human cxcl12 recombinant protein  (MedChemExpress)

Journal: Cell Death Discovery

Article Title: CXCL12 alone is enough to Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts

doi: 10.1038/s41420-025-02420-0

Figure Lengend Snippet: A Schematic diagram showing the generation of NFs treated with CAFs-CM. B Phase-contrast microscopy revealed the typical spindle-like features of fibroblasts in CAFs and NFs isolated from lung cancer tissues, Scale bar = 100 μm. C Western blot analysis showed the expression of the fibroblast markers (FAP and Vimentin), the epithelial markers (CK-19) and the endothelial marker (CD31) in CAFs and NFs. D The impact of NFs and CAFs on the migratory capabilities of H1299 and A549 was assessed using transwell assay. The results include representative images of cell migration counts (left) and statistical data (right). Data are presented as the mean ± SD of three biological replicates.*, p < 0.05; ** , p < 0.005. Scale bar = 200 μm. E Western blot analysis showed the expression of CXCL12, CXCR4, pSTAT3/STAT3, Vimentin, and α-SMA in NFs treated with DMEM or CAFs CM.

Article Snippet: Recombinant human CXCL12 protein was purchased from Sino Biological (Beijing, China).

Techniques: Microscopy, Isolation, Western Blot, Expressing, Marker, Transwell Assay, Migration

Journal: Cell Death Discovery

Article Title: CXCL12 alone is enough to Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts

doi: 10.1038/s41420-025-02420-0

Figure Lengend Snippet: A . Western blot analysis of the expression of CXCL12, p-STAT3/STAT3, Vimentin, and α-SMA in p53S-CAFs treated with DMEM and NFs treated with DMEM, p53 -/- fibroblast CM, and p53S-CAFs CM. B Immunofluorescence analysis of the expression of Vimentin and α-SMA in NFs treated with DMEM, p53 -/- fibroblast CM, and p53S-CAFs CM. C Calculation of the percentage of cells that incorporated EdU or the number of migration cells for Transwell migration assay in NFs alone and treated with p53S-CAFs-CM. *, p < 0.05. **, p < 0.005. D Transwell migration assay of lung cancer cells H1299 and A549 cultured with NFs CM or CEFs CM. Average migration ±SEM from three independent experiments performed( n = 3). **, p < 0.005. ***, p < 0.001.

Article Snippet: Recombinant human CXCL12 protein was purchased from Sino Biological (Beijing, China).

Techniques: Western Blot, Expressing, Immunofluorescence, Migration, Transwell Migration Assay, Cell Culture

Journal: Cell Death Discovery

Article Title: CXCL12 alone is enough to Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts

doi: 10.1038/s41420-025-02420-0

Figure Lengend Snippet: A Western blot analysis of the expression of CXCL12 in NFs and CAFs. B Correlation of CXCL12 expression with CAFs markers α-SMA and Vimentin ( P < 0.001, R > 0).

Article Snippet: Recombinant human CXCL12 protein was purchased from Sino Biological (Beijing, China).

Techniques: Western Blot, Expressing

Journal: Cell Death Discovery

Article Title: CXCL12 alone is enough to Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts

doi: 10.1038/s41420-025-02420-0

Figure Lengend Snippet: A Western blotting analysis was conducted on NFs that were either untreated or treated with CXCL12, p53S-CAFs-CM, or a combination of p53S-CAFs-CM and AMD3100. B EdU incorporation assay of NFs treated with DMEM, CXCL12, CXCL12 and AMD3100, p53S-CAFs CM, p53S-CAFs CM and AMD3100. Representative images (left) and statistics (right) of the percentage of cells that incorporated EdU were shown. **, p < 0.005. C Transwell assay of NFs treated with DMEM, CXCL12, CXCL12 and AMD3100, p53S-CAFs CM, p53S-CAFs CM and AMD3100. Representative images (left) and statistics (right) of migration assay were shown. **, p < 0.005. ***, p < 0.001. D Transwell co-culture assay was employed to evaluate the pro-migratory capacity of normal fibroblasts, CEFs-12 (normal fibroblasts treated with CXCL12), CEFs (normal fibroblasts treated with p53S-CAFs conditioned medium), and CEFs+AMD3100 towards lung cancer cells H1299 and A549. The results include representative images of cell migration (left) and statistical data (right). **, p < 0.005, ***, p < 0.0005. Scale bar = 200 μm. E The flowchart for the experimental design of xenograft tumor models. F Representative images show the xenograft tumors in the backs of nude mice formed by mixed subcutaneous injection of CEFs-12 (or NFs) and A549 cells. G Tumor growth graphs indicated the tumor volumes at different time course ( n = 3 or 4 mice per group). ** p < 0.01. H Precise weighing of the tumors was performed upon dissection, ** p < 0.01.

