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Titolo:
Butyrate sensitizes human colon cancer cells to TRAIL-mediated apoptosis
Autore:
Hernandez, A; Thomas, R; Smith, F; Sandberg, J; Kim, S; Chung, DH; Evers, BM;
Indirizzi:
Univ Texas, Med Branch, Dept Surg, Galveston, TX 77555 USA Univ Texas Galveston TX USA 77555 nch, Dept Surg, Galveston, TX 77555 USA
Titolo Testata:
SURGERY
fascicolo: 2, volume: 130, anno: 2001,
pagine: 265 - 272
SICI:
0039-6060(200108)130:2<265:BSHCCC>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
ADHERENT TUMOR-CELLS; SODIUM-BUTYRATE; EPITHELIAL-CELLS; DEATH; EXPRESSION; INDUCTION; FAMILY; CYCLE; RECEPTORS; PROTEINS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Evers, BM Univ Texas, Med Branch, Dept Surg, 301 Univ Blvd, Galveston, TX 77555 USA Univ Texas 301 Univ Blvd Galveston TX USA 77555 on, TX 77555 USA
Citazione:
A. Hernandez et al., "Butyrate sensitizes human colon cancer cells to TRAIL-mediated apoptosis", SURGERY, 130(2), 2001, pp. 265-272

Abstract

Background. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a novel member of the tumor necrosis factor family, induces apoptosis inTRAIL-sensitive tumors through the activation of the caspase pathway. Sodium butyrate (NaBT) induces differentiation and apoptosis in certain colorectal cancers; the molecular mechanisms for these effects have not been clearly defined. The purpose of our study was to determine whether NaBT sensitizes TRAIL-resistant human colon cancer cells to the effects of TRAIL. Methods. Human colon cancer cells (KM12C, KML4A, and KM20) that are resistant to TRAIL treatment alone were treated with TRAIL (100 ng/mL), NaBT (5 mmol/L), or a combination of these agents and harvested for total RNA and protein. Western blots were performed to assess intracellular expression of Flice-like inhibitory protein (FLIP), a caspase inhibitor Percent-specific apoptosis, relative caspase-3 activity, and Annexin-V immunofluorescence were determined at 24 and 48 hours. Cell cycle-related gene expression was assessed by RNase protection. Results. Treatment with NaBT for 24 and 48 hours decreased FLIP protein expression in all cell lines. Furthermore, NaBT sensitized these resistant cancer cells to the effects of TRAIL with significant increases noted in celldeath, caspase-3 activity, and Annexin-V staining compared with NaBT alone. Conclusions. Our findings suggest that the reduction of FLIP protein levels by NaBT renders TRAIL-resistant human colon cancer cells sensitive to TRAIL-mediated apoptosis. The combination of TRAIL with agents (such as NaBT, which target proteins that prevent cell death) may provide a more effectiveand less toxic regimen for the treatment of resistant colon cancers.

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Documento generato il 04/04/20 alle ore 12:16:12