIT3) in the supernatant of EPCs were detected by enzyme-linked immunosorbent assay. b) Alizarin red staining (ARS) was performed to detect mineralized nodules in osteoblasts. Scale bar: 50 μm. c) The protein level of p-SMAD2 and p-SMAD3 in EPCs was detected by western blot. d) was the immunofluorescence result of p-SMAD2. Scale bar: 100 μm. N = 5/group. Each value was presented as the mean (SD). ***p < 0.001 vs the control group; ##p < 0.01, ###p < 0.001 vs the small interfering RNA targeting transforming growth factor-β1 (si-TGF-β1) group.

Article Snippet: Three small interfering RNA sequences targeting TGF-β1 (si-TGF-β1 #1, si-TGF-β1 #2, si-TGF-β1 #3) and a negative control sequence (si-TGF-β1 NC) were synthesized separately by Sangon Biotech (China).

Techniques: Derivative Assay, Enzyme-linked Immunosorbent Assay, Staining, Western Blot, Immunofluorescence, Control, Small Interfering RNA

Journal: Bone & Joint Research

Article Title: Naringin targets TGF-β1-mediated angiogenesis to enhance the osteogenic effect of induced membrane

doi: 10.1302/2046-3758.155.BJR-2025-0412.R1

Figure Lengend Snippet: Interactions between naringin and transforming growth factor-β1 (TGF-β1). a) The basic chemical structure of naringin. b) 3D and 2D molecular docking patterns of naringin with TGF-β1. c) to g) Results of molecular dynamics simulation analysis illustrating root mean square deviation (RMSD), root mean square fluctuation (RMSF), radius of gyration (Rg), solvent-accessible surface area (SASA), and hydrogen-bond number for the TGF-β1-naringin complexes. h) Representative images of cellular thermal shift assay (CETSA) showing TGF-β1 thermal stability after naringin treatment. i) CETSA curve was performed using GraphPad Prism (GraphPad Software, USA). N = 5/group. Each value was presented as the mean (SD). *p < 0.05, **p < 0.01, ***p < 0.001 vs the dimethyl sulfoxide (DMSO) group.

Article Snippet: Three small interfering RNA sequences targeting TGF-β1 (si-TGF-β1 #1, si-TGF-β1 #2, si-TGF-β1 #3) and a negative control sequence (si-TGF-β1 NC) were synthesized separately by Sangon Biotech (China).

Techniques: Solvent, Thermal Shift Assay, Software

Journal: Oncology Reports

Article Title: TRIM46 deficiency-induced DNA damage enhances the sensitivity of cisplatin in non-small cell lung cancer by regulating the Akt signaling pathway

doi: 10.3892/or.2026.9063

Figure Lengend Snippet: TRIM46 expression is associated with DDP resistance in non-small cell lung cancer tissues. (A) Immunohistochemistry staining was performed using a TRIM46 antibody and normal, DDP-sensitive and DDP-resistant tissues. (B) Percentages of tissues with low or high TRIM46 expression in DDP-sensitive (n=38) or DDP-resistant (n=47) patients. (C) Percentages of patients with DDP-resistant or DDP-sensitive tissues and low (n=44) or high (n=41) TRIM46 expression. ***P<0.001. TRIM46, tripartite motif 46; DDP, cisplatin.

Article Snippet: The shRNA sequences targeting TRIM46 (shTRIM46-1, 5′-GGTGAGGATATGCAGACCT-3′; shTRIM46-2, 5′-GATATGCAGACCTTCACTT-3′; and shTRIM46-3, 5′-AGACCTTCACTTCCATCAT-3′), as well as the shNC (5′-GATACATACTAGATCGACT-3′) vector, were purchased from Shanghai GeneChem Co., Ltd and engineered into the pLKO.1 puro lentiviral vector (Addgene, Inc.).

