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R&D Systems human cxcl7 nap 2 duoset elisa kit
Human Cxcl7 Nap 2 Duoset Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human cxcl7 nap 2 duoset elisa kit - by Bioz Stars, 2026-07

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Increased inflammatory and oxidative stress levels in the PVT of DIO mice. A Quantification of CXCL7 in plasma from control or DIO mice. n = 3 mice per group, P = 0.0003. B and C Representative images ( B ) and summarized data ( C ) of the expression of CXCL7 in PVT Glu neurons from control and DIO mice. n = 5 mice per group, with one slice from each mouse. P < 0.0001. Scale bars, 10 μm. D - H Representative images ( D ) and quantification of IBA1 + cell numbers ( E ), intensity ( F ) and Imaris-based semiautomatic quantification of cell morphometry, including total branch length ( G ) and points ( H ) of IBA1 + -microglia from control and DIO mice. n = 5 mice per group for quantification of cell number and intensity, with one slice from each mouse. P (number) = 0.0081, P (intensity) = 0.0122. n= 6 mice for the control group and n = 7 mice for the DIO group in the quantification of branch length and points, with one slice from each mouse. P (length) = 0.014, P (intensity) = 0.0001. Scale bars, 10 μm (overview) and 3 μm (inset and rendering). I and J Representative images ( I ) and summarized data ( J ) of GPX4 in PVT Glu neurons from control and DIO mice. n = 6 mice per group, with one slice from each mouse. P = 0.0012. Scale bars, 10 μm. Statistical analysis was performed using Student’s t test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Journal: Journal of Neuroinflammation

Article Title: CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain

doi: 10.1186/s12974-025-03679-x

Figure Lengend Snippet: Increased inflammatory and oxidative stress levels in the PVT of DIO mice. A Quantification of CXCL7 in plasma from control or DIO mice. n = 3 mice per group, P = 0.0003. B and C Representative images ( B ) and summarized data ( C ) of the expression of CXCL7 in PVT Glu neurons from control and DIO mice. n = 5 mice per group, with one slice from each mouse. P < 0.0001. Scale bars, 10 μm. D - H Representative images ( D ) and quantification of IBA1 + cell numbers ( E ), intensity ( F ) and Imaris-based semiautomatic quantification of cell morphometry, including total branch length ( G ) and points ( H ) of IBA1 + -microglia from control and DIO mice. n = 5 mice per group for quantification of cell number and intensity, with one slice from each mouse. P (number) = 0.0081, P (intensity) = 0.0122. n= 6 mice for the control group and n = 7 mice for the DIO group in the quantification of branch length and points, with one slice from each mouse. P (length) = 0.014, P (intensity) = 0.0001. Scale bars, 10 μm (overview) and 3 μm (inset and rendering). I and J Representative images ( I ) and summarized data ( J ) of GPX4 in PVT Glu neurons from control and DIO mice. n = 6 mice per group, with one slice from each mouse. P = 0.0012. Scale bars, 10 μm. Statistical analysis was performed using Student’s t test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: Seven days later, a volume of 50 ng/μl CXCL7 protein (HY- P75698 , MCE, USA) dissolved in artificial cerebrospinal fluid (ACSF) was infused into the lateral ventricles (1 μl), or PVT (300 nl) was given once a day for three days in a row.

