Effects of propofol on the proliferation and migration of liver cancer cells

Liver cancer is a malignant cancer with worldwide prevalence. It has been reported that cancer cells are usually exposed to a hypoxic microenvironment, which is associated with a poor prognosis in patients with cancer. Propofol is an intravenous anesthetic that is widely used in cancer surgery. The...

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Veröffentlicht in:Experimental and therapeutic medicine 2021-07, Vol.22 (1), p.733-733, Article 733
Hauptverfasser: Li, Chan, Fu, Qingxia, Cai, Jin, Mei, Hongxia, Shangguan, Wangning
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Fu, Qingxia
Cai, Jin
Mei, Hongxia
Shangguan, Wangning
description Liver cancer is a malignant cancer with worldwide prevalence. It has been reported that cancer cells are usually exposed to a hypoxic microenvironment, which is associated with a poor prognosis in patients with cancer. Propofol is an intravenous anesthetic that is widely used in cancer surgery. The present study aimed to determine the effects of propofol stimulation on the viability, proliferation and migration of liver cancer cells under normoxia and cobalt chloride (Co[Cl.sub.2])-induced hypoxia. Under normoxia, HepG2 and HCCLM3 cells were randomly divided into six groups as follows: i) Control group; ii) 10 [micro]M propofol group; iii) 25 [micro]M propofol group; iv) 50 [micro]M propofol group; v) 100 [micro]M propofol group; and vi) DMSO group. Cell viability and proliferation were analyzed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays, respectively, following 24 or 48 h of propofol treatment. In addition, wound healing and Transwell migration assays were used to determine the changes in cell migration. Under Co[Cl.sub.2]-induced hypoxia, the protein levels of hypoxia inducible factor-1[alpha] (HIF-1[alpha]) of HepG2 cells were analyzed using western blotting. Subsequently, CCK-8 and wound healing assays were used to determine the effect of propofol on cell viability and migration. The results of the present study revealed that propofol stimulation had no significant effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxia. The protein levels of HIF-1[alpha] were significantly upregulated following the treatment with 200 [micro]M Co[Cl.sub.2] for 12 h. However, no significant differences were found in the viability and migration of HepG2 cells following the stimulation with propofol in the presence of Co[Cl.sub.2]. In conclusion, the findings of the present study revealed Keythat propofol exerted no effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxic and hypoxic conditions. Key words: propofol, liver cancer, viability, proliferation, migration
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It has been reported that cancer cells are usually exposed to a hypoxic microenvironment, which is associated with a poor prognosis in patients with cancer. Propofol is an intravenous anesthetic that is widely used in cancer surgery. The present study aimed to determine the effects of propofol stimulation on the viability, proliferation and migration of liver cancer cells under normoxia and cobalt chloride (Co[Cl.sub.2])-induced hypoxia. Under normoxia, HepG2 and HCCLM3 cells were randomly divided into six groups as follows: i) Control group; ii) 10 [micro]M propofol group; iii) 25 [micro]M propofol group; iv) 50 [micro]M propofol group; v) 100 [micro]M propofol group; and vi) DMSO group. Cell viability and proliferation were analyzed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays, respectively, following 24 or 48 h of propofol treatment. In addition, wound healing and Transwell migration assays were used to determine the changes in cell migration. Under Co[Cl.sub.2]-induced hypoxia, the protein levels of hypoxia inducible factor-1[alpha] (HIF-1[alpha]) of HepG2 cells were analyzed using western blotting. Subsequently, CCK-8 and wound healing assays were used to determine the effect of propofol on cell viability and migration. The results of the present study revealed that propofol stimulation had no significant effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxia. The protein levels of HIF-1[alpha] were significantly upregulated following the treatment with 200 [micro]M Co[Cl.sub.2] for 12 h. However, no significant differences were found in the viability and migration of HepG2 cells following the stimulation with propofol in the presence of Co[Cl.sub.2]. In conclusion, the findings of the present study revealed Keythat propofol exerted no effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxic and hypoxic conditions. 