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Cell Signaling Technology Inc phosphorylated p stat3

Knockdown of CCT2 inhibits <t>STAT3</t> signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, <t>p-STAT3,</t> MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

Phosphorylated P Stat3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 337 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 337 article reviews

phosphorylated p stat3 - by Bioz Stars, 2026-09

96/100 stars

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1) Product Images from "Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation"

Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation

Journal: Oncology Reports

doi: 10.3892/or.2026.9086

Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

Figure Legend Snippet: Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

Techniques Used: Knockdown, Activation Assay, Western Blot, Immunohistochemical staining, Staining, Negative Control, Sequencing

IL-6 abolishes the effects of CCT2 knockdown on the proliferation and invasion of hepatocellular carcinoma cells. The protein levels of STAT3 and p-STAT3 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The proliferation of (C) Huh-7 and (D) HCCLM3 cells following CCT2 knockdown and IL-6 treatment was detected using EdU incorporation assay. The invasion of (E) Huh-7 and (F) HCCLM3 cells was assessed using Transwell assay. *P<0.05, **P<0.01 vs. PBS. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; p-, phosphorylated.

Figure Legend Snippet: IL-6 abolishes the effects of CCT2 knockdown on the proliferation and invasion of hepatocellular carcinoma cells. The protein levels of STAT3 and p-STAT3 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The proliferation of (C) Huh-7 and (D) HCCLM3 cells following CCT2 knockdown and IL-6 treatment was detected using EdU incorporation assay. The invasion of (E) Huh-7 and (F) HCCLM3 cells was assessed using Transwell assay. *P<0.05, **P<0.01 vs. PBS. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; p-, phosphorylated.

Techniques Used: Knockdown, Western Blot, Transwell Assay

Incubation:

Article Title: GRIM-19-mediated induction of mitochondrial STAT3 alleviates systemic sclerosis by inhibiting fibrosis and Th2/Th17 cells
Article Snippet: Protein concentrations were determined via a Bradford protein assay (#23225, Thermo). .. Proteins were separated via SDS‒PAGE, transferred to Hybond enhanced chemiluminescence (ECL) membranes (#10600001, Cytiva), and incubated with antibodies against GRIM-19 (#ab186848, Abcam, 1:1000), phosphorylated (p)-STAT3 (Tyr705) (#9145 L, Cell Signaling, 1:1000), p727 STAT3 (Ser727) (#9134 L, Cell Signaling, 1:500), STAT3 (#9139, Cell Signaling, 1:1000), LC3B (#ab48394, Abcam, 1:1000), COX IV (#ab33985, Abcam, 1:1000), α-SMA (#ab7817, Abcam, 1:1000), connective tissue growth factor (CTGF) (#ab6992, Abcam, 1:1000), or β-actin (#sc-47778, Santa Cruz, 1:1000). .. Protein bands were visualized via the SNAP i.d. protein detection system (Millipore) and X-ray film (EA8EC, Agfa).

Article Title: Inhibition of CCL4 prevents renal inflammation and fibrosis in acute kidney injury
Article Snippet: .. Membranes were blocked with 1% BSA217 solution for 1 hour then incubated with antibodies against CCL4 (Santa Cruz,218 sc-393441, 1:1000, Dallas, TX, USA), kidney injury molecule-1 (KIM-1; R&D219 Systems, AF1817, 1:1000, Minneapolis, USA), phosphorylated (p)-STAT3 (Cell220 Signaling Technology, #9145S, 1:1000, Danvers, MA, USA), STAT3 (Cell Signaling221 Technology, #9139S, #12640, 1:1000, Danvers, MA, USA) , transforming growth222 factor-β (TGF-β; Cell Signaling Technology, #3711S, 1:1000, Danvers, MA, USA),223 p-Smad2/3 (Cell Signaling Technology, #8828S, 1:1000, Danvers, MA, USA),224 Smad2/3 (Cell Signaling Technology, #3102S, 1:1000,Danvers, MA, USA), collagen225 1 (Cell Signaling Technology, #91144S, 1:1000, Danvers, MA, USA), IL-1β (Santa226 Cruz, sc-7884, 1:1000, Dallas, TX, USA), IL-6 (Cell Signaling Technology, #12153S,227 1:1000, Danvers, MA, USA), and TNF-α (Cell Signaling, 3707S, 1:1000, Danvers,228 MA, USA). .. The immunoblotting expression of KIM-1, p-STAT3, STAT3, TGF-β,229 p-Smad2/3, Smad2/3, collagen 1, IL-1β, IL-6, and TNF-α was normalized to the actin230 expression determined using an anti-β-actin antibody (Santa Cruz Biotechnology,231 sc-81178, Dallas, TX, USA; 1:10,000).232 2.13 Statistical analysis233 All raw data were analyzed by Shapiro-Wilk normality test.

