Journal: Oncology Letters

Article Title: Inhibition of cancer cell‑platelet adhesion as a promising therapeutic target for preventing peritoneal dissemination of gastric cancer

doi: 10.3892/ol.2023.14125

Figure Lengend Snippet: Major candidate molecules involved in the interaction between cancer cells and platelets. Inhibitors targeting the candidate molecules are shown. CLEC-2, C-type lectin-like receptor 2; Co-HP, cobalt hematoporphyrin; GPVI, glycoprotein VI; Gal-3, galectin-3; PDPN, podoplanin.

Article Snippet: The Gal-3 inhibitor GB1107 was purchased from MedChemExpress (Monmouth Junction, NJ, USA), and a 10 μM solution was used. rat antimouse-GPVI monoclonal therapeutic antibody JAQ1 (M011-0) and its negative control, rat IgG, were purchased from EMFRET Analytics & Co. KG (Wurzburg, Germany).

Techniques:

Journal: Oncology Letters

Article Title: Inhibition of cancer cell‑platelet adhesion as a promising therapeutic target for preventing peritoneal dissemination of gastric cancer

doi: 10.3892/ol.2023.14125

Figure Lengend Snippet: Inhibitory effect of GPVI/galectin-3 inhibitors on tumor development in mouse cell lines (YTN16). Results of the (A) migration and (B) invasion assays and (C and D) their microscopic images show that JAQ1 significantly suppresses both the platelet-induced enhancement of migratory and invasive abilities of YTN16 cells (P=0.004, vs. mPLT group, and P=0.003, vs. mPLT group, respectively; magnification, ×100). Furthermore, the Gal-3 inhibitor GB1107 tended to suppress this enhanced ability, especially in migration assays (P=0.044 vs. mPLT group, and P=0.071 vs. mPLT group, respectively; magnification, ×100). Gal-3, galectin-3; hPLT, human platelets; mPLT, mouse platelets.

Article Snippet: The Gal-3 inhibitor GB1107 was purchased from MedChemExpress (Monmouth Junction, NJ, USA), and a 10 μM solution was used. rat antimouse-GPVI monoclonal therapeutic antibody JAQ1 (M011-0) and its negative control, rat IgG, were purchased from EMFRET Analytics & Co. KG (Wurzburg, Germany).

Techniques: Migration

Journal: Oncology Letters

Article Title: Inhibition of cancer cell‑platelet adhesion as a promising therapeutic target for preventing peritoneal dissemination of gastric cancer

doi: 10.3892/ol.2023.14125

Figure Lengend Snippet: Therapeutic effects of JAQ1 and GB1107 in peritoneal dissemination. Trends in (A) mouse weight, (B) number of peritoneal tumors, (C) weight of the tumor mass and (D) findings from each representative abdominal cavity can be observed. All groups, except for the mPLT group, show similar increasing trends in mouse weight. Both the number of tumors and their weights are enhanced by platelet contact (P=0.040 vs. NT group and P=0.037 vs. NT group, respectively) and reduced by coadministration of JAQ1 and GB1107 (P=0.042 vs. mPLT group). NT, nontreatment; mPLT, mouse platelet.

Article Snippet: The Gal-3 inhibitor GB1107 was purchased from MedChemExpress (Monmouth Junction, NJ, USA), and a 10 μM solution was used. rat antimouse-GPVI monoclonal therapeutic antibody JAQ1 (M011-0) and its negative control, rat IgG, were purchased from EMFRET Analytics & Co. KG (Wurzburg, Germany).

Techniques:

Journal: Current Oncology

Article Title: Prostate Cancer Biomarkers with a Focus on Galectin-3: Emerging Clinical and Therapeutic Implications

doi: 10.3390/curroncol33050280

Figure Lengend Snippet: Compartment-specific functions of Galectin-3 and therapeutic targeting strategies in prostate cancer.

Article Snippet: Lung & Pancreatic Cancer , KRAS Addiction: Gal-3 supports pro-survival pathways in KRAS-driven tumors. , GB1107 , Novel small molecule Galectin-3 inhibitor , Identified as a druggable vulnerability in hard-to-treat tumors, showing Gal-3 as a key mediator of oncogenic signaling beyond the AR pathway [ ]. .