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It has been reported that cancer cells are usually exposed to a hypoxic microenvironment, which is associated with a poor prognosis in patients with cancer. Propofol is an intravenous anesthetic that is widely used in cancer surgery. The present study aimed to determine the effects of propofol stimulation on the viability, proliferation and migration of liver cancer cells under normoxia and cobalt chloride (Co[Cl.sub.2])-induced hypoxia. Under normoxia, HepG2 and HCCLM3 cells were randomly divided into six groups as follows: i) Control group; ii) 10 [micro]M propofol group; iii) 25 [micro]M propofol group; iv) 50 [micro]M propofol group; v) 100 [micro]M propofol group; and vi) DMSO group. Cell viability and proliferation were analyzed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays, respectively, following 24 or 48 h of propofol treatment. In addition, wound healing and Transwell migration assays were used to determine the changes in cell migration. Under Co[Cl.sub.2]-induced hypoxia, the protein levels of hypoxia inducible factor-1[alpha] (HIF-1[alpha]) of HepG2 cells were analyzed using western blotting. Subsequently, CCK-8 and wound healing assays were used to determine the effect of propofol on cell viability and migration. The results of the present study revealed that propofol stimulation had no significant effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxia. The protein levels of HIF-1[alpha] were significantly upregulated following the treatment with 200 [micro]M Co[Cl.sub.2] for 12 h. However, no significant differences were found in the viability and migration of HepG2 cells following the stimulation with propofol in the presence of Co[Cl.sub.2]. In conclusion, the findings of the present study revealed Keythat propofol exerted no effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxic and hypoxic conditions. 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It has been reported that cancer cells are usually exposed to a hypoxic microenvironment, which is associated with a poor prognosis in patients with cancer. Propofol is an intravenous anesthetic that is widely used in cancer surgery. The present study aimed to determine the effects of propofol stimulation on the viability, proliferation and migration of liver cancer cells under normoxia and cobalt chloride (Co[Cl.sub.2])-induced hypoxia. Under normoxia, HepG2 and HCCLM3 cells were randomly divided into six groups as follows: i) Control group; ii) 10 [micro]M propofol group; iii) 25 [micro]M propofol group; iv) 50 [micro]M propofol group; v) 100 [micro]M propofol group; and vi) DMSO group. Cell viability and proliferation were analyzed using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays, respectively, following 24 or 48 h of propofol treatment. In addition, wound healing and Transwell migration assays were used to determine the changes in cell migration. Under Co[Cl.sub.2]-induced hypoxia, the protein levels of hypoxia inducible factor-1[alpha] (HIF-1[alpha]) of HepG2 cells were analyzed using western blotting. Subsequently, CCK-8 and wound healing assays were used to determine the effect of propofol on cell viability and migration. The results of the present study revealed that propofol stimulation had no significant effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxia. The protein levels of HIF-1[alpha] were significantly upregulated following the treatment with 200 [micro]M Co[Cl.sub.2] for 12 h. However, no significant differences were found in the viability and migration of HepG2 cells following the stimulation with propofol in the presence of Co[Cl.sub.2]. In conclusion, the findings of the present study revealed Keythat propofol exerted no effect on the viability, proliferation and migration of HepG2 and HCCLM3 cells under normoxic and hypoxic conditions. Key words: propofol, liver cancer, viability, proliferation, migration</abstract><cop>Athens</cop><pub>Spandidos Publications</pub><pmid>34055050</pmid><doi>10.3892/etm.2021.10165</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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ispartof Experimental and therapeutic medicine, 2021-07, Vol.22 (1), p.733-733, Article 733
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language eng
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subjects Biotechnology
Cancer cells
Cell migration
Cell proliferation
Development and progression
Hypoxia
Investigations
Liver cancer
Medical prognosis
Metastasis
Pharmacology, Experimental
Physiological aspects
Propofol
Proteins
Surgery
Tumors
title Effects of propofol on the proliferation and migration of liver cancer cells
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