Sequencing:

Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation.
Article Snippet: .. The primary antibodies were as follows: CCT2 (cat. no. 24896‐1‐AP), β‐actin (cat. no. 66009‐1‐Ig), MMP2 (cat. no. 10373‐2‐AP), myeloid cell leukemia sequence 1 (MCL1; cat. no. 16225‐1‐AP) and SRY‐box transcription factor 2 (SOX2; cat. no. 11064‐1‐AP; all Proteintech Group, Inc.) and STAT3 (cat. no. 4904) and phosphorylated (p‐)STAT3 (Tyr705; cat. no. 4113; both Cell Signaling Technology, Inc.) The membranes were washed three times in TBST (0.1% Tween‐20) for 5 min each at room temperature. ..

Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation
Article Snippet: .. The primary antibodies were as follows: CCT2 (cat. no. 24896-1-AP), β-actin (cat. no. 66009-1-Ig), MMP2 (cat. no. 10373-2-AP), myeloid cell leukemia sequence 1 (MCL1; cat. no. 16225-1-AP) and SRY-box transcription factor 2 (SOX2; cat. no. 11064-1-AP; all Proteintech Group, Inc.) and STAT3 (cat. no. 4904) and phosphorylated (p-)STAT3 (Tyr705; cat. no. 4113; both Cell Signaling Technology, Inc.) The membranes were washed three times in TBST (0.1% Tween-20) for 5 min each at room temperature. ..

Staining:

Article Title: Liraglutide attenuates doxorubicin-induced cardiomyocyte ferroptosis via DHHC7-mediated STAT3 palmitoylation.
Article Snippet: .. Tissue sections were differentially processed for histological evaluation: One subset was stained with H&E for morphological assessment, while another subset was subjected to immunofluorescence analysis to examine the spatial distribution of key proteins, including phosphorylated (p)-STAT3 (cat. no. 9145; Cell Signaling Technology, Inc.; 1:150) and GPX4 (cat. no. 67763–1-Ig; Proteintech Group, Inc.; 1:1000). .. Following overnight incubation with primary antibodies at 4 ◦C, the sections were thoroughly washed with PBS and subsequently exposed to Alexa Fluor® 488-conjugated goat anti-rabbit IgG secondary antibody (cat. no. 4412; Cell Signaling Technology, Inc.; 1:1000) for 60 min under light-protected conditions at room temperature.

Immunofluorescence:

Image Search Results

Journal: Oncology Reports

Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation

doi: 10.3892/or.2026.9086

Figure Lengend Snippet: Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

Article Snippet: The primary antibodies were as follows: CCT2 (cat. no. 24896-1-AP), β-actin (cat. no. 66009-1-Ig), MMP2 (cat. no. 10373-2-AP), myeloid cell leukemia sequence 1 (MCL1; cat. no. 16225-1-AP) and SRY-box transcription factor 2 (SOX2; cat. no. 11064-1-AP; all Proteintech Group, Inc.) and STAT3 (cat. no. 4904) and phosphorylated (p-)STAT3 (Tyr705; cat. no. 4113; both Cell Signaling Technology, Inc.) The membranes were washed three times in TBST (0.1% Tween-20) for 5 min each at room temperature.