Article Snippet: Recombinant human CXCL12 protein was purchased from Sino Biological (Beijing, China).

Techniques: Western Blot, Transwell Assay, Migration, Co-culture Assay, Injection, Dissection

Journal: Cell Death Discovery

Article Title: CXCL12 alone is enough to Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts

doi: 10.1038/s41420-025-02420-0

Figure Lengend Snippet: A p53S-CAFs-derived CXCL12 activated STAT3 pathway. NFs were treated with CXCL12 (20 ng/ml, 24 hours). The protein levels of CXCL12, CXCR4, IL6, p-JAK2, JAK2, p-STAT3, STAT3, SHP2, α-SMA, vimentin, p-ERK, ERK, p-AKT and AKT were detected by Western blot. B Western blot analysis of CXCL12, p-STAT3, STAT3, α-SMA and Vimentin from NFs alone and treated with CXCL12, or CXCL12 and Stattic. C Proliferative ability of NFs treated with CXCL12, CXCL12 and Stattic (upper), or p53S-CAFs CM, p53S-CAFs CM and Stattic(down) were measured by EdU incorporation assay. **, p < 0.005. D Migratory ability of NFs treated with CXCL12, CXCL12 and Stattic (upper), or p53S-CAFs CM, p53S-CAFs CM and Stattic(down) were measured by transwell migration assay. **, p < 0.005. ***, p < 0.001. Scale bar = 200 μm. E NFs were treated with CXCL12 and then transfected with STAT3 siRNA or control siRNA. STAT3 and p-STAT3 expression was measured by Western blot. *, p < 0.05. **, p < 0.005. F Proliferative and Migratory ability were measured by EdU incorporation assay and transwell assay. **, p < 0.005. ***, p < 0.001. G CEFs (NFs were treated with CXCL12) were transfected with STAT3 siRNA or control siRNA. Transwell assays detected the migration ability of H1299 and A549 co-cultured with CEFs or CEFs-SiSTAT3. **, p < 0.005. ***, p < 0.001. Scale bar = 200 μm.

Article Snippet: Recombinant human CXCL12 protein was purchased from Sino Biological (Beijing, China).

Techniques: Derivative Assay, Western Blot, Transwell Migration Assay, Transfection, Control, Expressing, Transwell Assay, Migration, Cell Culture

Journal: Cell Death Discovery

Article Title: CXCL12 alone is enough to Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts

doi: 10.1038/s41420-025-02420-0

Figure Lengend Snippet: A Western blot analysis of the knockdown efficiency following the transfection of CXCL12 siRNA into p53S-CAFs. B Western blot assessment of the impact on the expression of CAFs marker proteins in normal fibroblasts by conditioned medium after CXCL12 knockdown in p53S-CAFs. C Immunofluorescence analysis was conducted on the expression of CAFs markers α-SMA and Vimentin in p53 +/+ fibroblasts treated with either p53S-CAFs+NC CM or p53S-CAFs+siCXCL12 CM, in addition to the percentage of EdU-incorporated positive population. * p < 0.05, ** p < 0.005. D The impact of CEFs and CEFs+siCXCL12 on the migratory capabilities of H1299 and A549 was assessed using transwell assay. The results include representative images of cell migration counts (left) and statistical data (right). * p < 0.05; ** p < 0.005. Scale bar = 200 μm.

Article Snippet: Recombinant human CXCL12 protein was purchased from Sino Biological (Beijing, China).

Techniques: Western Blot, Knockdown, Transfection, Expressing, Marker, Immunofluorescence, Transwell Assay, Migration

Journal: bioRxiv

Article Title: IgE-producing cells on the move: CCR2 is a key regulator of IgE + plasma cell migration