Techniques: Clinical Proteomics, Control, Expressing

Infusion of CXCL7 improved PVT Glu neuronal activity and induced pain hypersensitivity in control mice. A Schematic of the experimental procedure. B Image showing the site of the cannula implanted in the lateral ventricle of control mice. Scale bar, 500 μm. C and D Effects of infusion of CXCL7 in the lateral ventricle on the pain threshold in control mice treated with ACSF or CXCL7, using von Frey test ( C ) and Hargreaves tests ( D ). n = 5 mice per group, P = 0.0079 ( C ), P = 0.0007 ( D ). E Representative heatmaps of travel trajectory of control mice treated with ACSF or CXCL7 in the CPA test. F and G Summarized data of aversion index ( F ) and preference index ( G ) for ( E ), n = 7 mice per group. P < 0.0001 ( F and G ). ( H ) Image showing the site of the cannula implanted in the PVT of control mice. Scale bar, 500 μm. I and J Representative images ( I ) and summarized data ( J ) of CXCL7 on PVT Glu neurons in control mice treated with ACSF or CXCL7. n = 6 mice, with one slice from each mouse, P < 0.0001. Scale bar, 10 μm. K and L Representative images ( K ) and summarized data ( L ) of c-Fos in PVT from control mice treated with ACSF or CXCL7. n = 5 mice, with one slice from each mouse. P = 0.0061. Scale bar, 200 μm. M and N Sample traces ( M ) and summarized number of spikes ( N ) in PVT Glu neurons recorded from control mice treated with ACSF or CXCL7. n = 14 cells from 4 mice per group. P (time × column factor) = 0.0019, P (time) < 0.0001, P (column factor) = 0.001, F (1, 26) = 13.79. O and P Effects of the infusion of CXCL7 in PVT Glu neurons on the pain threshold using the von Frey test ( O ) and Hargreaves tests ( P ) of control mice treated with ACSF or CXCL7. n = 7 mice per group, P = 0.0002 ( O ), P = 0.0015 ( P ). Q Representative heatmaps of travel trajectory of control mice treated with ACSF or CXCL7 within PVT in the CPA test. ( R and S ) Summarized data of aversion index ( R ) and preference index ( S ) for ( Q ), n = 7 mice per group. P = 0.0003 ( R and S ). Statistical analysis was performed using Student’s t test in ( C ), ( D) , ( F) , ( G) , ( J) , ( L) , ( O) , ( P) , ( R) and ( S ), and two-way ANOVA followed by Bonferroni’s post hoc correction in ( N ). ** P < 0.01, *** P < 0.001, **** P < 0.0001

Journal: Journal of Neuroinflammation

Article Title: CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain

doi: 10.1186/s12974-025-03679-x

Figure Lengend Snippet: Infusion of CXCL7 improved PVT Glu neuronal activity and induced pain hypersensitivity in control mice. A Schematic of the experimental procedure. B Image showing the site of the cannula implanted in the lateral ventricle of control mice. Scale bar, 500 μm. C and D Effects of infusion of CXCL7 in the lateral ventricle on the pain threshold in control mice treated with ACSF or CXCL7, using von Frey test ( C ) and Hargreaves tests ( D ). n = 5 mice per group, P = 0.0079 ( C ), P = 0.0007 ( D ). E Representative heatmaps of travel trajectory of control mice treated with ACSF or CXCL7 in the CPA test. F and G Summarized data of aversion index ( F ) and preference index ( G ) for ( E ), n = 7 mice per group. P < 0.0001 ( F and G ). ( H ) Image showing the site of the cannula implanted in the PVT of control mice. Scale bar, 500 μm. I and J Representative images ( I ) and summarized data ( J ) of CXCL7 on PVT Glu neurons in control mice treated with ACSF or CXCL7. n = 6 mice, with one slice from each mouse, P < 0.0001. Scale bar, 10 μm. K and L Representative images ( K ) and summarized data ( L ) of c-Fos in PVT from control mice treated with ACSF or CXCL7. n = 5 mice, with one slice from each mouse. P = 0.0061. Scale bar, 200 μm. M and N Sample traces ( M ) and summarized number of spikes ( N ) in PVT Glu neurons recorded from control mice treated with ACSF or CXCL7. n = 14 cells from 4 mice per group. P (time × column factor) = 0.0019, P (time) < 0.0001, P (column factor) = 0.001, F (1, 26) = 13.79. O and P Effects of the infusion of CXCL7 in PVT Glu neurons on the pain threshold using the von Frey test ( O ) and Hargreaves tests ( P ) of control mice treated with ACSF or CXCL7. n = 7 mice per group, P = 0.0002 ( O ), P = 0.0015 ( P ). Q Representative heatmaps of travel trajectory of control mice treated with ACSF or CXCL7 within PVT in the CPA test. ( R and S ) Summarized data of aversion index ( R ) and preference index ( S ) for ( Q ), n = 7 mice per group. P = 0.0003 ( R and S ). Statistical analysis was performed using Student’s t test in ( C ), ( D) , ( F) , ( G) , ( J) , ( L) , ( O) , ( P) , ( R) and ( S ), and two-way ANOVA followed by Bonferroni’s post hoc correction in ( N ). ** P < 0.01, *** P < 0.001, **** P < 0.0001