Techniques: Knockdown, Activation Assay, Western Blot, Immunohistochemical staining, Staining, Negative Control, Sequencing

Journal: Oncology Reports

Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation

doi: 10.3892/or.2026.9086

Figure Lengend Snippet: IL-6 abolishes the effects of CCT2 knockdown on the proliferation and invasion of hepatocellular carcinoma cells. The protein levels of STAT3 and p-STAT3 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The proliferation of (C) Huh-7 and (D) HCCLM3 cells following CCT2 knockdown and IL-6 treatment was detected using EdU incorporation assay. The invasion of (E) Huh-7 and (F) HCCLM3 cells was assessed using Transwell assay. *P<0.05, **P<0.01 vs. PBS. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; p-, phosphorylated.

Techniques: Knockdown, Western Blot, Transwell Assay

Determination of M1 vs. M2 polarization in iMac. a Pro-inflammatory M1 cytokines IL-1β, TNFα, IL-6, and IL-8 measured by ELISA. b Anti-inflammatory M2 cytokines IL-4, IL-10, IL-13, CCL5, CCL17, and CCL20 measured by ELISA. For a , b iMac were cultured in 6-well plates (3 × 10 6 cells/well). To challenge with tumor factors, iMac were co-cultured with 50% fresh supernatant from SK-MEL-28 cells every 24 h for 3 days. Supernatants were collected during the final 24 h for cytokine measurement. c Activation (phosphorylation) of NF-kB p65, STAT1, STAT3, and STAT6 in iMac was determined using Western blotting after conditioning with melanoma (SK-MEL-28) supernatant for 72 h. Protein band intensity was quantified using Odyssey version 3.0 software. After adjusting for loading using the β-actin band, data are presented as fold change to the iMac (Dox-) group, which is set as 1. For a – c , one-way ANOVA with Bonferroni’s correction for multiple comparisons was used to analyze group comparisons. Data are presented as means ± SD. Each experiment was performed three times, with triplicate samples each time. * p < 0.05, *** p < 0.001, and **** p < 0.0001

Journal: Signal Transduction and Targeted Therapy

Article Title: Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth

doi: 10.1038/s41392-026-02650-3

Figure Lengend Snippet: Determination of M1 vs. M2 polarization in iMac. a Pro-inflammatory M1 cytokines IL-1β, TNFα, IL-6, and IL-8 measured by ELISA. b Anti-inflammatory M2 cytokines IL-4, IL-10, IL-13, CCL5, CCL17, and CCL20 measured by ELISA. For a , b iMac were cultured in 6-well plates (3 × 10 6 cells/well). To challenge with tumor factors, iMac were co-cultured with 50% fresh supernatant from SK-MEL-28 cells every 24 h for 3 days. Supernatants were collected during the final 24 h for cytokine measurement. c Activation (phosphorylation) of NF-kB p65, STAT1, STAT3, and STAT6 in iMac was determined using Western blotting after conditioning with melanoma (SK-MEL-28) supernatant for 72 h. Protein band intensity was quantified using Odyssey version 3.0 software. After adjusting for loading using the β-actin band, data are presented as fold change to the iMac (Dox-) group, which is set as 1. For a – c , one-way ANOVA with Bonferroni’s correction for multiple comparisons was used to analyze group comparisons. Data are presented as means ± SD. Each experiment was performed three times, with triplicate samples each time. * p < 0.05, *** p < 0.001, and **** p < 0.0001

Article Snippet: The polyvinylidene difluoride (PVDF) membranes were incubated with specific primary antibodies against ACE (R&D Systems, MAB9291, 1:1,000), GAPDH (Sigma-Aldrich, SAB5600208, 1:2,000), β-actin (Sigma-Aldrich, A3854; 1:1000), phosphorylated NF-kB p65 (Novus, NB100-82086, 1:500), phosphorylated STAT1 (R&D Systems, AF2894, 1 μg/ml), phosphorylated STAT3 (Novus, NBP2-24463, 0.5 μg/ml), or phosphorylated STAT6 (Millipore, 06-937, 1:1000).

