Journal: Journal of Cancer

Article Title: Elevated CXCL12 in the plasma membrane of locally advanced rectal cancer after neoadjuvant chemoradiotherapy: a potential prognostic marker

doi: 10.7150/jca.64082

Figure Lengend Snippet: Changes in CXCL12, CXCR4, and FAPα expression after neoadjuvant chemoradiotherapy (nCRT) in LARC patients. (A) and (B) Boxplot of CXCL12, CXCR4, and FAPα expression in tumor and irradiated tumor tissues (using dataset GSE15781 and GSE94104). (C) Boxplot of CXCL12, CXCR4, and FAPα expression in normal and irradiated normal adjacent tissues (using dataset GSE15781). * p < 0.05, ** p < 0.01, ns: not significant. Mann-Whitney U test (A, B, and C).

Article Snippet: The tissue sections were incubated at 37 °C for 30 min with the mouse monoclonal anti-human CXCL12 (1:300, catalog #MA5-23759, Invitrogen, Rockford, IL, USA), the rabbit monoclonal anti-human CXCR4 (1:100, catalog #ab124824, Abcam, Cambridge, UK), and the rabbit polyclonal anti-human FAPα (1:20, catalog #AHP1322, BIO-RAD, Hercules, CA, USA).

Techniques: Expressing, Irradiation, MANN-WHITNEY

Journal: Journal of Cancer

Article Title: Elevated CXCL12 in the plasma membrane of locally advanced rectal cancer after neoadjuvant chemoradiotherapy: a potential prognostic marker

doi: 10.7150/jca.64082

Figure Lengend Snippet: Correlation of CXC chemokine ligand 12 (CXCL12), CXC chemokine type 4 (CXCR4), and fibroblast activation protein-α (FAPα) expression with clinicopathological factors in 121 patients with locally advanced rectal cancer.

Article Snippet: The tissue sections were incubated at 37 °C for 30 min with the mouse monoclonal anti-human CXCL12 (1:300, catalog #MA5-23759, Invitrogen, Rockford, IL, USA), the rabbit monoclonal anti-human CXCR4 (1:100, catalog #ab124824, Abcam, Cambridge, UK), and the rabbit polyclonal anti-human FAPα (1:20, catalog #AHP1322, BIO-RAD, Hercules, CA, USA).

Techniques: Activation Assay, Expressing

Journal: Journal of Cancer

Article Title: Elevated CXCL12 in the plasma membrane of locally advanced rectal cancer after neoadjuvant chemoradiotherapy: a potential prognostic marker

doi: 10.7150/jca.64082

Figure Lengend Snippet: Images showing immunohistochemical staining of CXCL12, CXCR4, and FAPα in the case of each pathways in locally advanced rectal cancer (LARC) after neoadjuvant chemoradiotherapy (LARC-nCRT) (A,C,E) and LARC with no nCRT (LARC-no nCRT) (B,D,E). In the case of LARC-nCRT, the expression of CXCL12, CXCR4, and FAPα is higher than in the case of LARC-no nCRT (original magnification 400× ; scale bar= 50 µm).

Article Snippet: The tissue sections were incubated at 37 °C for 30 min with the mouse monoclonal anti-human CXCL12 (1:300, catalog #MA5-23759, Invitrogen, Rockford, IL, USA), the rabbit monoclonal anti-human CXCR4 (1:100, catalog #ab124824, Abcam, Cambridge, UK), and the rabbit polyclonal anti-human FAPα (1:20, catalog #AHP1322, BIO-RAD, Hercules, CA, USA).