Techniques: Activity Assay, Control

Mechanism of CXCL7-CXCR2 interaction in PVT Glu →BLA Glu neuronal circuit promotes the onset of obesity-related pain. In obese mice, elevated expression of the chemokine, CXCL7, results in the binding of CXCR2 receptors of PVT Glu neurons, thereby leading to increased activity in PVT Glu →BLA Glu neuronal circuit, which mediate obesity-related pain

Journal: Journal of Neuroinflammation

Article Title: CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain

doi: 10.1186/s12974-025-03679-x

Figure Lengend Snippet: Mechanism of CXCL7-CXCR2 interaction in PVT Glu →BLA Glu neuronal circuit promotes the onset of obesity-related pain. In obese mice, elevated expression of the chemokine, CXCL7, results in the binding of CXCR2 receptors of PVT Glu neurons, thereby leading to increased activity in PVT Glu →BLA Glu neuronal circuit, which mediate obesity-related pain

Techniques: Expressing, Binding Assay, Activity Assay

Figure 5. Differential regulation of CXCL7 (PPBP) gene expression in MDMs infected with HIV-1 or HIV-2. (A) The expression profiles of chemokine genes in MDMs infected with HIV-1 Ada or HIV-2 B5, B9, or Rod was analyzed by Affymetrix array using cell samples collected on day 15 post-infection. (B) The expression levels of CXCL7 mRNA in MDMs infected with HIV-1 Ada, 92UG024, BCF03, or Bal or HIV-2 B4, B5, B7, B8, or Rod isolates were measured by qPCR. The expression levels of CXCL7 mRNA were examined using cells harvested on day 15 post-infection, normalized by the levels of GAPDH mRNA and presented as the amount relative to uninfected cells (Cell only). Statistical analysis was performed using one-way ANOVA with Dunnett’s test for multiple testing corrections. The asterisks on the long bar line indicate a significant difference between the uninfected group and the nine HIV-1 and HIV-2-infected groups (**, p < 0.005, n = 3), as found using one-way ANOVA. The asterisks on the short bar lines indicate significant differences (*, p < 0.05) between the HIV infected group under the bar lines and the HIV-1 Ada control group, as assessed using Dunnett’s test for multiple comparisons.

Journal: International journal of molecular sciences

Article Title: Macrophage-Derived Factors with the Potential to Contribute to the Pathogenicity of HIV-1 and HIV-2: Roles of M-CSF and CXCL7.

doi: 10.3390/ijms26115028

Figure Lengend Snippet: Figure 5. Differential regulation of CXCL7 (PPBP) gene expression in MDMs infected with HIV-1 or HIV-2. (A) The expression profiles of chemokine genes in MDMs infected with HIV-1 Ada or HIV-2 B5, B9, or Rod was analyzed by Affymetrix array using cell samples collected on day 15 post-infection. (B) The expression levels of CXCL7 mRNA in MDMs infected with HIV-1 Ada, 92UG024, BCF03, or Bal or HIV-2 B4, B5, B7, B8, or Rod isolates were measured by qPCR. The expression levels of CXCL7 mRNA were examined using cells harvested on day 15 post-infection, normalized by the levels of GAPDH mRNA and presented as the amount relative to uninfected cells (Cell only). Statistical analysis was performed using one-way ANOVA with Dunnett’s test for multiple testing corrections. The asterisks on the long bar line indicate a significant difference between the uninfected group and the nine HIV-1 and HIV-2-infected groups (**, p < 0.005, n = 3), as found using one-way ANOVA. The asterisks on the short bar lines indicate significant differences (*, p < 0.05) between the HIV infected group under the bar lines and the HIV-1 Ada control group, as assessed using Dunnett’s test for multiple comparisons.

Article Snippet: CXCL7 concentrations in the supernatants collected from cultures of HIV-infected MDMs throughout the time course of infections were measured using ELISA kits (Cat# EA100464) purchased from Origene (Gaithersburg, MD, USA), following the manufacturer’s instructions.