Techniques: Expressing, Immunohistochemistry, Staining

Journal: Oncology Reports

Article Title: TRIM46 deficiency-induced DNA damage enhances the sensitivity of cisplatin in non-small cell lung cancer by regulating the Akt signaling pathway

doi: 10.3892/or.2026.9063

Figure Lengend Snippet: TRIM46 upregulation contributes to DDP resistance in non-small cell lung cancer cells. (A) RT-qPCR (left) and western blot (right) analysis of TRIM46 expression in 16HBE, A549 and A549/DDP cells. (B) RT-qPCR (left) and western blot (right) analysis of TRIM46 expression in A549 cells infected with TRIM46 overexpression lentivirus. (C) Cell apoptosis was measured after transduction with TRIM46-overexpression lentivirus and/or DDP treatment (0, 5 and 10 µM) in A549 cells. (D) Quantitative analysis of cell apoptosis. (E) Representative images of the comet assay showing DNA fragmentation after transduction with TRIM46-overexpression lentivirus and/or DDP treatment (0, 5 and 10 µM) in A549 cells (scale bar, 50 µm; magnification, ×400). (F) Quantification of tail DNA (%) revealing DNA damage after transduction with TRIM46-overexpression lentivirus and/or DDP treatment (0, 5 and 10 µM) in A549 cells. *P<0.05, **P<0.01, ***P<0.001. TRIM46, tripartite motif 46; DDP, cisplatin; RT-qPCR, reverse transcription-quantitative polymerase chain reaction; PI, propidium iodide.

Article Snippet: The shRNA sequences targeting TRIM46 (shTRIM46-1, 5′-GGTGAGGATATGCAGACCT-3′; shTRIM46-2, 5′-GATATGCAGACCTTCACTT-3′; and shTRIM46-3, 5′-AGACCTTCACTTCCATCAT-3′), as well as the shNC (5′-GATACATACTAGATCGACT-3′) vector, were purchased from Shanghai GeneChem Co., Ltd and engineered into the pLKO.1 puro lentiviral vector (Addgene, Inc.).

Techniques: Quantitative RT-PCR, Western Blot, Expressing, Infection, Over Expression, Transduction, Single Cell Gel Electrophoresis, Reverse Transcription, Real-time Polymerase Chain Reaction

Journal: Oncology Reports

Article Title: TRIM46 deficiency-induced DNA damage enhances the sensitivity of cisplatin in non-small cell lung cancer by regulating the Akt signaling pathway

doi: 10.3892/or.2026.9063

Figure Lengend Snippet: TRIM46 knockdown alleviates DDP resistance in non-small cell lung cancer cells. (A) Reverse transcription-quantitative polymerase chain reaction (left) and western blot (right) analysis of TRIM46 expression in A549/DPP cells infected with TRIM46 knockdown lentiviruses. (B) Cell apoptosis was measured after transduction with TRIM46 knockdown lentivirus and/or DDP treatment (0, 50 and 100 µM) in A549/DDP cells. (C) Quantitative analysis of cell apoptosis. (D) Representative images of the comet assay showing DNA fragmentation after transduction with TRIM46 knockdown lentivirus and/or DDP treatment (0, 50 and 100 µM) in A549/DDP cells (scale bar, 50 µm; magnification, ×400). (E) Quantification of tail DNA (%) revealing DNA damage after transduction with TRIM46 knockdown lentivirus and/or DDP treatment (0, 50 and 100 µM) in A549/DDP cells. ***P<0.001. TRIM46, tripartite motif 46; DDP, cisplatin; sh, short hairpin; NC, negative control; PI, propidium iodide.

Article Snippet: The shRNA sequences targeting TRIM46 (shTRIM46-1, 5′-GGTGAGGATATGCAGACCT-3′; shTRIM46-2, 5′-GATATGCAGACCTTCACTT-3′; and shTRIM46-3, 5′-AGACCTTCACTTCCATCAT-3′), as well as the shNC (5′-GATACATACTAGATCGACT-3′) vector, were purchased from Shanghai GeneChem Co., Ltd and engineered into the pLKO.1 puro lentiviral vector (Addgene, Inc.).

Techniques: Knockdown, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Expressing, Infection, Transduction, Single Cell Gel Electrophoresis, Negative Control

Journal: Oncology Reports

Article Title: TRIM46 deficiency-induced DNA damage enhances the sensitivity of cisplatin in non-small cell lung cancer by regulating the Akt signaling pathway

doi: 10.3892/or.2026.9063

Figure Lengend Snippet: TRIM46 depletion inhibits cell proliferation by regulating the Akt signaling pathway. (A) Cell proliferation of A549/DDP cells transduced with TRIM46-knockdown lentiviruses. (B) Western blot analysis of p-Akt, Akt, caspase 3, cleaved-caspase 3 and RAD51 expression in A549/DDP cells transduced with TRIM46-knockdown lentiviruses. (C) Cell proliferation of A549 cells transduced with TRIM46-overexpression lentivirus and/or treated with LY294002 (20 µM) or vehicle. (D) Western blot analysis of p-Akt, Akt, caspase 3, cleaved-caspase 3 and RAD51 in A549 cells transduced with TRIM46-overexpression lentivirus and/or treated with LY294002 (20 µM) or vehicle. ***P<0.001 vs. shNC or Vector + Vehicle; ### P<0.001 vs. TRIM46 + Vehicle. TRIM46, tripartite motif 46; DDP, cisplatin; sh, short hairpin; NC, negative control; OD, optical density; p-, phosphorylated.