Techniques: Immunohistochemical staining, Staining, Expressing

Journal: Journal of Cancer

Article Title: Elevated CXCL12 in the plasma membrane of locally advanced rectal cancer after neoadjuvant chemoradiotherapy: a potential prognostic marker

doi: 10.7150/jca.64082

Figure Lengend Snippet: Comparison of the levels of CXCL12, CXCR4, and FAPα by immunohistochemical staining among pathways in locally advanced rectal cancer (LARC) after neoadjuvant chemoradiotherapy (nCRT) (LARC-nCRT) (n = 61), LARC untreated with nCRT (LARC-no nCRT) (n = 60) and high-grade dysplasia of colorectal adenoma (HD) (n = 16). The levels of the three proteins were higher in LARC-nCRT than in LARC-no nCRT or HD (p < 0.001 for each). (A) CXCL12 positivity: 62.3%, 38/61 LARC-nCRT cases; 5.0%, 3/60 LARC-no nCRT cases; and 0.0%, 0/16 HD cases. (B) CXCR4 positivity: 47.5%, 29/61 LARC-nCRT cases; 0.0%, 0/60 LARC-no nCRT cases; and 0.0%, 0/16 HD cases. (C) FAPα positivity: 62.3%, 38/61 LARC-nCRT cases; 25.0%, 15/60 LARC-no nCRT cases; and 0.0%, 0/16 HD cases.

Article Snippet: The tissue sections were incubated at 37 °C for 30 min with the mouse monoclonal anti-human CXCL12 (1:300, catalog #MA5-23759, Invitrogen, Rockford, IL, USA), the rabbit monoclonal anti-human CXCR4 (1:100, catalog #ab124824, Abcam, Cambridge, UK), and the rabbit polyclonal anti-human FAPα (1:20, catalog #AHP1322, BIO-RAD, Hercules, CA, USA).

Techniques: Comparison, Immunohistochemical staining, Staining

Journal: Journal of Cancer

Article Title: Elevated CXCL12 in the plasma membrane of locally advanced rectal cancer after neoadjuvant chemoradiotherapy: a potential prognostic marker

doi: 10.7150/jca.64082

Figure Lengend Snippet: Univariate analysis of overall survival and freedom from recurrence in 61 cases of locally advanced rectal cancer with neoadjuvant chemoradiotherapy.

Article Snippet: The tissue sections were incubated at 37 °C for 30 min with the mouse monoclonal anti-human CXCL12 (1:300, catalog #MA5-23759, Invitrogen, Rockford, IL, USA), the rabbit monoclonal anti-human CXCR4 (1:100, catalog #ab124824, Abcam, Cambridge, UK), and the rabbit polyclonal anti-human FAPα (1:20, catalog #AHP1322, BIO-RAD, Hercules, CA, USA).

Techniques: Expressing

Journal: Journal of Cancer

Article Title: Elevated CXCL12 in the plasma membrane of locally advanced rectal cancer after neoadjuvant chemoradiotherapy: a potential prognostic marker

doi: 10.7150/jca.64082

Figure Lengend Snippet: Multivariate analysis of overall survival and Freedom from recurrence in 61 cases of locally advanced rectal cancer with neoadjuvant chemoradiotherapy.

Article Snippet: The tissue sections were incubated at 37 °C for 30 min with the mouse monoclonal anti-human CXCL12 (1:300, catalog #MA5-23759, Invitrogen, Rockford, IL, USA), the rabbit monoclonal anti-human CXCR4 (1:100, catalog #ab124824, Abcam, Cambridge, UK), and the rabbit polyclonal anti-human FAPα (1:20, catalog #AHP1322, BIO-RAD, Hercules, CA, USA).

Techniques: Expressing

Journal: Journal of Cancer

Article Title: Elevated CXCL12 in the plasma membrane of locally advanced rectal cancer after neoadjuvant chemoradiotherapy: a potential prognostic marker

doi: 10.7150/jca.64082

Figure Lengend Snippet: Kaplan-Meier survival curves-estermates of freedom from recurrence of colorectal cancer in 61 cases of locally advanced rectal cancer (LARC) with neoadjuvant chemoradiotherapy according to plasma membrane expressions of CXCL12, CXCR4 and FAPα in tumor cells. (A) CXCL12, (B) CXCR4, and (C) FAPα.