Techniques: Gene Expression, Infection, Expressing, Control

Figure 6. Differential CXCL7 production by MDMs following infection with HIV-1 or HIV-2. (A,B) Time course of virus replication and CXCL7 production following infection of MDMs with HIV-1 or HIV-2 isolates. MDMs differentiated for 10 days in DMEM containing 10% PHS were harvested, replated, and infected with the indicated HIV isolates. RT activities (A) and CXCL7 levels (B) of the culture supernatants collected from day 6 to day 36 were assessed at 6-day intervals. Data shown are results from three donors (Mean ± SEM, n = 3). (C) The concentrations of CXCL7 in the supernatants harvested from MDMs infected with the indicated HIV isolates at the peak viral- replication time points were determined by ELISA. The concentrations of CXCL7 in the supernatants of each infection group were normalized to the expression levels of CXCL7 in the supernatants harvested from uninfected MDMs and presented as relative CXCL7 levels. Each symbol represents an individual donor. Data are shown as the mean ± SEM (n = 6–8). The asterisks on the long bar line indicate a significant difference among the five HIV-infection groups (p < 0.0001, n = 6–8), as analyzed using one-way ANOVA. The asterisks on the short bar lines indicate significant differences (***, p < 0.0005, ****, p < 0.0001) between the HIV-infection groups under the bar lines and the HIV-1 Ada control group, as assessed using Dunnett’s test for multiple comparisons.

Journal: International journal of molecular sciences

Article Title: Macrophage-Derived Factors with the Potential to Contribute to the Pathogenicity of HIV-1 and HIV-2: Roles of M-CSF and CXCL7.

doi: 10.3390/ijms26115028

Figure Lengend Snippet: Figure 6. Differential CXCL7 production by MDMs following infection with HIV-1 or HIV-2. (A,B) Time course of virus replication and CXCL7 production following infection of MDMs with HIV-1 or HIV-2 isolates. MDMs differentiated for 10 days in DMEM containing 10% PHS were harvested, replated, and infected with the indicated HIV isolates. RT activities (A) and CXCL7 levels (B) of the culture supernatants collected from day 6 to day 36 were assessed at 6-day intervals. Data shown are results from three donors (Mean ± SEM, n = 3). (C) The concentrations of CXCL7 in the supernatants harvested from MDMs infected with the indicated HIV isolates at the peak viral- replication time points were determined by ELISA. The concentrations of CXCL7 in the supernatants of each infection group were normalized to the expression levels of CXCL7 in the supernatants harvested from uninfected MDMs and presented as relative CXCL7 levels. Each symbol represents an individual donor. Data are shown as the mean ± SEM (n = 6–8). The asterisks on the long bar line indicate a significant difference among the five HIV-infection groups (p < 0.0001, n = 6–8), as analyzed using one-way ANOVA. The asterisks on the short bar lines indicate significant differences (***, p < 0.0005, ****, p < 0.0001) between the HIV-infection groups under the bar lines and the HIV-1 Ada control group, as assessed using Dunnett’s test for multiple comparisons.

Techniques: Infection, Virus, Enzyme-linked Immunosorbent Assay, Expressing, Control

