We are analyzing https://link.springer.com/article/10.1007/s10585-011-9376-x.

Title:
Transient silencing of galectin-3 expression promotes both in vitro and in vivo drug-induced apoptosis of human pancreatic carcinoma cells | Clinical & Experimental Metastasis
Description:
Pancreatic cancer demonstrates a strong resistance to anticancer drugs, presumably due to its resistance to drug induced apoptosis. Although gemcitabine (GEM) might be partially effective for treating advanced pancreatic cancer, its efficacy is still less than satisfactory. Galectin-3 (gal-3), a member of the β-galactoside-binding protein family, is a multifunctional protein with roles in tumor cell adhesion, proliferation, differentiation, angiogenesis, metastasis, and apoptosis. We have utilized gal-3 small interfering RNA (siRNA) to probe whether gal-3 regulates anticancer drug-induced apoptosis in pancreatic cancer cells. We found that Gal-3 siRNA augmented GEM- and cisplatin-induced apoptosis in pancreatic cancer cell lines in vitro. Mitochondrial depolarization induction was increased in gal-3-silenced cells after GEM treatment, resulting in activation of caspase-9, but not caspase-8. Akt phosphorylation was significantly downregulated in gal-3- silenced cells in association with apoptosis. Moreover, intratumoral administration of gal-3 siRNA increased the GEM sensitivity of tumor xenografts produced by subcutaneous inoculation of pancreatic cancer cells into nude mice. These results suggest that gal-3 might provide a novel therapeutic target in pancreatic cancer.
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article, pubmed, google, scholar, cas, cancer, galectin, pancreatic, apoptosis, cells, cell, gemcitabine, tumor, gal, res, human, expression, akt, nangiamakker, privacy, cookies, content, vitro, vivo, carcinoma, raz, drug, gem, protein, regulates, phosphorylation, access, role, clin, biol, publish, research, search, metastasis, promotes, kobayashi, shimura, resistance, family, sirna, patients, death, trial, survival, fukumori,

Topics {✒️}

igf-ii-overexpressing rhabdomyosarcomas cells animal beta-galactoside-binding lectins β-galactoside-binding protein family month download article/chapter gli-sox2 signaling axis galectin-3 mediates genistein-induced cell-intrinsic death machinery vivo drug-induced apoptosis phosphoinositide 3-kinase/akt pathway phosphorylated galectin-3 regulates related subjects drug induced apoptosis pancreatic carcinoma cells full article pdf cisplatin-induced apoptosis pancreatic cancer cells tumor cell adhesion transient silencing resected pancreatic cancer japanese study group advanced pancreas cancer privacy choices/manage cookies protein kinase akt melanoma cell plasticity gal-3-silenced cells gal-3- silenced cells tumor xenografts produced inhibits apoptosis interleukin-3-induced phosphorylation human matrix metalloproteinases-2 plasmid pgex-gal-3 karmanos cancer institute growing breast cancers epithelial-specific galectin tumor immune response mitochondrial depolarization induction influencing mitochondrial homeostasis cancer drug resistance prostate cancer progression randomized controlled trial article kobayashi galectin-3 expression promotes galectin-3 overexpression protects european economic area tension homolog deleted membrane lipid rafts tensin homologue deleted malignant thyroid carcinomas central control point grant 3r37-ca46120-21

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         headline:Transient silencing of galectin-3 expression promotes both in vitro and in vivo drug-induced apoptosis of human pancreatic carcinoma cells
         description:Pancreatic cancer demonstrates a strong resistance to anticancer drugs, presumably due to its resistance to drug induced apoptosis. Although gemcitabine (GEM) might be partially effective for treating advanced pancreatic cancer, its efficacy is still less than satisfactory. Galectin-3 (gal-3), a member of the β-galactoside-binding protein family, is a multifunctional protein with roles in tumor cell adhesion, proliferation, differentiation, angiogenesis, metastasis, and apoptosis. We have utilized gal-3 small interfering RNA (siRNA) to probe whether gal-3 regulates anticancer drug-induced apoptosis in pancreatic cancer cells. We found that Gal-3 siRNA augmented GEM- and cisplatin-induced apoptosis in pancreatic cancer cell lines in vitro. Mitochondrial depolarization induction was increased in gal-3-silenced cells after GEM treatment, resulting in activation of caspase-9, but not caspase-8. Akt phosphorylation was significantly downregulated in gal-3- silenced cells in association with apoptosis. Moreover, intratumoral administration of gal-3 siRNA increased the GEM sensitivity of tumor xenografts produced by subcutaneous inoculation of pancreatic cancer cells into nude mice. These results suggest that gal-3 might provide a novel therapeutic target in pancreatic cancer.
         datePublished:2011-02-18T00:00:00Z
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      headline:Transient silencing of galectin-3 expression promotes both in vitro and in vivo drug-induced apoptosis of human pancreatic carcinoma cells
      description:Pancreatic cancer demonstrates a strong resistance to anticancer drugs, presumably due to its resistance to drug induced apoptosis. Although gemcitabine (GEM) might be partially effective for treating advanced pancreatic cancer, its efficacy is still less than satisfactory. Galectin-3 (gal-3), a member of the β-galactoside-binding protein family, is a multifunctional protein with roles in tumor cell adhesion, proliferation, differentiation, angiogenesis, metastasis, and apoptosis. We have utilized gal-3 small interfering RNA (siRNA) to probe whether gal-3 regulates anticancer drug-induced apoptosis in pancreatic cancer cells. We found that Gal-3 siRNA augmented GEM- and cisplatin-induced apoptosis in pancreatic cancer cell lines in vitro. Mitochondrial depolarization induction was increased in gal-3-silenced cells after GEM treatment, resulting in activation of caspase-9, but not caspase-8. Akt phosphorylation was significantly downregulated in gal-3- silenced cells in association with apoptosis. Moreover, intratumoral administration of gal-3 siRNA increased the GEM sensitivity of tumor xenografts produced by subcutaneous inoculation of pancreatic cancer cells into nude mice. These results suggest that gal-3 might provide a novel therapeutic target in pancreatic cancer.
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         Pancreatic cancer
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