BACKGROUND: The natural history of colorectal neoplasia may be influenced by steroid hormones and nutritional compounds. We evaluated the effect of the anti-estrogenic tamoxifen (Tx), and the synthetic retinoid fenretinimide (4-HPR) on the growth of human colorectal cancer cells. METHODS: DLD-1, CACO-2, SW-620, and COLO-205 colon cancer cells, and SW-1463 and SW-837 rectal cancer cells were cultured under serum-free conditions. Quadruplicates wells (4 x 10(4) cells/well) were created for each treated, and untreated groups in each cell line. Cells were treated with 1 microM Tx, 5 microM Tx, 1 microM 4-HPR, 1 microM Tx with 1 microM 4-HPR, and 5 microM Tx with microM 4-HPR. Cell growth was measured colorimetrically with the hexosaminidase assay (405 nm), and was compared among the different groups. Cells were analyzed for estrogen receptors using an enzyme immunoassay. RESULTS: Tamoxifen, 4-HPR, or both, inhibited the growth in DLD-1 (P = .001), COLO-205 (P = .02), SW-620 (P = .001), and CACO-2 (P = .02) cell lines. Tamoxifen with 4-HPR inhibited cell growth more (P = .03) than did either Tx or 4-HPR in DLD-1, COLO-205, and SW620 cancer cells. Tamoxifen, 4-HPR, or both, had no effect on the growth of SW-837 (P = .14) cancer cells. Tamoxifen with 4-HPR promoted (P = .02) growth in SW-1463 cells, but not when added separately. Estrogen receptors were not found in any of the cells. CONCLUSIONS: Under serum-free conditions, Tx, 4-HPR, or both, inhibit the growth of human colon cancer cells but not of rectal cancer cells. Combined treatment with Tx and 4-HPR is more effective than treatment with either of the agents alone in inhibiting of cell growth. The mechanism of inhibition is not clear yet, and further studies are warranted.
BACKGROUND: The natural history of colorectal neoplasia may be influenced by steroid hormones and nutritional compounds. We evaluated the effect of the anti-estrogenic tamoxifen (Tx), and the synthetic retinoidfenretinimide (4-HPR) on the growth of humancolorectal cancer cells. METHODS: DLD-1, CACO-2, SW-620, and COLO-205 colon cancer cells, and SW-1463 and SW-837 rectal cancer cells were cultured under serum-free conditions. Quadruplicates wells (4 x 10(4) cells/well) were created for each treated, and untreated groups in each cell line. Cells were treated with 1 microM Tx, 5 microM Tx, 1 microM 4-HPR, 1 microM Tx with 1 microM 4-HPR, and 5 microM Tx with microM 4-HPR. Cell growth was measured colorimetrically with the hexosaminidase assay (405 nm), and was compared among the different groups. Cells were analyzed for estrogen receptors using an enzyme immunoassay. RESULTS:Tamoxifen, 4-HPR, or both, inhibited the growth in DLD-1 (P = .001), COLO-205 (P = .02), SW-620 (P = .001), and CACO-2 (P = .02) cell lines. Tamoxifen with 4-HPR inhibited cell growth more (P = .03) than did either Tx or 4-HPR in DLD-1, COLO-205, and SW620 cancer cells. Tamoxifen, 4-HPR, or both, had no effect on the growth of SW-837 (P = .14) cancer cells. Tamoxifen with 4-HPR promoted (P = .02) growth in SW-1463 cells, but not when added separately. Estrogen receptors were not found in any of the cells. CONCLUSIONS: Under serum-free conditions, Tx, 4-HPR, or both, inhibit the growth of humancolon cancer cells but not of rectal cancer cells. Combined treatment with Tx and 4-HPR is more effective than treatment with either of the agents alone in inhibiting of cell growth. The mechanism of inhibition is not clear yet, and further studies are warranted.
Authors: Judith G Villablanca; Wendy B London; Arlene Naranjo; Patrick McGrady; Matthew M Ames; Joel M Reid; Renee M McGovern; Sarah A Buhrow; Hollie Jackson; Enno Stranzinger; Brenda J Kitchen; Paul M Sondel; Marguerite T Parisi; Barry Shulkin; Gregory A Yanik; Susan L Cohn; C Patrick Reynolds Journal: Clin Cancer Res Date: 2011-09-09 Impact factor: 12.531
Authors: Elena Doldo; Gaetana Costanza; Sara Agostinelli; Chiara Tarquini; Amedeo Ferlosio; Gaetano Arcuri; Daniela Passeri; Maria Giovanna Scioli; Augusto Orlandi Journal: Biomed Res Int Date: 2015-03-24 Impact factor: 3.411