Fig. 1 CXCL7 upregulation in chemotherapy-resistant colorectal cancer. A Differential gene expression proﬁling between chemosensitive and chemoresistant colorectal tumors (TCGA cohort) treated with 5-FU/oxaliplatin combination therapy. B Representative immunohisto- chemical (IHC) staining of CXCL7 in chemotherapy-resistant versus chemotherapy-sensitive CRC specimens (Scale bar, 100 μm). C Gene Set Enrichment Analysis (GSEA) demonstrating cisplatin resistance pathway activation in CXCL7-high versus CXCL7-low expression subgroups. D Comparative histopathological analysis using H&E staining and IHC evaluation of CXCL7/CD68 expression in paired pre- and post- chemotherapy CRC specimens from individual patients (Scale bar, 100 μm). E CXCL7 protein localization by IHC in chemotherapy-treated CRC lesions versus matched adjacent normal mucosa (Scale bar, 100 μm). F Quantitative comparison of CXCL7 expression levels between chemotherapeutically treated malignant tissues and non-neoplastic colorectal tissues. G Stage-dependent IHC expression patterns of CXCL7 across colorectal cancer progression (Scale bar, 100 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 1 CXCL7 upregulation in chemotherapy-resistant colorectal cancer. A Differential gene expression proﬁling between chemosensitive and chemoresistant colorectal tumors (TCGA cohort) treated with 5-FU/oxaliplatin combination therapy. B Representative immunohisto- chemical (IHC) staining of CXCL7 in chemotherapy-resistant versus chemotherapy-sensitive CRC specimens (Scale bar, 100 μm). C Gene Set Enrichment Analysis (GSEA) demonstrating cisplatin resistance pathway activation in CXCL7-high versus CXCL7-low expression subgroups. D Comparative histopathological analysis using H&E staining and IHC evaluation of CXCL7/CD68 expression in paired pre- and post- chemotherapy CRC specimens from individual patients (Scale bar, 100 μm). E CXCL7 protein localization by IHC in chemotherapy-treated CRC lesions versus matched adjacent normal mucosa (Scale bar, 100 μm). F Quantitative comparison of CXCL7 expression levels between chemotherapeutically treated malignant tissues and non-neoplastic colorectal tissues. G Stage-dependent IHC expression patterns of CXCL7 across colorectal cancer progression (Scale bar, 100 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Article Snippet: CT26 murine colorectal cancer cells were subcutaneously injected into BALB/c mice, followed by treatment with anti-CXCL7 antibody (20 μg/mouse, R&D Systems, AF793) or isotype control antibodies, with tumor volume monitoring and subsequent tumor collection for apoptosis assays and IHC analysis.

Techniques: Gene Expression, Immunohistochemistry, Activation Assay, Expressing, Staining, Comparison

Fig. 2 Macrophage-derived CXCL7 promotes chemoresistance in colorectal cancer cells. A CXCL7-associated single-cell analysis of CRC_GSE146771 using the TISCH2 database. B Correlation analysis of CXCL7 with macrophage inﬁltration via TCGA database. C Left: mIHC staining of chemotherapy-sensitive versus resistant CRC tissues showing CK+ (purple), CXCL7+ (white), and CD68+ macrophages (green), with DAPI nuclear staining (blue) (scale bar, 50 μm). Right: CXCL7+ macrophage proportions in chemotherapy-sensitive versus resistant patients. D Schematic of tumor cell-macrophage co-culture system. E CXCL7 mRNA and F CXCL7 protein levels in macrophages co-cultured with HCT116 cells ± 5-FU (5 μM), oxaliplatin (5 μM), or combination. F The expression of CXCL7 in chemotherapy-treated colorectal cancer tissues compared with non-tumor tissues was analyzed. G Representative images and quantiﬁcation for colony formation of CRC cells with CXCL7 + Mø versus CXCL7- Mø under 5-FU/oxaliplatin treatment. H Annexin V/PI apoptosis rates and (I) TUNEL+ cells (green) in CRC cells co-cultured with CXCL7 + Mø versus CXCL7- Mø under chemotherapy (scale bar, 50 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 2 Macrophage-derived CXCL7 promotes chemoresistance in colorectal cancer cells. A CXCL7-associated single-cell analysis of CRC_GSE146771 using the TISCH2 database. B Correlation analysis of CXCL7 with macrophage inﬁltration via TCGA database. C Left: mIHC staining of chemotherapy-sensitive versus resistant CRC tissues showing CK+ (purple), CXCL7+ (white), and CD68+ macrophages (green), with DAPI nuclear staining (blue) (scale bar, 50 μm). Right: CXCL7+ macrophage proportions in chemotherapy-sensitive versus resistant patients. D Schematic of tumor cell-macrophage co-culture system. E CXCL7 mRNA and F CXCL7 protein levels in macrophages co-cultured with HCT116 cells ± 5-FU (5 μM), oxaliplatin (5 μM), or combination. F The expression of CXCL7 in chemotherapy-treated colorectal cancer tissues compared with non-tumor tissues was analyzed. G Representative images and quantiﬁcation for colony formation of CRC cells with CXCL7 + Mø versus CXCL7- Mø under 5-FU/oxaliplatin treatment. H Annexin V/PI apoptosis rates and (I) TUNEL+ cells (green) in CRC cells co-cultured with CXCL7 + Mø versus CXCL7- Mø under chemotherapy (scale bar, 50 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Techniques: Derivative Assay, Single-cell Analysis, Staining, Co-Culture Assay, Cell Culture, Expressing, TUNEL Assay