doi: 10.64898/2025.12.18.695109

Figure Lengend Snippet: (A) Switched tonsil B cells were stained for surface CXCR4 followed by intracellular for IgE and IgG1. The histogram shows CXCR4 expression on IgE + (red) and IgG1 + (blue) gated cells. The filled grey histogram represents the isotype control staining. The accompanying graph shows CXCR4 median fluorescence intensity (MFI) on the surface of IgE + and IgG1 + cells. (B) CXCL12 induced migration of IgE + and IgG1 + cells was assessed using the transwell assay. After 3h of migration, the number of migrating cells was quantified by flow cytometry. Migration of IgE + and IgG1 + cells in response to 300 ng/mL (30nM) of CXCL12 is shown as a percentage of the cells migrating in response to RPMI control. (C) Flow cytometry dot plots of the IgE + and IgG1 + gated GC-like B cells, a PC-like “plasmablast” and PCs. Representative histograms show the CXCR4 expression on each of these gated IgE + and IgG1 + cells. (D) Bar chart showing the CXCR4 expression (MFI) across different IgE + and IgG1 + cell populations. (E) Flow cytometry staining of IgE + and IgG1 + GC-like B cells, PC-like PBs and PC after 3h of migration to the bottom chamber of the transwell. (F) CXCL12 induced migration shown as a percentage of the cells migrating in response to RPMI control. Data are mean + s.d. Statistical analysis was performed using one-way ANOVA with Tukey’s multiple comparison test (D, F) or paired two-tailed t -test with Welch’s correction (A, B); *p< 0.05; **p< 0.01; ***p< 0.001; and ****p< 0.0001. Non-significant values are not shown.

Article Snippet: More specifically, we tested the migration of IgE + and IgG1 + cells in response to recombinant human CXCL12 (R&D systems; 300ng/mL), CCL2 (Biolegend; 10ng/mL, 100ng/mL and 300ng/mL) and CCL28 (R&D systems; 300ng/mL and 1.5ug/mL).

Techniques: Staining, Expressing, Control, Fluorescence, Migration, Transwell Assay, Flow Cytometry, Comparison, Two Tailed Test

Journal: Frontiers in Immunology

Article Title: The tropomyosin 3.1/3.2 inhibitor ATM-3507 alters B-cell actin dynamics and impairs the growth and motility of diffuse large B-cell lymphoma cell lines

doi: 10.3389/fimmu.2025.1668379

Figure Lengend Snippet: ATM-3507 inhibits the migration of DLBCL cells toward CXCL12. (A, B) NU-DUL-1 or Toledo cells were pre-treated with ATM-3507 or 0.03% DMSO (equivalent to the highest ATM-3507 concentration) for 1 h before being added to the upper chamber of a Transwell. The lower chamber contained 100 nM CXCL12 plus the same concentration of ATM-3507 or DMSO as in the upper chamber. After 4 h, the number of cells that had migrated into the lower chamber was determined using flow cytometry. The data are expressed as a percent of the number of DMSO-treated cells that migrated into the bottom chamber. The 100% values (percent of DMSO-treated cells that migrated into the lower chamber) in individual experiments ranged from 15-30% for NU-DUL-1 cells and from 50-70% for Toledo cells. Each symbol is an independent experiment. Means ± SEM are shown for 3 independent experiments. (C) NU-DUL-1 or Toledo cells were treated with 3 µM ATM-3507 or 0.03% DMSO for 1 h or 5 h before quantifying cell surface levels of CXCR4 by flow cytometry. Means ± SEM are shown for 3 independent experiments. p-values were calculated using two-tailed paired t -tests.

Article Snippet: Imaging medium (600 μL) with the same concentration of ATM-3507 or DMSO plus 100 nM recombinant human CXCL12 (R&D Systems, Minneapolis, MN, USA #460-SD) was added to the bottom chamber.

Techniques: Migration, Concentration Assay, Flow Cytometry, Two Tailed Test

Journal: Frontiers in Immunology

Article Title: The tropomyosin 3.1/3.2 inhibitor ATM-3507 alters B-cell actin dynamics and impairs the growth and motility of diffuse large B-cell lymphoma cell lines

doi: 10.3389/fimmu.2025.1668379

Figure Lengend Snippet: ATM-3507 inhibits the 2D motility of DLBCL cells on FN. Toledo DLBCL cells were added to FN-coated coverslips in the presence of 100 nM CXCL12 and either 10 µM ATM-3507 or 0.1% DMSO. After a 1 h pre-treatment period, time-lapse images were acquired every 30 s for 1 h. Cell tracks were generated from the time-lapse videos. Representative videos of DMSO-treated cells ( Supplementary Video 1 ) and ATM-3507-treated cells ( Supplementary Video 2 ) are in the Supplementary Material . (A) Individual cell tracks from a representative experiment. In each experiment, 40–100 cell tracks were analyzed per condition. (B) Compiled data from 3 independent experiments. Each symbol represents the median value from an individual experiment. Means ± SEM are shown. p-values were calculated using two-tailed paired t -tests.

Article Snippet: Imaging medium (600 μL) with the same concentration of ATM-3507 or DMSO plus 100 nM recombinant human CXCL12 (R&D Systems, Minneapolis, MN, USA #460-SD) was added to the bottom chamber.

