Inhibitory effect of statins on the proliferation of human breast cancer cells

Mück, A. O.; Seeger, Harald; Wallwiener, D.

doi:10.5414/cpp42695

Cited by 59 publications

(47 citation statements)

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“…In addition to their role in lowering cholesterol, the statin family of drugs has shown a broad range of functions including suppression of cancer cell growth in vitro and in vivo [9][10][11][12][13][14][15][16] in many cell types. Sur prisingly, the eVect of statins on ovarian cancer is limited to one study documenting lovastatin-induced growth inhibi tion [35].…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have revealed that statins inhibit certain can cer cell proliferation, invasion and migration in vitro and in vivo [9][10][11][12][13][14][15][16]. To determine the direct eVect of statins on ovarian cancer cells, we treated Hey 1B cells, a human ovarian carcinoma cell line, with lovastatin, a member of the statin family, at various doses for 48 h and the lova statin-induced Hey 1B cell death could be observed by a phase contrast microscope (Fig.1a).…”

Section: Statins Induce Apoptosis In Ovarian Cancer Cellsmentioning

confidence: 99%

“…The anticancer function of statins is based on preclinical evidence of their antiprolifer ative, pro-apoptotic and anti-invasive properties. Statins can induce apoptosis and inhibit proliferation in a variety of cancer cell types [9][10][11][12][13]. In vivo studies have revealed that statins can inhibit tumor cell growth, invasion and metasta sis [14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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Statins induce apoptosis in ovarian cancer cells through activation of JNK and enhancement of Bim expression

Liu

Liang

Kumar

et al. 2008

Cancer Chemother Pharmacol

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Purpose Ovarian cancer is the leading cause of death among all gynecological malignancies in Western coun tries. Although therapy for ovarian cancer has been greatly improved in the past 20 years, the overall survival for patients with advanced ovarian cancer has not changed sig niWcantly. The poor survival rates in patients with advanced ovarian cancer are due both to late diagnosis and to lack of eVective drugs for the majority of patients who have a relapse and develop resistance to current chemotherapy agents used for ovarian cancer. Thus, developing and dis covering eVective novel drugs with diVerent molecular structures from conventional chemotherapy agents have become an urgent clinical need.

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Section: Discussionmentioning

confidence: 99%

Section: Statins Induce Apoptosis In Ovarian Cancer Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Statins induce apoptosis in ovarian cancer cells through activation of JNK and enhancement of Bim expression

Liu

Liang

Kumar

et al. 2008

Cancer Chemother Pharmacol

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“…Additionally, several statins, including atrovastatin and fluvastatin, have proapoptotic functions within MCF-7 cells, suggesting that the statins, as a group, possess properties that may be beneficial in the treatment of breast cancer patients. 53 Interestingly, women taking statins have a 68% reduction in the risk of breast cancer. 40 Recently, work in SpragueDawley rats has demonstrated that atorvastatin treatment increases PTEN protein expression.…”

Section: Discussionmentioning

confidence: 99%

Increased PTEN expression due to transcriptional activation of PPARγ by Lovastatin and Rosiglitazone

Teresi

Shaiu

Chen

et al. 2006

Intl Journal of Cancer

107

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Germline mutations in the tumor suppressor gene PTEN (protein phosphatase and tensin homolog located on chromosome ten) predispose to heritable breast cancer. The transcription factor PPARc has also been implicated as a tumor suppressor pertinent to a range of neoplasias, including breast cancer. A putative PPARc binding site in the PTEN promoter indicates that PPARc may regulate PTEN expression. We show here that the PPARc agonist Rosiglitazone, along with Lovastatin, induce PTEN in a dose-and time-dependent manner. Lovastatin-or Rosiglitazoneinduced PTEN expression was accompanied by a decrease in phosphorylated-AKT and phosphorylated-MAPK and an increase in G1 arrest. We demonstrate that the mechanism of Lovastatin-and Rosiglitazone-associated PTEN expression was a result of an increase in PTEN mRNA, suggesting that this increase was transcriptionally-mediated. Compound-66, an inactive form of Rosiglitazone, which is incapable of activating PPARc, was unable to elicit the same response as Rosiglitazone, signifying that the Rosiglitazone response is PPARc-mediated. To support this, we show, using reporter assays including dominant-negative constructs of PPARc, that both Lovastatin and Rosiglitazone specifically mediate PPARc activation. Additionally, we demonstrated that cells lacking PTEN or PPARc were unable to induce PTEN mediated cellular events in the presence of Lovastatin or Rosiglitazone. These data are the first to demonstrate that Lovastatin can signal through PPARc and directly demonstrate that PPARc can upregulate PTEN at the transcriptional level. Since PTEN is constitutively active, our data indicates it may be worthwhile to examine Rosiglitazone and Lovastatin stimulation as mechanisms to increase PTEN expression for therapeutic and preventative strategies including cancer, diabetes mellitus and cardiovascular disease. ' 2006 Wiley-Liss, Inc.

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“…The in vitro effects of statins on cancer, cell cycle regulation (13)(14)(15) and apoptosis induction (16)(17)(18)(19) have been shown and cancer cell proliferation suppression has been confirmed (10)(11)(12). Statins also inhibit growth of cancer in vivo and reduce metastasis at clinical doses (20,21).…”

Section: Introductionmentioning

confidence: 99%

Statins induce apoptosis and inhibit proliferation in cholangiocarcinoma cells

Kamigaki

2011

Int J Oncol

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Abstract. Given the poor prognosis for cholangiocarcinoma, new and effective treatments are urgently needed. HMG-CoA reductase inhibitors (statins) reportedly exert anticancer effects in a variety of diseases, but there have been no reports of these effects in cholangiocarcinoma. In this study, we investigated the utility of statins for cholangiocarcinoma treatment. Proliferation suppression by pitavastatin and atorvastatin was investigated in the human cholangiocarcinoma cell lines HuCCT1 and YSCCC while changes in the cell cycle and intracellular signals were examined by FACS and Western blotting, respectively. Additive proliferation suppression by statins and pre-existing anticancer drugs was also investigated. HuCCT1 and YSCCC cell proliferation was dramatically suppressed by incubation with statins for 72 h or longer. Cell cycle analysis revealed a reduction in the G2M fraction and an increase in the sub-G1 fraction in statin-treated cells, while Western blotting showed increased levels of cleaved caspase-3 and a reduction in p-ERK. Furthermore, statins in combination with gemcitabine, cisplatin and 5-FU showed additive proliferation suppression. In this study, treatment of human cholangiocarcinoma cells with statins induced apoptosis via suppression of the classical MAPK pathway. Together, these results suggest that statins may be a new cholangiocarcinoma treatment option that could potentially enhance the anticancer effect of pre-existing anticancer drugs.

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Inhibitory effect of statins on the proliferation of human breast cancer cells

Cited by 59 publications

References 0 publications

Statins induce apoptosis in ovarian cancer cells through activation of JNK and enhancement of Bim expression

Statins induce apoptosis in ovarian cancer cells through activation of JNK and enhancement of Bim expression

Increased PTEN expression due to transcriptional activation of PPARγ by Lovastatin and Rosiglitazone

Statins induce apoptosis and inhibit proliferation in cholangiocarcinoma cells

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