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Mechanism of antimitogenic action of vitamin D in human colon carcinoma cells: relevance for suppression of epidermal growth factor-stimulated cell growth.
Oncol Res. 1999; 11(2):77-84.OR

Abstract

Because the efficacy of 1alpha,25-dihydroxyvitamin D3 [1alpha,25-(OH)2D3] in treatment of colon cancer might critically depend on its ability to specifically counteract epidermal growth factor (EGF)-stimulated tumor cell growth, we utilized human colon adenocarcinoma-derived cells in primary culture as well as the Caco-2 cell line to elucidate possible sites of interaction of 1alpha,25-(OH)2D3 with signaling from EGF receptor activation. In both types of colon cancer cells investigated, 10(-8) M 1alpha,25-(OH)2D3 reduced basal cell proliferation by about 50%, and prevented any rise in proliferation when colon cancer cells were treated with 25 ng/ml EGF: this can be explained by a marked inhibitory effect of 1alpha,25-(OH)2D3 on EGFR mRNA and protein expression. The steroid hormone also seemingly promotes EGF-induced internalization of apical and basolateral membrane EGFR. In addition, 1alpha,25-(OH)2D3 significantly reduced basal and EGF-stimulated expression of cyclin D1 at the mRNA and protein level in primary cultures as well as in the Caco-2 cell line. The ability of 1alpha,25-(OH)2D3 to interfere with a key event in cell cycle control and thereby to block mitogenic signaling from EGF could be seen as advantageous for the potential use of vitamin D compounds in colon cancer therapy.

Authors+Show Affiliations

Department of General and Experimental Pathology, University of Vienna Medical School, Austria.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10489163

Citation

Tong, W M., et al. "Mechanism of Antimitogenic Action of Vitamin D in Human Colon Carcinoma Cells: Relevance for Suppression of Epidermal Growth Factor-stimulated Cell Growth." Oncology Research, vol. 11, no. 2, 1999, pp. 77-84.
Tong WM, Hofer H, Ellinger A, et al. Mechanism of antimitogenic action of vitamin D in human colon carcinoma cells: relevance for suppression of epidermal growth factor-stimulated cell growth. Oncol Res. 1999;11(2):77-84.
Tong, W. M., Hofer, H., Ellinger, A., Peterlik, M., & Cross, H. S. (1999). Mechanism of antimitogenic action of vitamin D in human colon carcinoma cells: relevance for suppression of epidermal growth factor-stimulated cell growth. Oncology Research, 11(2), 77-84.
Tong WM, et al. Mechanism of Antimitogenic Action of Vitamin D in Human Colon Carcinoma Cells: Relevance for Suppression of Epidermal Growth Factor-stimulated Cell Growth. Oncol Res. 1999;11(2):77-84. PubMed PMID: 10489163.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanism of antimitogenic action of vitamin D in human colon carcinoma cells: relevance for suppression of epidermal growth factor-stimulated cell growth. AU - Tong,W M, AU - Hofer,H, AU - Ellinger,A, AU - Peterlik,M, AU - Cross,H S, PY - 1999/9/17/pubmed PY - 1999/9/17/medline PY - 1999/9/17/entrez SP - 77 EP - 84 JF - Oncology research JO - Oncol Res VL - 11 IS - 2 N2 - Because the efficacy of 1alpha,25-dihydroxyvitamin D3 [1alpha,25-(OH)2D3] in treatment of colon cancer might critically depend on its ability to specifically counteract epidermal growth factor (EGF)-stimulated tumor cell growth, we utilized human colon adenocarcinoma-derived cells in primary culture as well as the Caco-2 cell line to elucidate possible sites of interaction of 1alpha,25-(OH)2D3 with signaling from EGF receptor activation. In both types of colon cancer cells investigated, 10(-8) M 1alpha,25-(OH)2D3 reduced basal cell proliferation by about 50%, and prevented any rise in proliferation when colon cancer cells were treated with 25 ng/ml EGF: this can be explained by a marked inhibitory effect of 1alpha,25-(OH)2D3 on EGFR mRNA and protein expression. The steroid hormone also seemingly promotes EGF-induced internalization of apical and basolateral membrane EGFR. In addition, 1alpha,25-(OH)2D3 significantly reduced basal and EGF-stimulated expression of cyclin D1 at the mRNA and protein level in primary cultures as well as in the Caco-2 cell line. The ability of 1alpha,25-(OH)2D3 to interfere with a key event in cell cycle control and thereby to block mitogenic signaling from EGF could be seen as advantageous for the potential use of vitamin D compounds in colon cancer therapy. SN - 0965-0407 UR - https://www.unboundmedicine.com/medline/citation/10489163/Mechanism_of_antimitogenic_action_of_vitamin_D_in_human_colon_carcinoma_cells:_relevance_for_suppression_of_epidermal_growth_factor_stimulated_cell_growth_ L2 - https://antibodies.cancer.gov/detail/CPTC-EGFR-12 DB - PRIME DP - Unbound Medicine ER -