Techniques: Generated, Two Tailed Test

Journal: Frontiers in Immunology

Article Title: The tropomyosin 3.1/3.2 inhibitor ATM-3507 alters B-cell actin dynamics and impairs the growth and motility of diffuse large B-cell lymphoma cell lines

doi: 10.3389/fimmu.2025.1668379

Figure Lengend Snippet: Tpm3.1/3.2 regulates actin organization and actin-dependent processes in B cells. Tpm3.1/3.2 dimers associate with actin filaments, form homopolymers along the filament, stabilize the actin filament, and recruit myosin II. Myosin II dimers can crosslink actin filaments and mediate actomyosin contractility. Inhibition of Tpm3.1/3.2 by ATM-3507 impairs multiple actin-dependent processes in B cells, including the assembly of a peripheral actin ring that drives BCR-induced cell spreading via the formation of protrusive lamellipodia, and the formation of actomyosin arcs (indicated by the yellow arrow) at the inner face of the peripheral actin ring. ATM-3507 also inhibits the growth of DLBCL cells as well as their CXCL12-dependent migration and motility. Created with BioRender.com.

Article Snippet: Imaging medium (600 μL) with the same concentration of ATM-3507 or DMSO plus 100 nM recombinant human CXCL12 (R&D Systems, Minneapolis, MN, USA #460-SD) was added to the bottom chamber.

Techniques: Inhibition, Migration

Journal: Scientific reports

Article Title: GliaTrap is a biodegradable, non-swelling and non-inflammatory hydrogel with tuned release of CXCL12 to attract migrating glioblastoma cells.

doi: 10.1038/s41598-025-02977-x

Figure Lengend Snippet: Fig. 2. CXCL12 induces GSC chemotaxis in a biomimetic device. (A) Design of the negative mold for the biomimetic device and development of the PDMS device. (B) Time-lapse images between T = 0 and T = 42 h for dextran release from our hyaluronic acid/collagen II-based (HA/Col) hydrogel in the device using Zen 2.5D visualization software (Zeiss). (C) Time-lapse images of GSC migration in the device in the presence or absence of GliaTrap + CXCL12. Images were acquired each day for 4 consecutive days. GSC spheroids were embedded in the middle chamber of the device in Collagen I. (D) Coordinates of each migrating GSC in control or GliaTrap devices at day 4 were plotted using R. (E) Quantification of the ratio of migrating GSCs between the left and right side of the middle line of each GSC spheroid. GliaTrap induces significant increase in the number of GSCs migrating towards the GliaTrap containing chamber of the device (*p < 0.05, Student’s t-test). (F) Coordinate single cell migration data were used to calculate the polar coordinates and degrees from the origin and visualized as a rose plot using the R package ggplot2.

Article Snippet: Preparation and characteristics of HA/Col II hydrogel CXCL12-loaded liposomes were formed by mixing Lipofectamine 2000 (Thermo Fisher) and carrier-free human CXCL12 protein (R&D systems) at 1:1 molar ratio and the mixture was incubated at room temperature for 2 h. The particle size, size distribution (polydispersity index, PDI), and surface charge of liposomes were characterized using Zetasizer Nano ZS90 (Malvern Instruments Ltd., Malvern, UK).

Techniques: Chemotaxis Assay, Software, Migration, Control

Journal: Scientific reports

Article Title: GliaTrap is a biodegradable, non-swelling and non-inflammatory hydrogel with tuned release of CXCL12 to attract migrating glioblastoma cells.

doi: 10.1038/s41598-025-02977-x

Figure Lengend Snippet: Fig. 4. GliaTrap does not induce inflammatory infiltration in vivo. Mouse brain coronal Sect. (4 μm thickness) at the level of injection site across three experimental groups: subhippocampal needle stick only (A–E), injection of hydrogel vehicle only (F–J), and injection of hydrogel containing CXCL12 (GliaTrap) (K–O). Representative images are shown, chosen from among n = 3 mice in each experimental group. From left to right, slices were prepared with H&E staining; F4/80 mAb 1:250 to identify macrophages; CD4 mAb 1:100 to identify CD4 + T-Cells; CD8a mAb 1:400 to identify CD8 + T-Cells; and Granzyme B mAb 1:100 to identify activated T cells and natural killer cells. All antibodies and concentrations were the same as for spleen positive control staining from the injection-only mice, as shown in (Supplementary Fig. 3). Antibody positivity was observed in F4/80 in all three groups adjacent to the injection site (purple arrows), but not in slices prepared using the other three antibodies. Images were captured using an Axio Observer Z1/7 microscope, Axiocam 705 1X Camera Adapter, and EC Plan-Neuofluar 10X / 0.30 M27 Objective.