Techniques:

Journal: Molecular Medicine Reports

Article Title: Galectin-3 blockade suppresses the growth of cetuximab-resistant human oral squamous cell carcinoma

doi: 10.3892/mmr.2021.12325

Figure Lengend Snippet: Effects of cetuximab and GB1107 on growth of regular and cet-R HSC3 tumors in mice xenografts. (A) Tumor growth curve of cet-R HSC3 tumors (n=4). BALB/c nude mice were injected with HSC3 cells. When the tumor volume reached 80 mm 3 , mice were treated with 0.2 mg/kg cetuximab once per week via tail vein injection, and resistance developed after ~85 days. (B) GB1107 significantly inhibited cet-R tumor xenograft growth compared with the PBS treatment group. BALB/c nude mice were injected with cet-R HSC3 cells (n=10/group). When the tumor volume reached 80 mm 3 , mice were treated with 10 mg/kg GB1107 per day via oral gavage for 36 days. GB1107 treatment significantly decreased tumor volumes compared with those observed in mice treated with PBS. (C) GB1107 and cetuximab combination treatment displayed a synergistic antitumor effect in regular HSC3 tumors. BALB/c nude mice (n=10/group) were injected with regular HSC3 cells. When the tumor volume reached 80 mm 3 , mice were treated with a placebo (IgG or PBS), GB1107, cetuximab or cetuximab + GB1107 for 36 days. Treatment with cetuximab resulted in a 59.52% inhibition rate compared with the IgG treatment group, whereas treatment with GB1107 resulted in a 18.73% inhibition rate compared with the PBS treatment group. By contrast, the combination treatment of GB1107 and cetuximab resulted in a 73.81% inhibition rate compared with the IgG treatment group. Data are presented as the mean ± SEM. Data presented in were analyzed using two-way mixed ANOVA followed by Tukey's post hoc test. *P<0.05 and **P<0.01. cet-R, cetuximab-resistant.

Article Snippet: Mice (n=10/group; male to female ratio=1:1) were randomly assigned to the following treatment groups: i) mice received 0.2 mg/kg cetuximab (Erbitux ® ; diluted with saline solution; Merck KGaA) once per week via tail vein injection ( ); ii) mice received 10 mg/kg GB1107 (a Gal-3 inhibitor; diluted with PBS; Aobious, Inc.) once per day by oral gavage ( ); and iii) the control group received PBS (100 μl) or IgG (0.2 mg/kg).

Techniques: Injection, Inhibition

Journal: Molecular Medicine Reports

Article Title: Galectin-3 blockade suppresses the growth of cetuximab-resistant human oral squamous cell carcinoma

doi: 10.3892/mmr.2021.12325

Figure Lengend Snippet: GB1107 inhibits the expression of Gal-3, p-ERK1/2 and p-Akt in cet-R tumors of mice xenografts. Tumors were collected from the following three groups: i) cet-R HSC3 tumor xenografts treated with GB1107; ii) cet-R HSC3 tumor xenografts treated with PBS; and iii) regular HSC3 tumor xenograft treated with PBS (control; non-resistant tumors). Gal-3, p-ERK1/2 and p-Akt expression was examined by IHC and then quantified. Gal-3, p-ERK1/2 and p-Akt expression was significantly increased in cet-R tumors compared with regular HSC3 tumors. However, GB1107 significantly inhibited the expression of Gal-3, p-ERK1/2 and p-Akt in cet-R tumors. Data are presented as the mean ± SEM (n=10/group). Data were analyzed by one-way ANOVA followed by Tukey's post hoc test. *P<0.05 and **P<0.01. Gal-3, galectin-3; p, phosphorylated; OD, optical density; IHC, immunohistochemistry; cet-R, cetuximab-resistant.

Article Snippet: Mice (n=10/group; male to female ratio=1:1) were randomly assigned to the following treatment groups: i) mice received 0.2 mg/kg cetuximab (Erbitux ® ; diluted with saline solution; Merck KGaA) once per week via tail vein injection ( ); ii) mice received 10 mg/kg GB1107 (a Gal-3 inhibitor; diluted with PBS; Aobious, Inc.) once per day by oral gavage ( ); and iii) the control group received PBS (100 μl) or IgG (0.2 mg/kg).