Article Snippet: The tissue sections were incubated at 37 °C for 30 min with the mouse monoclonal anti-human CXCL12 (1:300, catalog #MA5-23759, Invitrogen, Rockford, IL, USA), the rabbit monoclonal anti-human CXCR4 (1:100, catalog #ab124824, Abcam, Cambridge, UK), and the rabbit polyclonal anti-human FAPα (1:20, catalog #AHP1322, BIO-RAD, Hercules, CA, USA).

Techniques: Clinical Proteomics, Membrane

Journal: Viruses

Article Title: A Renaissance for Oncolytic Adenoviruses?

doi: 10.3390/v15020358

Figure Lengend Snippet: Adenoviral vectors currently in clinical trials for cancer therapy. Replication defective viruses that are used for gene delivery only are shaded in grey.

Article Snippet: NG-641 , Ad11/Ad3 chimera , untouched (Ad11) , Ad11 , secreted Interferon alpha, the chemokines CXCL9, CXCL10 and an anti-FAP/anti-CD3 bispecific T-cell activator , near complete deletion , , PsiOxus Therapeutics.

Techniques: Modification, Plasmid Preparation, Mutagenesis

Journal: The FASEB Journal

Article Title: FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6

doi: 10.1096/fj.202501823R

Figure Lengend Snippet: ELOVL6 inhibits VSMC de‐differentiation through M2 macrophages and directly in HASMCs. (A) Schematic protocol for preparing macrophage CM following ELOVL6 transfection. M0 macrophages were infected with adenovirus (Ad‐NC or Ad‐ELOVL6) or transfected with siRNA (siRNA‐NC or siRNA‐ELOVL6) and then induced to polarize into M2 macrophages. The resulting supernatant was added to HASMCs. (B) Representative images and quantitative analysis of the EdU assay show the effect on HASMC proliferation cultured in CM ( n = 5). Scale bar = 75 μm. (C) Representative images and quantitative analysis of the scratch assay showing the effect on the migration of HASMCs cultured in CM ( n = 5). Images were taken at 0 and 24 h post‐scratch (enhanced edge image). Scale bar = 200 μm. (D) Representative western blot and quantitative analysis of VSMC contractile marker (CNN1 and TAGLN) protein expression in HASMCs cultured in CM ( n = 3). β‐Tubulin was used as a loading control. (E) Schematic protocol for the HASMC culture assay following ELOVL6 transfection. HASMCs were infected with adenovirus (Ad‐NC or Ad‐ELOVL6) and transfected with siRNA (siRNA‐NC or siRNA‐ELOVL6), then incubated with PDGF‐BB to induce de‐differentiation. (F) Representative images and quantification of HASMCs assessed by the EdU assay ( n = 5). Scale bar = 75 μm. (G) Representative images and quantification of HASMCs assessed by the scratch assay ( n = 5). Images were taken at 0 and 24 h post‐scratch (enhanced edge image). Scale bar = 200 μm. (H) Representative western blot and quantitative analysis of VSMC contractile marker (CNN1 and TAGLN) protein expression in HASMCs ( n = 3). β‐Tubulin was used as a loading control. Data represent the mean ± SEM from n independent experiments. Independent measures one‐way ANOVA with Bonferroni's correction or Kruskal‐Wallis nonparametric test for multiple comparisons. *p < 0.05, **p < 0.01, ****p < 0.0001. HASMC, human aortic smooth muscle cell; CM, conditioned media; EdU, 5‐ethynyl‐2′‐deoxyuridine; CNN1, calponin 1, basic; TAGLN, transgelin; DAPI, 4′,6‐diamidino‐2‐phenylindole; NC, normal control; Ad, adenovirus; siRNA, small interfering RNA.

Article Snippet: FPR2 was knocked down by siRNA (Vigene Bioscience, Jinan, China) in both M2 macrophages and HASMCs, along with negative controls (siRNA‐NC).