Article Snippet: Preparation and characteristics of HA/Col II hydrogel CXCL12-loaded liposomes were formed by mixing Lipofectamine 2000 (Thermo Fisher) and carrier-free human CXCL12 protein (R&D systems) at 1:1 molar ratio and the mixture was incubated at room temperature for 2 h. The particle size, size distribution (polydispersity index, PDI), and surface charge of liposomes were characterized using Zetasizer Nano ZS90 (Malvern Instruments Ltd., Malvern, UK).

Techniques: In Vivo, Injection, Staining, Positive Control, Microscopy

Journal: Cell

Article Title: Inflammation switches the chemoattractant requirements for naive lymphocyte entry into lymph nodes

doi: 10.1016/j.cell.2024.11.031

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Human CXCL12 (SDF-1a) Recombinant Protein , PeproTech , Cat# 300–28A.

Techniques: Control, Virus, Recombinant, Adjuvant, Reverse Transcription, RNAscope, SYBR Green Assay, Plasmid Preparation, Software

Journal: iScience

Article Title: Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells

doi: 10.1016/j.isci.2024.111269

Figure Lengend Snippet: iCAFs enhanced lung cancer cell migration and invasion via CXCL12 (A) mRNA levels of CXCL12 in fibroblasts were detected by qPCR. (B) The secreted CXCL12 by cells were examined by ELISA assay. (C) Lung cancer cells were treated with CXCL12. Cell proliferation was examined by CCK-8 kit after 48 h. (D and E) Lung cancer cells were treated with CXCL12. Cell migration was detected by wound healing assay after 24 h. (F and G) Lung cancer cells were treated with CXCL12. Cell invasion was detected by trans-well assay after 24 h (scale bar, 100 μm). (H and I) Lung cancer cells were treated with CXCL12, CM, or CM + CXCX12 neutralizing antibody. Cell migration was detected by wound healing assay after 24 h. (J and K) Lung cancer cells were treated with CXCL12, CM, or CM + CXCX12 neutralizing antibody. Cell invasion was detected by trans-well assay after 24 h (scale bar, 100 μm). (L) Lung cancer cells were treated with CM. The expressions of CXCR4 were detected by western blotting. Ab, neutralizing antibody. Data represents the mean ± SD from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 .

Article Snippet: Recombinant human CXCL12 , Sino Biological , Cat#10118-H01H.

Techniques: Migration, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Wound Healing Assay, Western Blot

Journal: iScience

Article Title: Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells

doi: 10.1016/j.isci.2024.111269

Figure Lengend Snippet: CXCL12 mediated the activation of AKT/NF-κB pathway (A) Lung cancer cells were treated with CM. Gene expressions were detected by western blotting. (B) Lung cancer cells were treated with CM, CXCL12, or CM + CXCX12 neutralizing antibody. Gene expressions were detected by western blotting. (C and D) Lung cancer cells were treated with CM. Gene expressions were detected by western blotting. (E) Lung cancer cells were pretreated with AKT inhibitor perifosine (10 μM) or NF-κB inhibitor JSH23 (10 μM) for 1 h and then treated with CM. Gene expressions were detected by western blotting. (F and G) Lung cancer cells were pretreated with AKT inhibitor perifosine (10 μM) or NF-κB inhibitor JSH23 (10 μM) for 1 h and then treated with CM. Cell migration was detected by wound healing assay after 24 h. (H and I) Lung cancer cells were pretreated with AKT inhibitor perifosine (10 μM) or NF-κB inhibitor JSH23 (10 μM) for 1 h and then treated with CM. Cell invasion was detected by trans-well assay after 24 h (scale bar, 100 μm). Ab, neutralizing antibody. Data represent the mean ± SD from three independent experiments. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 .

Article Snippet: Recombinant human CXCL12 , Sino Biological , Cat#10118-H01H.

Techniques: Activation Assay, Western Blot, Migration, Wound Healing Assay

Journal: iScience

Article Title: Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells

doi: 10.1016/j.isci.2024.111269

Figure Lengend Snippet:

Article Snippet: Recombinant human CXCL12 , Sino Biological , Cat#10118-H01H.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay

Journal: iScience

Article Title: Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells

doi: 10.1016/j.isci.2024.111269

Figure Lengend Snippet: PCR primer sequences

Article Snippet: Recombinant human CXCL12 , Sino Biological , Cat#10118-H01H.

Techniques: