Journal: Acta Pharmaceutica Sinica. B

Article Title: Neutralizing dentin sialophosphoprotein facilitates tumor vascular normalization in colorectal cancer by blocking the crosstalk between tumor cells and endothelial cells

doi: 10.1016/j.apsb.2026.06.011

Figure Lengend Snippet: DSPP/ α v β 3/MAPK signaling axis promotes tumor vessel abnormalization. (A, B) Investigating the potential regulatory functions of DSPP in CRC by the WiKi (A) and KEGG (B) pathway enrichment analysis. (C) The mitogen-activated protein kinase (MAPK)-related pathways were enriched in CRC with high DSPP expression by GSEA analysis. (D) Western blot assays showing the expression of the FAK/ERK pathway components in HUVEC treated with CM from the indicated CRC cells (E, F) Representative tubular structures formed by HUVECs treated with indicated CM from indicated HCT8/Caco-2 cells. Data are presented as mean ± SD ( n = 3). (G) Heat map demonstrates the differentially expressed genes related to angiogenesis and matrix metalloproteinase family in HUVEC treated with CM from control and sg DSPP HCT116 cells. (H) Detecting the effect of AZD6244 on the DSPP-upregulated expression of angiogenesis and matrix metalloproteinase family-related genes by real-time quantitative PCR. Data are presented as mean ± SD ( n = 4). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: Inhibitors, including the mitogen-activated protein kinase (MAPK) kinase inhibitor selumetinib (AZD6244, MCE, Monmouth Junction, NJ, USA) or cyclo (-RGDfK) TFA (HY-P0023A, MCE), were introduced into the cultured cells.

Techniques: Expressing, Western Blot, Control, Real-time Polymerase Chain Reaction

Journal: Acta Pharmaceutica Sinica. B

Article Title: Neutralizing dentin sialophosphoprotein facilitates tumor vascular normalization in colorectal cancer by blocking the crosstalk between tumor cells and endothelial cells

doi: 10.1016/j.apsb.2026.06.011

Figure Lengend Snippet: A schematic diagram shows the action mechanism of DSPP in regulating tumor vascular abnormalization to induce tumor metastasis. In the tumor microenvironment, IL-7F enhances the expression and secretion of DSPP in CRC. The CRC-secreted DSPP binds to the integrin α v β 3 on the endothelial cell surface and activates the downstream FAK/MAPK signaling to induce tumor vascular abnormalization, finally promote tumor metastasis.

Article Snippet: Inhibitors, including the mitogen-activated protein kinase (MAPK) kinase inhibitor selumetinib (AZD6244, MCE, Monmouth Junction, NJ, USA) or cyclo (-RGDfK) TFA (HY-P0023A, MCE), were introduced into the cultured cells.

Techniques: Expressing

Journal: Journal of Cell Science

Article Title: Apical-out polarity in epithelial spheroids requires α6β4 integrins, cell proliferation and anchorage independence

doi: 10.1242/jcs.264323

Figure Lengend Snippet: Anchorage independence is required for apical-out polarity. (A) MDCK cells were seeded into soft agar. Cells were left untreated or were treated with RhoA activator II. (B) Quantification of colonies formed in the agar assay. Each data point represents the mean (from a minimum of three field of view) from each experimental replicate (three replicate experiments were performed in total) (error bars are overall mean±s.d.). * P <0.05 (paired two-tailed t -test). (C) MDCK cysts were grown in Matrigel for 7 days and then treated with RhoA activator II for 72 h, pre-treated with FAK inhibitor Y15 24 h followed by Y15+Rho Activator II for an additional 48 h, or treated with Rho activator II for 24 h, followed by Y15+Rho activator II for an additional 48 h (post treatment). (D) Quantification of normal, disrupted lumen and eversion for each condition. Each data point represents the mean (expressed as a percentage) of each condition per replicate experiment (minimum of 10 cysts analyzed per condition per experiment, five replicate experiments performed in total; error bars are overall mean±s.d.). ** P <0.01; ns, not significant (two-way ANOVA with Tukey's multiple comparison test).

Article Snippet: Focal adhesion kinase (FAK) inhibitor Y15 (also known as FAK inhibitor 14) was used at a final concentration of 2.5 μM (Medchem express, catalog HY-12444).

Techniques: Two Tailed Test, Comparison

Journal: Neural Regeneration Research

Article Title: Trans-spinal magnetic stimulation upregulates microglial SOCS3 to attenuate neuroinflammation in chronic constriction injury–induced neuropathic pain