Article Snippet: The shRNA sequences targeting TRIM46 (shTRIM46-1, 5′-GGTGAGGATATGCAGACCT-3′; shTRIM46-2, 5′-GATATGCAGACCTTCACTT-3′; and shTRIM46-3, 5′-AGACCTTCACTTCCATCAT-3′), as well as the shNC (5′-GATACATACTAGATCGACT-3′) vector, were purchased from Shanghai GeneChem Co., Ltd and engineered into the pLKO.1 puro lentiviral vector (Addgene, Inc.).

Techniques: Transduction, Knockdown, Western Blot, Expressing, Over Expression, Plasmid Preparation, Negative Control

Journal: Oncology Reports

Article Title: TRIM46 deficiency-induced DNA damage enhances the sensitivity of cisplatin in non-small cell lung cancer by regulating the Akt signaling pathway

doi: 10.3892/or.2026.9063

Figure Lengend Snippet: TRIM46 knockdown increases the sensitivity of xenograft tumors to DDP treatment. (A) Tumor volumes and (B) images of xenograft tumors in the designated groups (scale bar, 1 cm; n=6 per group). (C) TUNEL assay of xenograft tumor samples (scale bar, 100 µm; magnification, ×200). (D) Statistical analysis of the TUNEL assay (n=6 per group). (E) Western blot analysis of TRIM46 and RAD51 expression in xenograft tumors. ***P<0.001. TRIM46, tripartite motif 46; DDP, cisplatin; sh, short hairpin; NC, negative control.

Article Snippet: The shRNA sequences targeting TRIM46 (shTRIM46-1, 5′-GGTGAGGATATGCAGACCT-3′; shTRIM46-2, 5′-GATATGCAGACCTTCACTT-3′; and shTRIM46-3, 5′-AGACCTTCACTTCCATCAT-3′), as well as the shNC (5′-GATACATACTAGATCGACT-3′) vector, were purchased from Shanghai GeneChem Co., Ltd and engineered into the pLKO.1 puro lentiviral vector (Addgene, Inc.).

Techniques: Knockdown, TUNEL Assay, Western Blot, Expressing, Negative Control

Journal: Oncology Reports

Article Title: TRIM46 deficiency-induced DNA damage enhances the sensitivity of cisplatin in non-small cell lung cancer by regulating the Akt signaling pathway

doi: 10.3892/or.2026.9063

Figure Lengend Snippet: Mechanism of TRIM46 deficiency-induced DNA damage, enhancing the sensitivity of DDP in NSCLC by regulating Akt signaling pathway. (A) TRIM46 expression was positively associated with DDP resistance in NSCLC tissues. (B) TRIM46 overexpression significantly suppressed DDP-induced apoptosis and enhanced DDP resistance in A549 cells. (C) TRIM46 knockdown induced DNA damage by modulating the protein levels of p-AKT, RAD51, caspase 3, and cleaved-caspase 3, thereby resulting in cell proliferation inhibition in NSCLC cells. (D) TRIM46 knockdown increased the sensitivity of xenograft tumors to DDP treatment. NSCLC, non-small cell lung cancer; TRIM46, tripartite motif 46; DDP, cisplatin; p-, phosphorylated.

Article Snippet: The shRNA sequences targeting TRIM46 (shTRIM46-1, 5′-GGTGAGGATATGCAGACCT-3′; shTRIM46-2, 5′-GATATGCAGACCTTCACTT-3′; and shTRIM46-3, 5′-AGACCTTCACTTCCATCAT-3′), as well as the shNC (5′-GATACATACTAGATCGACT-3′) vector, were purchased from Shanghai GeneChem Co., Ltd and engineered into the pLKO.1 puro lentiviral vector (Addgene, Inc.).

Techniques: Expressing, Over Expression, Knockdown, Inhibition