Phosphatidylinositol 3-Kinase Mediates the Ability of Retinol to Decrease Colorectal Cancer Cell Invasion.

Previously, we showed that retinol (vitamin A) decreased both colorectal cancer cell invasion and phosphatidylinositol 3-kinase (PI3K) activity through a retinoic acid receptor–independent mechanism. Here, we determined if these phenomena were related by using parental HCT-116 cells that harbor 1 al...

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Publicado en:Nutrition & Cancer Vol. 66; no. 8; pp. 1352 - 1362
Autores principales: Griffin Lengyel, Jennifer N., Park, Eun Young, Brunson, Anna R., Pinali, Daniel, Lane, Michelle A.
Formato: research tables/charts Journal Article
Publicado: Taylor & Francis Ltd Nov/Dec2014
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Nov/Dec2014
      vid: 66
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      pub: Taylor & Francis Ltd
      place: Philadelphia, Pennsylvania
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        10.1080/01635581.2014.956258
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        atl: Phosphatidylinositol 3-Kinase Mediates the Ability of Retinol to Decrease Colorectal Cancer Cell Invasion.
      aug:
        au:
          Griffin Lengyel, Jennifer N.
          Park, Eun Young
          Brunson, Anna R.
          Pinali, Daniel
          Lane, Michelle A.
        affil: School of Family and Consumer Sciences, Nutrition and Foods Program, Texas State University—San Marcos, San Marcos, Texas, USA
      sug:
        subj:
          Inositol Phosphates
          Phosphotransferases
          Retinoids Therapeutic Use
          Colorectal Neoplasms Prevention and Control
          Cell Physiology
          Nutrition
          Neoplasms
          Human
          Cancer Patients Evaluation
          Biological Assay
          Blotting, Western
          Animal Studies
          Mice
          Xenografts
          Immunohistochemistry
          Data Analysis
          Data Analysis Software
          Descriptive Statistics
          Gene Expression
          Genetics
      ab: Previously, we showed that retinol (vitamin A) decreased both colorectal cancer cell invasion and phosphatidylinositol 3-kinase (PI3K) activity through a retinoic acid receptor–independent mechanism. Here, we determined if these phenomena were related by using parental HCT-116 cells that harbor 1 allele of wild-type PI3K and 1 allele of constitutively active (ca) PI3K and 2 mutant HCT-116 cell lines homozygous for caPI3K. In vitro, treatment of parental HCT-116 cells with 10 μM retinol reduced cell invasion whereas treatment of mutant HCT-116 cell lines with retinol did not. Treatment with 10 μM retinol also decreased the activity of matrixmetalloproteinase-9 and increased tissue inhibitor of matrixmetalloproteinase-I levels in parental, but not mutant, HCT-116 cells. Finally, parental or mutant cells were intrasplenically injected into athymic mice consuming diets with or without supplemental vitamin A. As expected, vitamin A supplementation tended (P= 0.18) to reduce the incidence of metastases in mice injected with the parental cell line and consuming the supplemented diet. In contrast, metastatic incidence was not affected (P= 1.00) by vitamin A supplementation in mice injected with mutant cells. These data indicate that the capacity of retinol to inhibit PI3K activity confers its ability to decrease colorectal cancer metastasis.
      pubtype: Academic Journal
      doctype:
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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