doi: 10.4103/NRR.NRR-D-24-00912

Figure Lengend Snippet: rMS-induced upregulation of SOCS3 in microglia is CaMKKβ/AMPK-dependent in vitro . (A) A schematic diagram of the in vitro study. (B) Western blotting data indicating that the p-CaMKKβ protein level in BV-2 cells increased at 5 minutes after a single administration of rMS and was highest at 15 minutes post-rMS ( n = 4). (C) Western blotting data showing that the p-AMPK protein level in BV-2 cells increased significantly at 30 minutes after rMS ( n = 4). (D, E) Representative western blotting results show that STO-609 and compound C alleviated rMS-induced activation of AMPK in vitro ( n = 4). (F–H) Representative western blotting data showing that compound C abrogated rMS-induced upregulation of SOCS3 and inhibition of p38 and STAT3 in vitro ( n = 4). (I) Representative immunofluorescence images showing that rMS inhibited the translocation of NF-κB p65 (green, Alexa Fluor 488) from the cytosol to the nucleus after LPS treatment in vitro , where this effect was reversed by administration of compound C (20 μmol/mL) 0.5 hours before LPS pretreatment ( n = 3). Arrows indicate BV-2 cells. Scale bars: 10 μm. Data are expressed as mean ± SD. # P < 0.05, ## P < 0.01, vs . Control group; * P < 0.05, ** P < 0.01, **** P < 0.001, vs . LPS group; † P < 0.05, †† P < 0.01, vs. LPS + rMS group (one‐way analysis of variance followed by Tukey’s multiple comparisons tests). AMPK: Adenosine 5′-monophosphate-activated protein kinase; CaMKKβ: calmodulin-dependent protein kinase kinase beta; Compound C: an AMPK inhibitor; DAPI: 4′,6-diamidino-2-phenylindole; LPS: lipopolysaccharide; NF-κB: nuclear factor kappa-B; p-AMPK: phosphorylated AMPK(Thr172); p-CaMKKβ: phospho-CaMKKβ(Ser511); rMS: repetitive magnetic stimulation; SOCS3: suppressor of cytokine signaling 3; STAT3: transducer and activator of transcription 3; STO-609: a CaMKKβ inhibitor.

Article Snippet: Intrathecal injections of compound C, an adenosine 5′-monophosphate-activated protein kinase (AMPK) inhibitor (10 μg/10 μL; MedChemExpress, Newark, NJ, USA, Cat# HY-13418A), and SOCS3 siRNA (500 pmol/10 μL; Santa Cruz Biotechnology, Santa Cruz, CA, USA, Cat# SC-270156) were performed as described previously by Mestre et al. (1994).

Techniques: In Vitro, Western Blot, Activation Assay, Inhibition, Immunofluorescence, Translocation Assay, Control

Journal: Neural Regeneration Research

Article Title: Trans-spinal magnetic stimulation upregulates microglial SOCS3 to attenuate neuroinflammation in chronic constriction injury–induced neuropathic pain

doi: 10.4103/NRR.NRR-D-24-00912

Figure Lengend Snippet: The pain-relieving effect and upregulation of SOCS3 induced by focal rTSMS depended on the activation of AMPK. (A) Timeline diagram of CCI modeling, rTSMS treatment, mechanical withdrawal threshold assessment, and experimental analysis in rats. (B) Western blotting data illustrates that the p-AMPK protein level decreased in CCI model rats and increased in CCI + rTSMS + Vehicle rats ( n = 5). (C, D) Intrathecal injection of compound C largely prevented the pain-relieving effects of focal rTMS, when applied once or repeatedly, in rats with CCI neuropathic pain ( n = 8). (E–H) Representative western blotting results showing that compound C alleviated the rTSMS-induced activation of AMPK, increase in SOCS3, and downregulation of p38 and STAT3 ( n = 5). (I, J) Representative immunofluorescence images showing that compound C abrogated the rTSMS-induced upregulation of SOCS3 (green, Alexa Fluor 488) in the dorsal horn of the spinal cord ( n = 3). Dashed box indicates the region of interest in the dorsal horn of the spinal cord. Scale bars: 100 μm. Data are expressed as mean ± SD. # P < 0.05, ## P < 0.01, ### P < 0.001, vs. Sham + Vehicle group; * P < 0.05, ** P < 0.01, **** P < 0.0001, vs . CCI + Vehicle group; † P < 0.05, †† P < 0.01, ††† P < 0.001, †††† P < 0.0001, vs . CCI + rTSMS + Compound C group (C, D: two‐way analysis of variance; B, E–H, J: one‐way analysis of variance followed by Tukey’s multiple comparisons tests). AMPK: Adenosine 5′-monophosphate-activated protein kinase; CCI: chronic constrictive injury; DAPI: 4′,6-diamidino-2-phenylindole; Iba-1: ionized calcium binding adaptor molecule-1; p-AMPK: phosphorylated AMPK(Thr172); p-p38: phospho-p38 mitogen-activated protein kinase; p-STAT3: phospho-STAT3; rTSMS: repetitive trans-spinal magnetic stimulation; SOCS3: suppressor of cytokine signaling 3; STAT3: transducer and activator of transcription 3.

Article Snippet: Intrathecal injections of compound C, an adenosine 5′-monophosphate-activated protein kinase (AMPK) inhibitor (10 μg/10 μL; MedChemExpress, Newark, NJ, USA, Cat# HY-13418A), and SOCS3 siRNA (500 pmol/10 μL; Santa Cruz Biotechnology, Santa Cruz, CA, USA, Cat# SC-270156) were performed as described previously by Mestre et al. (1994).

Techniques: Activation Assay, Western Blot, Injection, Immunofluorescence, Binding Assay