Techniques: Enzyme-linked Immunosorbent Assay, Cell Culture, Activation Assay, Phospho-proteomics, Western Blot, Software

KSM inhibits CHI3L1-stimulated M2 macrophage activation via EGFR. Bulk RNA-seq sequencing analysis on the differentiated macrophages from THP-1 cells was used to evaluate mRNA expression in the macrophage differentiation regulated by CHI3L1 and KSM. ( A ). Volcano plots showing differentially expressed genes regulated by CHI3L1. ( B ) Representative plots of the top 20 genes that are upregulated (> 2-fold) by CHI3L1 stimulation but downregulated (< 2-fold) by KSM treatment. ( C ) Representative mRNA expression of EGFR in differentiated macrophages with CHI3L1 and KSM treatment was detected by real-time qRT-PCR. ( D ) Representative immunoblots showing p-EGFR (Tyr1068) and total EGFR expression in differentiated macrophages with CHI3L1 and KSM. Right panel, densitometric quantitation on the blots of EGFR and p-EGFR. ( E ) Effect of EGFR inhibition on the expression of p-STAT3 and total-STAT3 in CHI3L1-stimulated, differentiated macrophages by gefitinib (Tocris Bioscience, #3000) treatment (1 μM, 72 hours). Right panel, densitometric quantitation on the blots of p-STAT3 and total STAT3. ( F ) Effects of EGFR inhibition on the expression of CD163 and CD206 in CHI3L1-stimulated, differentiated macrophages by gefitinib treatment (0.1 and 1 μM, 72 hours). Right panel, densitometric quantitation on the blots of CD163 and CD206. The values in ( C – F ) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).

Journal: ImmunoTargets and Therapy

Article Title: Kasugamycin Inhibits Melanoma Lung Metastasis and CHI3L1-Driven M2-Like Tumor-Associated Macrophage Differentiation

doi: 10.2147/ITT.S563951

Figure Lengend Snippet: KSM inhibits CHI3L1-stimulated M2 macrophage activation via EGFR. Bulk RNA-seq sequencing analysis on the differentiated macrophages from THP-1 cells was used to evaluate mRNA expression in the macrophage differentiation regulated by CHI3L1 and KSM. ( A ). Volcano plots showing differentially expressed genes regulated by CHI3L1. ( B ) Representative plots of the top 20 genes that are upregulated (> 2-fold) by CHI3L1 stimulation but downregulated (< 2-fold) by KSM treatment. ( C ) Representative mRNA expression of EGFR in differentiated macrophages with CHI3L1 and KSM treatment was detected by real-time qRT-PCR. ( D ) Representative immunoblots showing p-EGFR (Tyr1068) and total EGFR expression in differentiated macrophages with CHI3L1 and KSM. Right panel, densitometric quantitation on the blots of EGFR and p-EGFR. ( E ) Effect of EGFR inhibition on the expression of p-STAT3 and total-STAT3 in CHI3L1-stimulated, differentiated macrophages by gefitinib (Tocris Bioscience, #3000) treatment (1 μM, 72 hours). Right panel, densitometric quantitation on the blots of p-STAT3 and total STAT3. ( F ) Effects of EGFR inhibition on the expression of CD163 and CD206 in CHI3L1-stimulated, differentiated macrophages by gefitinib treatment (0.1 and 1 μM, 72 hours). Right panel, densitometric quantitation on the blots of CD163 and CD206. The values in ( C – F ) are the mean ± SEM. * P <0.05, ** P <0.01, *** P <0.001 (One-Way ANOVA, multiple comparisons).