Fig. 3 CXCL7 Mediates Tumor Chemotherapy Resistance in vivo. A Representative images and body weights of mice injected with CXCL7 + Mø or CXCL7- Mø under 5-FU/oxaliplatin treatment (n = 5 mice per group). B CT26 tumor growth in immunocompetent BALB/c mice treated with control or macrophage depletion (n = 5 mice per group). C CXCL7 expression levels in macrophage-intact versus macrophage- depleted tumors analyzed by RT-qPCR. D IHC staining of CD11b+ cells and CXCL7+ expression in control versus clodronate-treated tumors (scale bar, 50 μm). E CT26 tumor progression in mice treated with isotype control or CXCL7-neutralizing antibodies (n = 5 mice per group). F TUNEL-positive cells and representative IHC images of CXCL7 in the tumors obtained from mice treated with isotype control or CXCL7 neutralizing antibodies (scale bar for TUNEL, 10 μm; scale bar for IHC, 100 μm). G Intestinal polyp quantiﬁcation (number/size) and representative images from AOM/DSS mice treated with control or CXCL7-neutralizing antibodies (scale bar, 100 μm). H HE and IHC detection of CXCL7 expression across different groups of mice, as indicated (scale bar, 100 μm). I TUNEL+ apoptotic cell counts in AOM/DSS mice with/ without CXCL7 antibody treatment. All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 3 CXCL7 Mediates Tumor Chemotherapy Resistance in vivo. A Representative images and body weights of mice injected with CXCL7 + Mø or CXCL7- Mø under 5-FU/oxaliplatin treatment (n = 5 mice per group). B CT26 tumor growth in immunocompetent BALB/c mice treated with control or macrophage depletion (n = 5 mice per group). C CXCL7 expression levels in macrophage-intact versus macrophage- depleted tumors analyzed by RT-qPCR. D IHC staining of CD11b+ cells and CXCL7+ expression in control versus clodronate-treated tumors (scale bar, 50 μm). E CT26 tumor progression in mice treated with isotype control or CXCL7-neutralizing antibodies (n = 5 mice per group). F TUNEL-positive cells and representative IHC images of CXCL7 in the tumors obtained from mice treated with isotype control or CXCL7 neutralizing antibodies (scale bar for TUNEL, 10 μm; scale bar for IHC, 100 μm). G Intestinal polyp quantiﬁcation (number/size) and representative images from AOM/DSS mice treated with control or CXCL7-neutralizing antibodies (scale bar, 100 μm). H HE and IHC detection of CXCL7 expression across different groups of mice, as indicated (scale bar, 100 μm). I TUNEL+ apoptotic cell counts in AOM/DSS mice with/ without CXCL7 antibody treatment. All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Techniques: In Vivo, Injection, Control, Expressing, Quantitative RT-PCR, Immunohistochemistry, TUNEL Assay

Fig. 4 CXCL7 upregulates PHGDH and activates serine metabolism in cancer cells. A Left: GSEA of enriched pathways in differentially expressed genes (DEGs) between HT29-control and HT29-CXCL7 groups. Right: Comparative analysis of PHGDH FPKM values between groups. B The expression level of PHGDH in control and CXCL7-overexpressing cells with or without the CXCR2 inhibitor, as determined by RT-qPCR. C Western blot detection of serine biosynthesis enzymes (PHGDH, PSAT1, PSPH).GAPDH was used as the loading control. D Kaplan‒Meier analysis of overall survival in TCGA-CRC patients stratiﬁed by PHGDH expression. E Left: Metabolite enrichment pathway bubble plot. Middle: Heatmap of differential metabolites. Right: Schematic of serine/one-carbon metabolism. F Heatmap visualization of DEGs in glycine, serine, and threonine metabolism pathways. G ELISA analysis of SAM levels in CXCL7-overexpressing cells and PHGDH-inhibited cells. H TUNEL assays of CXCL7-overexpressing cells transfected with NC-siRNA or PHGDH-siRNA, with or without SAM treatment(scale bar, 50 μm). I The drug sensitivity of CXCL7-overexpressing cells transfected with NC-siRNA or PHGDH-siRNA, with or without SAM treatment. All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 4 CXCL7 upregulates PHGDH and activates serine metabolism in cancer cells. A Left: GSEA of enriched pathways in differentially expressed genes (DEGs) between HT29-control and HT29-CXCL7 groups. Right: Comparative analysis of PHGDH FPKM values between groups. B The expression level of PHGDH in control and CXCL7-overexpressing cells with or without the CXCR2 inhibitor, as determined by RT-qPCR. C Western blot detection of serine biosynthesis enzymes (PHGDH, PSAT1, PSPH).GAPDH was used as the loading control. D Kaplan‒Meier analysis of overall survival in TCGA-CRC patients stratiﬁed by PHGDH expression. E Left: Metabolite enrichment pathway bubble plot. Middle: Heatmap of differential metabolites. Right: Schematic of serine/one-carbon metabolism. F Heatmap visualization of DEGs in glycine, serine, and threonine metabolism pathways. G ELISA analysis of SAM levels in CXCL7-overexpressing cells and PHGDH-inhibited cells. H TUNEL assays of CXCL7-overexpressing cells transfected with NC-siRNA or PHGDH-siRNA, with or without SAM treatment(scale bar, 50 μm). I The drug sensitivity of CXCL7-overexpressing cells transfected with NC-siRNA or PHGDH-siRNA, with or without SAM treatment. All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Techniques: Control, Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, TUNEL Assay, Transfection

