Fluvastatin inhibits growth and alters the malignant phenotype of the C6 glioma cell line

Sławińska-Brych, Adrianna; Zdzisińska, Barbara; Kandefer‐Szerszeń, Martyna

doi:10.1016/j.pharep.2014.01.002

Cited by 37 publications

(31 citation statements)

References 44 publications

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“…SIM exerted more cytotoxic effect than ATOR due to the difference in pharmacokinetic properties especially lipophilicity. Sławińska-Brych A et al (2014) reported the IC50 of SIM on MCF7 and MDM-231 ranging 1.26 to 91 µM and different with other cancerous cells [20] . The cytotoxicity of SIM and ATOR and DOX were measured by MTT.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of anti-proliferative activity of simvastatin and atorvastatin on MCF7 cell line compared with doxorubicin using MTT test

Al-khafaji

Arif

2018

AJPS

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Statins are effective to lower the cholesterol level and protect against cardiovascular disease. Recent studies showed that statins have pleiotropic effect and can be used to treat many types of diseases like neurodegenerative disorders, stroke, and cancer. Statins inhibit cell proliferation by suppression of mevalonate pathway leading to desregu-lation of cell signal transduction of some membrane receptor protein which is important for gene transcription. This study was done to evaluate the anti-proliferative activity of simvastatin and atorvastatin on MCF7 cell line alone and in combination with anathracycline chemotherapy drug (doxo-rubicin) using MTT assay. The results showed that simvastatin and atorvastatin had significant anti-proliferative effect on MCF7 cell line in dose-dependent manner with an IC50 10.10 μM and 12.3 μM respect-tively. Moreover, the combination of atorvastatin and simvastatin with (1 μM) doxorubicin had higher cytotoxic effect with an IC50 = 0.07 μM and 0.05μM respectively than doxoru-bicin alone IC50 = 1.9 μM. In conclusion, simvastatin and atorvastatin had anti-proliferative effect on MCF7 cell line and displayed significant synergism with doxorubicin which will help in enhancing efficacy of doxorubicin and decrease the adverse effect.

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Section: Discussionmentioning

confidence: 99%

Evaluation of anti-proliferative activity of simvastatin and atorvastatin on MCF7 cell line compared with doxorubicin using MTT test

Al-khafaji

Arif

2018

AJPS

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“…Statins are inhibitors of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMGCR), which is the rate-limiting enzyme in the melavonate pathway; a pathway producing a range of cell signalling molecules with the potential to regulate oncogenesis. This is supported by strong laboratory evidence that statins induce anticarcinogenic effects on cell proliferation and survival in various cell lines [1][2][3][4] , and reduce tumour growth in a range of in vivo models [5][6][7][8][9][10] .…”

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confidence: 82%

Predicting the effect of statins on cancer risk using genetic variants: a Mendelian randomization study in UK Biobank

Carter

Vithayathil

Kar

et al. 2020

Preprint

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Laboratory studies have suggested oncogenic roles of lipids, as well as anticarcinogenic effects of statins. We here assess the potential effect of statin therapy on cancer risk in Mendelian randomization analyses. We obtained genetic associations with the risk of overall and 22 site-specific cancers for 367,703 individuals in UK Biobank. In total, 75,037 individuals had a cancer event. Variants in the HMGCR gene region, which represent proxies for statin treatment, were associated with overall cancer risk (OR per 1 standard deviation increase in LDL-cholesterol 1.32, 95% CI 1.13-1.53, p=0.0003), but variants in gene regions representing alternative lipid-lowering treatment targets (PCSK9, LDLR, NPC1L1, APOC3, LPL) were not. Genetically-predicted LDL-cholesterol was not associated with overall cancer risk (OR 1.01, 95% CI 0.98-1.05, p=0.50). Our results predict that statins reduce cancer risk, but other lipid-lowering treatments do not. This suggests that statins reduce cancer risk through a cholesterol independent pathway.

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“…In addition to its cholesterol-lowering activities, fluvastatin has selective anti-cancer effects, such as the induction of tumor cell apoptosis in specific cancer cell lines (e.g., glioma and breast cancer cell lines) [5, 6]. Fluvastatin has also been suggested to have therapeutic potential for the treatment of HCC [7].…”

Section: Introductionmentioning

confidence: 99%

Synergistic anti-tumor efficacy of sorafenib and fluvastatin in hepatocellular carcinoma

et al. 2017

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Drug resistance to sorafenib is common in patients with hepatocellular carcinoma(HCC). We examined the effects of a combination of sorafenib and fluvastatin on HCC using in vitro and in vivo models. The dual treatment induced apoptosis and reduced cellular viability in HCC more effectively than either drug alone. The combination treatment also inhibited activation of hepatic stellate cells, whereas single drug treatments did not. On a molecular level, combined treatment inhibited activation of the MAPK and NF-κB pathways via Toll-like receptor 4 in HCC cells. Combined treatment also inhibited expression of stromal cell-derived factor 1α in HCC cells, which further inhibited the MAPK pathway in hepatic stellate cells. These results suggest that a combination of sorafenib and fluvastatin may be a promising therapeutic strategy for patients with advanced HCC.

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Fluvastatin inhibits growth and alters the malignant phenotype of the C6 glioma cell line

Cited by 37 publications

References 44 publications

Evaluation of anti-proliferative activity of simvastatin and atorvastatin on MCF7 cell line compared with doxorubicin using MTT test

Evaluation of anti-proliferative activity of simvastatin and atorvastatin on MCF7 cell line compared with doxorubicin using MTT test

Predicting the effect of statins on cancer risk using genetic variants: a Mendelian randomization study in UK Biobank

Synergistic anti-tumor efficacy of sorafenib and fluvastatin in hepatocellular carcinoma

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