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Cancer caveolin status: the dependence of anesthetic exposure to postoperative cancer chemotherapy in induction of cell death and survival
Author(s) -
Okada Sunaho,
Kawaraguchi Yoshitaka,
Patel Piyush M.,
Roth David M.,
Patel Hemal H.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.620.10
Volatile anesthetics have a dual effect on cell survival and death: they induce apoptosis in developing neurons but protect adult heart and brain from injury. The effect of volatile anesthetics on cancer cell survival and death, especially the sensitivity for anticancer therapy post anesthetic exposure is not clear. Therefore, we examined the effects of brief isoflurane exposure on TRAIL (TNF‐related apoptosis‐inducing ligand)‐induced apoptosis and its regulation by caveolin‐1 (Cav‐1). We exposed human colon cancer cell lines, HCT116 (high Cav‐1 expressing) and HT29 (low/none Cav‐1 expressing), to isoflurane. After isoflurane treatment, to mimic postoperative anticancer therapy, apoptosis was induced by TRAIL. To confirm the role of Cav‐1 in this response, we induced apoptosis by TRAIL in HT29 cells (which normally do not expression Cav‐1) stably expressing Cav‐1. Isoflurane exposure alone did not significantly induce apoptosis compared to the control group in both cell lines. However, TRAIL‐induced apoptosis was enhanced by isoflurane in HT29 and decreased in HCT116. By overexpressing Cav‐1 in HT29, the sensitivity to TRAIL‐induced apoptosis by isoflurane was attenuated. Brief isoflurane exposure leads to resistance against TRAIL‐induced apoptosis via a Cav‐1‐dependent mechanism, suggesting that Cav‐1 status of cancer may be an important consideration for postoperative anticancer therapy.