Fig. 5 STAT1 mediates CXCL7-induced PHGDH transcription and chemotherapy resistance. A GSEA analysis illustrating the correlation between CXCL7 and the interferon signaling pathway. B Predicted STAT1-binding sequences in the PHGDH promoter region using the JASPAR database. C The correlationship between STAT1 and PHGDH mRNA expression. D ChIP-qPCR results showing STAT1 enrichment at the PHGDH promoter. E Luciferase reporter assay results demonstrating PHGDH promoter activity in response to CXCL7 treatment with or without JAK1 inhibition. F Effects of JAK1 inhibition on PHGDH mRNA expression following CXCL7 treatment. G Western blot analysis of p-JAK1, JAK1, p-STAT1, STAT1, PHGDH, and IRF9 protein levels in cells treated with CXCL7 with or without JAK1 inhibition. H Cell viability assessment for cell treatment with CXCL7, following PHGDH inhibition or JAK1 inhibition. I Effects of PHGDH or JAK1 inhibition on tumor growth in mice with CXCL7-overexpressing cell. J IHC analysis of p-STAT1, PHGDH, and CD206 expression, along with TUNEL staining for apoptosis, in CXCL7-overexpressing tumors treated with PHGDH or JAK1 inhibitor (scale bar for IHC, 50 μm; scale bar for TUNEL, 10 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 5 STAT1 mediates CXCL7-induced PHGDH transcription and chemotherapy resistance. A GSEA analysis illustrating the correlation between CXCL7 and the interferon signaling pathway. B Predicted STAT1-binding sequences in the PHGDH promoter region using the JASPAR database. C The correlationship between STAT1 and PHGDH mRNA expression. D ChIP-qPCR results showing STAT1 enrichment at the PHGDH promoter. E Luciferase reporter assay results demonstrating PHGDH promoter activity in response to CXCL7 treatment with or without JAK1 inhibition. F Effects of JAK1 inhibition on PHGDH mRNA expression following CXCL7 treatment. G Western blot analysis of p-JAK1, JAK1, p-STAT1, STAT1, PHGDH, and IRF9 protein levels in cells treated with CXCL7 with or without JAK1 inhibition. H Cell viability assessment for cell treatment with CXCL7, following PHGDH inhibition or JAK1 inhibition. I Effects of PHGDH or JAK1 inhibition on tumor growth in mice with CXCL7-overexpressing cell. J IHC analysis of p-STAT1, PHGDH, and CD206 expression, along with TUNEL staining for apoptosis, in CXCL7-overexpressing tumors treated with PHGDH or JAK1 inhibitor (scale bar for IHC, 50 μm; scale bar for TUNEL, 10 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not signiﬁcant.

Techniques: Binding Assay, Expressing, ChIP-qPCR, Luciferase, Reporter Assay, Activity Assay, Inhibition, Western Blot, Paraffin-embedded Immunohistochemistry, TUNEL Assay, Staining

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