Article Snippet: Protein lysates (25 μg) from lung tissues or cells were subjected to SDS-PAGE, transferred to membranes, and immunoblotted with primary antibodies against CD163 (#PA5-109327, Thermo Fisher Scientific), CD206 (E6T5J, #24595S, Cell Signaling Technology), phosphorylated AKT (p-Akt) (193H12, #4058S, Cell Signaling Technology), and total Akt (11E7, #4685S, Cell Signaling Technology), phosphorylated EGFR (Tyr1068) (p-EGFR) (#44-788G, Thermo Fisher Scientific), EGFR (D38B1, #4267S, Cell Signaling Technology), phosphorylated Erk (p-Erk) (#9101S, Cell Signaling Technology), total Erk (#9102S, Cell Signaling Technology), phosphorylated STAT3 (Tyr705) (p-STAT3) (D3A7, #9145, Cell Signaling Technology), total STAT3 (79D7, #4904, Cell Signaling Technology) and b-actin (C4, #sc-47778 HRP, Santa Cruz Biotechnology).

Techniques: Activation Assay, RNA Sequencing, Sequencing, Expressing, Quantitative RT-PCR, Western Blot, Quantitation Assay, Inhibition

Protein expression of IL-21, p-STAT3, SOCS1, PTEN and PIAS3. (A) IL-21 expression in HC and SLE patients non-stimulated, (B) p-STAT3 expression in HC and SLE patients non-stimulated, (C) SOCS1 expression in HC and SLE patients non-stimulated, (D) PTEN expression in HC and SLE patients non-stimulated, (E) PIAS3 expression in HC and SLE patients non-stimulated, (F) IL-21 expression after stimulation with PMA+IONO in HC and SLE patients, (G) p-STAT3 expression after stimulation with PMA+IONO in HC and SLE patients, (H) SOCS1 expression after stimulation with PMA+IONO in HC and SLE patients, (I) PTEN expression after stimulation with PMA+IONO in HC and SLE patients, (J) PIAS3 expression after stimulation with PMA+IONO in HC and SLE patients. Data are shown in median and IQR. p-value was obtained through Mann-Whitney’s U test. β-actin served as an internal reference.

Journal: Frontiers in Immunology

Article Title: Aberrant STAT3 activation and overproduction of IL-21 in systemic lupus erythematosus: role of miR-155 and miR-21 in target genes SOCS1, PTEN and PIAS3

doi: 10.3389/fimmu.2026.1664409

Figure Lengend Snippet: Protein expression of IL-21, p-STAT3, SOCS1, PTEN and PIAS3. (A) IL-21 expression in HC and SLE patients non-stimulated, (B) p-STAT3 expression in HC and SLE patients non-stimulated, (C) SOCS1 expression in HC and SLE patients non-stimulated, (D) PTEN expression in HC and SLE patients non-stimulated, (E) PIAS3 expression in HC and SLE patients non-stimulated, (F) IL-21 expression after stimulation with PMA+IONO in HC and SLE patients, (G) p-STAT3 expression after stimulation with PMA+IONO in HC and SLE patients, (H) SOCS1 expression after stimulation with PMA+IONO in HC and SLE patients, (I) PTEN expression after stimulation with PMA+IONO in HC and SLE patients, (J) PIAS3 expression after stimulation with PMA+IONO in HC and SLE patients. Data are shown in median and IQR. p-value was obtained through Mann-Whitney’s U test. β-actin served as an internal reference.

Article Snippet: Subsequently, the membranes were immunoblotted with the specific primary antibodies, anti-IL-21 (ABCAM, Cambridge, UK) (1:3000), phosphorylated STAT3 (p-STAT3) on tyrosine 705 (Y705) (Santa Cruz Biotechnology, Dallas, TX, USA) (1:400), SOCS1 (Santa Cruz Biotechnology, Dallas, TX, USA) (1:500), PTEN (Santa Cruz Biotechnology, Dallas, TX, USA) (1:500) and PIAS3 (Santa Cruz Biotechnology, Dallas, TX, USA) (1:200) overnight at 4°C.

Techniques: Expressing

Impact of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway on tumor stem cell self-renewal and migration invasion. (A, B) Western blot analysis of JAK-STAT and nuclear factor kappa B (NF-κB) signaling pathway-related proteins: protein expression levels of phosphorylated-Janus kinase 2 (p-JAK2), JAK2, phosphorylated signal transducer and activator of transcription (p-STAT3), STAT3, NF-κB, and phosphorylated NF-κB (p-NF-κB) in FTC238-S cells co-cultured with different modified myeloid‑derived suppressor cells (MDSCs) (A), and protein levels of p-JAK2, JAK2, p-STAT3, and STAT3 in FTC238-S cells treated with anti-immunoglobulin G (anti-IgG) or anti-C-X-C motif chemokine ligand 8 (anti-CXCL8) antibodies (B). (C) Schematic diagram of monocyte treatment and co-culturing with FTC238-S cells. (D) Western blot analysis of JAK-STAT signaling pathway-related proteins in FTC238-S cells from each group. (E) Protein expression levels of stemness markers neuroepithelial stem cell protein (NESTIN), octamer-binding transcription factor 4 (OCT4), and SRY-box transcription factor 2 (SOX2) in FTC238-S cells from each group examined by Western blot. (F) Cell sphere formation assay assessing the sphere formation capability of FTC238-S cells in co-culture systems of each group. (G) Clonogenic assay evaluating the clonogenic capacity of FTC238-S cells in co-culture systems of each group. (H) Cell Counting Kit-8 (CCK-8) assay measuring the proliferation ability of FTC238-S cells in co-culture systems of each group. (I) Transwell assay determining the migration and invasion capability of FTC238-S cells in co-culture systems of each group, ∗ P < 0.05 compared between the two groups, and all cell experiments were repeated three times. M_oe-NC + S_sh-NC: FTC238-S cells transfected with short hairpin RNA-negative control (sh-NC) and treated with conditioned medium from monocytes transfected with oe-NC; M_oe-CXCL8 + S_sh-NC: FTC238-S cells transfected with sh-NC and treated with conditioned medium from monocytes transfected with oe-CXCL8; M_oe-CXCL8 + S_sh-SDC1: FTC238-S cells transfected with short hairpin RNA-SDC1 (sh-SDC1) and treated with conditioned medium from monocytes transfected with oe-CXCL8; M_oe-CXCL8 + S_DMSO: FTC238-S cells treated with conditioned medium from monocytes transfected with oe-CXCL8 and supplemented with an equal amount of dimethyl sulfoxide (DMSO); M_oe-CXCL8 + S_SD_1008: FTC238-S cells treated with conditioned medium from monocytes transfected with oe-CXCL8 and supplemented with SD-1008; THP-1 cells: Tohoku Hospital Pediatrics-1 cells; OD: optical density.

Journal: Journal of Pharmaceutical Analysis

Article Title: CXCL8/SDC1 axis mediates tumor stem cell interactions to drive remote transfer in thyroid cancer

