Journal of B.U.ON. : official journal of the Balkan Union of Oncology · 2019
Antiproliferative effects of propofol and lidocaine on the colon adenocarcinoma microenvironment.
СтатьяНазвание и аннотация: Перевод в очереди
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Tat Tiberiu, Jurj Ancuta, Selicean Cristina, Pasca Sergiu, Ionescu Daniela
Аннотация
PURPOSE: Certain anesthetic interventions may influence the postoperative outcome in surgical cancer patients. Our study investigated the antiproliferative effects of propofol and lidocaine in two colon cancer cells lines, fibroblasts and in co-cultures.
METHODS: The antiproliferative effects of concentrations of propofol and lidocaine were assessed in HCT-116 and RKO cell lines, in fibroblasts (CCD-18Co) and in co-culture system.
RESULTS: Both propofol (2-4 mcg/ml) and lidocaine (2-4 µM) inhibited significantly colon cancer cell proliferation (p<0.05). Caspase-8, heat-shock proteins (HSP-27 and HSP-60), insulin growth factor (IGF)-II, insulin growth factor binding proteins, p53 protein and survivin were significantly differentially expressed in malignant cells and in fibroblasts exposed to lidocaine.
CONCLUSION: Lidocaine and propofol selectively inhibited colon cancer cells proliferation. Antiproliferative effects were tumor-, dose- and time-dependent and may be at least partially explained by activation of apoptosis protein pathways. Further studies are necessary to confirm the clinical impact of our data.
METHODS: The antiproliferative effects of concentrations of propofol and lidocaine were assessed in HCT-116 and RKO cell lines, in fibroblasts (CCD-18Co) and in co-culture system.
RESULTS: Both propofol (2-4 mcg/ml) and lidocaine (2-4 µM) inhibited significantly colon cancer cell proliferation (p<0.05). Caspase-8, heat-shock proteins (HSP-27 and HSP-60), insulin growth factor (IGF)-II, insulin growth factor binding proteins, p53 protein and survivin were significantly differentially expressed in malignant cells and in fibroblasts exposed to lidocaine.
CONCLUSION: Lidocaine and propofol selectively inhibited colon cancer cells proliferation. Antiproliferative effects were tumor-, dose- and time-dependent and may be at least partially explained by activation of apoptosis protein pathways. Further studies are necessary to confirm the clinical impact of our data.