Techniques: Transfection, Infection, EdU Assay, Cell Culture, Wound Healing Assay, Migration, Western Blot, Marker, Expressing, Control, Incubation, Small Interfering RNA

Journal: The FASEB Journal

Article Title: FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6

doi: 10.1096/fj.202501823R

Figure Lengend Snippet: BMS‐986235 attenuates VSMC de‐differentiation through the FPR2/ELOVL6 axis in macrophages. (A) Representative images and quantification of EdU‐positive cells in HASMCs treated with siRNA‐NC + Vehicle/BMS‐986235‐CM and siRNA‐FPR2 + Vehicle/BMS‐986235‐CM ( n = 5). Scale bar = 75 μm. (B) Representative images and quantitative analysis of the scratch assay in HASMCs treated with siRNA‐NC + Vehicle/BMS‐986235‐CM and siRNA‐FPR2 + Vehicle/BMS‐986235‐CM ( n = 5). Images were captured at 0 and 24 h post‐scratch (enhanced edge image). Scale bar = 200 μm. (C) Representative western blot and quantitative analysis of ELOVL6 expression and VSMC contractile markers (CNN1 and TAGLN) in HASMCs treated with siRNA‐NC + Vehicle/BMS‐986235‐CM or siRNA‐FPR2 + Vehicle/BMS 986235‐CM ( n = 3). β‐Tubulin served as a loading control. Data represent the mean ± SEM from n independent experiments. Independent measures one‐way ANOVA with Bonferroni's correction or Kruskal‐Wallis nonparametric test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. HASMC, human aortic smooth muscle cell; CM, conditioned media; EdU, 5‐ethynyl‐2′‐deoxyuridine; CNN1, calponin 1, basic; TAGLN, transgelin; DAPI, 4′,6‐diamidino‐2‐phenylindole; NC, normal control; Ad, adenovirus; siRNA, small interfering RNA.

Article Snippet: FPR2 was knocked down by siRNA (Vigene Bioscience, Jinan, China) in both M2 macrophages and HASMCs, along with negative controls (siRNA‐NC).

Techniques: Wound Healing Assay, Western Blot, Expressing, Control, Small Interfering RNA

Journal: The FASEB Journal

Article Title: FPR2 Agonism Attenuates Restenosis by Mitigating Neointimal Hyperplasia via ELOVL6

doi: 10.1096/fj.202501823R

Figure Lengend Snippet: BMS‐986235 suppresses VSMC de‐differentiation by directly targeting the FPR2/ELOVL6 signaling axis in HASMCs. (A) Representative images and quantitative analysis of the EdU assay in HASMCs treated with BMS‐986235 after transfection with siRNA‐FPR2 or siRNA‐NC ( n = 5). Scale bar = 75 μm. (B) Representative images and quantitative analysis of scratch assay in HASMCs treated with BMS‐986235 following transfection with siRNA‐FPR2 or siRNA‐NC ( n = 5). Images were captured at 0 and 24 h post‐scratch (enhanced edge image). Scale bar = 200 μm. (C) Representative western blot and quantitative analysis of ELOVL6 expression and VSMC contractile markers (CNN1 and TAGLN) in HASMCs treated with BMS‐986235 post‐transfection with siRNA‐FPR2 or siRNA‐NC ( n = 3). β‐Tubulin was used as a loading control. Data represent the mean ± SEM from n independent experiments. Independent measures one‐way ANOVA with Bonferroni's correction or Kruskal‐Wallis nonparametric test for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. HASMC, human aortic smooth muscle cell; CM, conditioned media; EdU, 5‐ethynyl‐2′‐deoxyuridine; CNN1, calponin 1, basic; TAGLN, transgelin; DAPI, 4′,6‐diamidino‐2‐phenylindole; NC, normal control; Ad, adenovirus; siRNA, small interfering RNA.

Article Snippet: FPR2 was knocked down by siRNA (Vigene Bioscience, Jinan, China) in both M2 macrophages and HASMCs, along with negative controls (siRNA‐NC).

Techniques: EdU Assay, Transfection, Wound Healing Assay, Western Blot, Expressing, Control, Small Interfering RNA