doi: 10.1016/j.jpha.2025.101354

Figure Lengend Snippet: Impact of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway on tumor stem cell self-renewal and migration invasion. (A, B) Western blot analysis of JAK-STAT and nuclear factor kappa B (NF-κB) signaling pathway-related proteins: protein expression levels of phosphorylated-Janus kinase 2 (p-JAK2), JAK2, phosphorylated signal transducer and activator of transcription (p-STAT3), STAT3, NF-κB, and phosphorylated NF-κB (p-NF-κB) in FTC238-S cells co-cultured with different modified myeloid‑derived suppressor cells (MDSCs) (A), and protein levels of p-JAK2, JAK2, p-STAT3, and STAT3 in FTC238-S cells treated with anti-immunoglobulin G (anti-IgG) or anti-C-X-C motif chemokine ligand 8 (anti-CXCL8) antibodies (B). (C) Schematic diagram of monocyte treatment and co-culturing with FTC238-S cells. (D) Western blot analysis of JAK-STAT signaling pathway-related proteins in FTC238-S cells from each group. (E) Protein expression levels of stemness markers neuroepithelial stem cell protein (NESTIN), octamer-binding transcription factor 4 (OCT4), and SRY-box transcription factor 2 (SOX2) in FTC238-S cells from each group examined by Western blot. (F) Cell sphere formation assay assessing the sphere formation capability of FTC238-S cells in co-culture systems of each group. (G) Clonogenic assay evaluating the clonogenic capacity of FTC238-S cells in co-culture systems of each group. (H) Cell Counting Kit-8 (CCK-8) assay measuring the proliferation ability of FTC238-S cells in co-culture systems of each group. (I) Transwell assay determining the migration and invasion capability of FTC238-S cells in co-culture systems of each group, ∗ P < 0.05 compared between the two groups, and all cell experiments were repeated three times. M_oe-NC + S_sh-NC: FTC238-S cells transfected with short hairpin RNA-negative control (sh-NC) and treated with conditioned medium from monocytes transfected with oe-NC; M_oe-CXCL8 + S_sh-NC: FTC238-S cells transfected with sh-NC and treated with conditioned medium from monocytes transfected with oe-CXCL8; M_oe-CXCL8 + S_sh-SDC1: FTC238-S cells transfected with short hairpin RNA-SDC1 (sh-SDC1) and treated with conditioned medium from monocytes transfected with oe-CXCL8; M_oe-CXCL8 + S_DMSO: FTC238-S cells treated with conditioned medium from monocytes transfected with oe-CXCL8 and supplemented with an equal amount of dimethyl sulfoxide (DMSO); M_oe-CXCL8 + S_SD_1008: FTC238-S cells treated with conditioned medium from monocytes transfected with oe-CXCL8 and supplemented with SD-1008; THP-1 cells: Tohoku Hospital Pediatrics-1 cells; OD: optical density.

Article Snippet: Proteins were transferred to a polyvinylidene difluoride (PVDF) membrane and blocked with 5% skim milk at room temperature for 1 h. The PVDF membrane was incubated overnight at 4 °C with primary antibodies against CXCL8 (1:1000, ab235584, Abcam, Cambridge, UK), SDC1 (1:2000, ab128936, Abcam, Cambridge, UK), NESTIN (1:100, ab105389, Abcam, Cambridge, UK), OCT4 (1:10000, ab200834, Abcam, Cambridge, UK), SRY-Box transcription factor 2 (SOX2, 1:1500, ab92494, Abcam, Cambridge, UK), phosphorylated STAT3 (p-STAT3) (1:1000, NB100-82213, Novus Biologicals, Centennial, CO, USA), STAT3 (1:1000, MAB1799, Novus Biologicals, Centennial, CO, USA), phosphorylated-JAK2 (p-JAK2) (1:1500, ab32101, Abcam, Cambridge, UK), JAK2 (1:1000, ab108596, Abcam, Cambridge, UK), nuclear factor kappa B (NF-κB, 1:1000, 8242T, CST, Boston, MA, USA), phosphorylated NF-κB (p-NF-κB) (1:1000, 3033T, CST, Boston, MA, USA), glyceraldehyde 3-phosphate dehydrogenase (GAPDH) (1:2500, ab9485, Abcam, Cambridge, UK), and Tubulin (1:5000, ab7291, Abcam, Cambridge, UK).

Techniques: Migration, Western Blot, Expressing, Cell Culture, Modification, Binding Assay, Tube Formation Assay, Co-Culture Assay, Clonogenic Assay, Cell Counting, CCK-8 Assay, Transwell Assay, Transfection, shRNA, Negative Control

