Abstract
Fentanyl is used as an analgesic to treat pain in a variety of patients with cancer and recently it has become considered to also act as an antitumor agent. The study present was designed to investigate the effects of fentanyl on colorectal cancer cell growth and plausible mechanisms. The human colorectal carcinoma cell line HCT116 was subcutaneously injected into nude mice. The viability of HCT116 was tested by MTT assay, and apoptosis by flow cytometry and caspase-3 activity. The expression of Sirt1 and NF-κB were evaluated by Western blotting and the levels of Sirt1 and NF-κB by fluorescence method. SiRNA was used to silence and Ad-Sirt1 to overexpress Sirt1. Our data showed that fentanyl could inhibit tumor growth, with increased expression of Sirt1 and down-regulation of Ac-p65 in tumors. Compared with control cells without treatment, HCT116 cells that were incubated with fentanyl had a higher apoptotic rate. Moreover, fentanyl could increase expression and activity of Sirt1 and inhibitor expression and activity of NF-κB, which might be mechanisms of fentanyl action. Fentanyl increased colorectal carcinoma cell apoptosis by inhibition of NF-κB activation in a Sirt1-dependent manner.
Highlights
Worldwide, colorectal cancer is one of the most prevalent and incident common malignant tumors, followed by lung and breast cancers, and it was the fourth leading cause of cancer death (Jemal et al, 2011)
Fentanyl decreased the Growth of Colon Tumor Xenograft To test the role of fentanyl in tumor formation, HCT116 colorectal cells were stably subcutaneously injected into the flank of the nude mice and the tumors were injected with dosage of fentanyl at 0.04 mg/kg, 0.08
Results showed that the increased decetylation activity of Sirt1 and the decreased transcriptional activity of p65 were both in a dose-dependent manner(Figure 3B, C)
Summary
Colorectal cancer is one of the most prevalent and incident common malignant tumors, followed by lung and breast cancers, and it was the fourth leading cause of cancer death (Jemal et al, 2011). Studies reported that fentanyl has a activity of inhibiting of cancer cell proliferation and cancer progression (Huffman et al, 2007; Qin et al, 2012), which suggested that a potential antitumor role of fentanyl. It remains unknown whether fentanyl has a sustain effect on colorectal cancer. Fentanyl is used as an analgesic to treat pain in a variety of patients with cancer and recently it has become considered to act as an antitumor agent. Conclusions: Fentanyl increased colorectal carcinoma cell apoptosis by inhibition of NF-κB activation in a Sirt1-dependent manner
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