Techniques: Expressing, Control, Immunohistochemistry

Journal: Molecular Medicine Reports

Article Title: Galectin-3 blockade suppresses the growth of cetuximab-resistant human oral squamous cell carcinoma

doi: 10.3892/mmr.2021.12325

Figure Lengend Snippet: IC 50 values of cetuximab and GB1107 in HSC3 cells. HSC3 cells were cultured in vitro and treated with cetuximab (0.01–200 µM) or GB1107 (0.01–200 µM) for 72 h. Cell viability was measured using a Cell Counting Kit-8 assay. (A) IC 50 value of cetuximab in cet-R HSC3 cells was notably higher compared with that in regular HSC3 cells (437.6±12.04 µM vs. 7.67±1.31 µM). (B) IC 50 value of GB1107 in cet-R HSC3 cells was similar to that in regular HSC3 cells (1.28±1.12 µM vs. 0.88±1.15 µM). (C) siRNA-mediated Gal-3 knockdown in cet-R HSC3 cells was validated by western blotting. A scramble siRNA was used as the control. IC 50 value of cetuximab in Gal-3-knockdown cet-R HSC3 cells was notably decreased compared with that in scramble probe-transfected cells (437.6±12.04 µM vs. 26.68±2.35 µM). All results were representative of three independent experiments performed in triplicate. Data are presented as the mean ± SEM. cet-R, cetuximab-resistant; siRNA, small interfering RNA; Gal-3, galectin-3; KD, knockdown.

Article Snippet: Mice (n=10/group; male to female ratio=1:1) were randomly assigned to the following treatment groups: i) mice received 0.2 mg/kg cetuximab (Erbitux ® ; diluted with saline solution; Merck KGaA) once per week via tail vein injection ( ); ii) mice received 10 mg/kg GB1107 (a Gal-3 inhibitor; diluted with PBS; Aobious, Inc.) once per day by oral gavage ( ); and iii) the control group received PBS (100 μl) or IgG (0.2 mg/kg).

Techniques: Cell Culture, In Vitro, Cell Counting, Knockdown, Western Blot, Control, Transfection, Small Interfering RNA

Journal: Molecular Medicine Reports

Article Title: Galectin-3 blockade suppresses the growth of cetuximab-resistant human oral squamous cell carcinoma

doi: 10.3892/mmr.2021.12325

Figure Lengend Snippet: Regulatory effect of Gal-3 inhibitor on the proliferation, invasion and apoptosis of oral squamous cell carcinoma cells. Regular and cet-R HSC3 cells were cultured in vitro and treated with GB1107 (Gal-3 inhibitor) for 72 h. In addition, cet-R-HSC3 cells were transfected with Gal-3 small interfering RNA to knock down Gal-3 expression, followed by culture for 72 h. Subsequently, cell proliferation, invasion, colony formation and apoptosis were examined by performing Cell Counting Kit-8, Transwell, colony formation and flow cytometry assays, respectively. Compared with the PBS group, GB1107 treatment significantly decreased the (A) proliferation, (B) invasion (scale bar, 200 µm) and (C) colony formation (scale bar, 400 µm), but increased the (D) apoptotic rate of regular and cet-R HSC3 cells. In addition, the results demonstrated that Gal-3 knockdown inhibited the proliferation, invasion and colony formation, but induced the apoptosis of cet-R HSC3 cells. All experiments were performed in triplicate. Data are presented as the mean ± SEM. Data were analyzed using one-way ANOVA followed by Tukey's post hoc test (4A) or Student's t -test (4B-D). *P<0.05 and **P<0.01. Gal-3, galectin-3; cet-R, cetuximab-resistant; KD, knockdown.

Article Snippet: Mice (n=10/group; male to female ratio=1:1) were randomly assigned to the following treatment groups: i) mice received 0.2 mg/kg cetuximab (Erbitux ® ; diluted with saline solution; Merck KGaA) once per week via tail vein injection ( ); ii) mice received 10 mg/kg GB1107 (a Gal-3 inhibitor; diluted with PBS; Aobious, Inc.) once per day by oral gavage ( ); and iii) the control group received PBS (100 μl) or IgG (0.2 mg/kg).

Techniques: Cell Culture, In Vitro, Transfection, Small Interfering RNA, Knockdown, Expressing, Cell Counting, Flow Cytometry