Impact of the C-X-C motif chemokine ligand 8/syndecan-1 (CXCL8/SDC1) axis on tumor initiation, growth, and metastasis of thyroid cancer (THCA) stem cells i n Vivo . (A) Diagram of the in vivo animal experiment protocol, with the green syringe representing anti-immunoglobulin G (anti-IgG) and anti-CXCL8 treatments. (B) Western blot analysis of Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway-related proteins in subcutaneous tumor tissues of nude mice from each group. (C) Gross anatomy of subcutaneous transplant tumors in nude mice (left) and corresponding weight statistics (right). (D) Images of primary tumors in nude mice from each group (left) and diameter analysis (right). (E) Statistical analysis of axillary lymph node (LN) metastasis in subcutaneous transplant tumors of nude mice from each group. (F) Hematoxylin and eosin (H&E) staining to assess bone metastasis of primary tumors in nude mice from each group. (G) Images of lung metastasis in nude mice from each group (left) and diameter analysis (right). (H) H&E staining to evaluate lung metastasis in nude mice from each group. ∗ P < 0.05 compared between two groups, ∗∗ P < 0.01 with 6 nude mice in each group. p-JAK2: phosphorylated-JAK2; p-STAT3: phosphorylated STAT3; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; S_sh-NC: FTC238-S cells transfected with short hairpin RNA-negative control (sh-NC); S_sh-SDC1: FTC238-S cells transfected with short hairpin RNA-SDC1 (sh-SDC1).

Journal: Journal of Pharmaceutical Analysis

Article Title: CXCL8/SDC1 axis mediates tumor stem cell interactions to drive remote transfer in thyroid cancer

doi: 10.1016/j.jpha.2025.101354

Figure Lengend Snippet: Impact of the C-X-C motif chemokine ligand 8/syndecan-1 (CXCL8/SDC1) axis on tumor initiation, growth, and metastasis of thyroid cancer (THCA) stem cells i n Vivo . (A) Diagram of the in vivo animal experiment protocol, with the green syringe representing anti-immunoglobulin G (anti-IgG) and anti-CXCL8 treatments. (B) Western blot analysis of Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway-related proteins in subcutaneous tumor tissues of nude mice from each group. (C) Gross anatomy of subcutaneous transplant tumors in nude mice (left) and corresponding weight statistics (right). (D) Images of primary tumors in nude mice from each group (left) and diameter analysis (right). (E) Statistical analysis of axillary lymph node (LN) metastasis in subcutaneous transplant tumors of nude mice from each group. (F) Hematoxylin and eosin (H&E) staining to assess bone metastasis of primary tumors in nude mice from each group. (G) Images of lung metastasis in nude mice from each group (left) and diameter analysis (right). (H) H&E staining to evaluate lung metastasis in nude mice from each group. ∗ P < 0.05 compared between two groups, ∗∗ P < 0.01 with 6 nude mice in each group. p-JAK2: phosphorylated-JAK2; p-STAT3: phosphorylated STAT3; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; S_sh-NC: FTC238-S cells transfected with short hairpin RNA-negative control (sh-NC); S_sh-SDC1: FTC238-S cells transfected with short hairpin RNA-SDC1 (sh-SDC1).

Techniques: In Vivo, Western Blot, Staining, Transfection, shRNA, Negative Control

Schematic diagram of the molecular mechanism by which monocytes promote self-renewal, migration, and invasion of thyroid cancer (THCA) stem cells through the C-X-C motif chemokine ligand 8/syndecan-1 (CXCL8/SDC1) axis. JAK2: Janus kinase 2; STAT3: signal transducer and activator of transcription 3.

Journal: Journal of Pharmaceutical Analysis

Article Title: CXCL8/SDC1 axis mediates tumor stem cell interactions to drive remote transfer in thyroid cancer

doi: 10.1016/j.jpha.2025.101354

Figure Lengend Snippet: Schematic diagram of the molecular mechanism by which monocytes promote self-renewal, migration, and invasion of thyroid cancer (THCA) stem cells through the C-X-C motif chemokine ligand 8/syndecan-1 (CXCL8/SDC1) axis. JAK2: Janus kinase 2; STAT3: signal transducer and activator of transcription 3.

Techniques: Migration

Review

phosphorylated p stat3 (Cell Signaling Technology Inc)

Structured Review

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1) Product Images from "Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation"

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