Atorvastatin suppresses glioma invasion and migration by reducing microglial MT1-MMP expression

Yi, Yong-jun; Huang, Shuyun; Chen, Lei; Chen, Xiangrong; Yang, Zhen; Ke, Yiquan

doi:10.1016/j.jneuroim.2013.04.020

Cited by 45 publications

(53 citation statements)

References 27 publications

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“…These observations are comparable to recent studies in breast, liver, melanoma and lung cancer, showing promising anti-tumorigenic effects of statins on the growth of cancer in vitro and in vivo (19)(20)(21)(22)(23). Studies in other cancer cell types have also shown statins to have anti-metastatic effects such as inhibition of adhesion and invasion (24)(25)(26). Lastly, statin treatment has also been found to decrease metastatic burden in cancer mouse models (27,28).…”

Section: Discussionsupporting

confidence: 84%

Simvastatin, an HMG-CoA reductase inhibitor, exhibits antimetastatic and antitumorigenic effects in endometrial cancer

Stine

Schointuch

Zhou

et al. 2014

Gynecologic Oncology

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OBJECTIVE-Our goal was to evaluate the effects of simvastatin on endometrial cancer cell lines and primary cultures of endometrial cancer cells.METHODS-Cell proliferation in the ECC-1 and Ishikawa endometrial cancer cell lines and primary cultures of endometrial cancer cells was assessed by MTT assay. Apoptosis and cell cycle were detected by Annexin V assay and propidium iodide staining, respectively. Reactive oxygen species and cell adhesion were assessed using ELISA assays. Invasion was analyzed using a transwell invasion assay. Mitochondrial DNA damage was confirmed using qPCR. The effects of simvastatin on the AKT/mTOR and MAPK pathways were determined by Western blotting.RESULTS-Simvastatin inhibited cell proliferation in a dose-dependent manner in both endometrial cancer cell lines and 5/8 primary cultures of endometrial cancer cells. Simvastatin treatment resulted in G1 cell cycle arrest, a reduction in the enzymatic activity of HMG-CoA, induction of apoptosis as well as DNA damage and cellular stress. Treatment with simvastatin resulted in inhibition of the MAPK pathway and exhibited differential effects on the AKT/mTOR pathway in the ECC-1 and Ishikawa cells. Minimal change in AKT phosphorylation was seen in both cell lines. An increase in phosphorylated S6 was seen in ECC-1 and a decrease was seen in Ishikawa. Treatment with simvastatin reduced cell adhesion and invasion (p<0.01) in both cell lines. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access

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Section: Discussionsupporting

confidence: 84%

Simvastatin, an HMG-CoA reductase inhibitor, exhibits antimetastatic and antitumorigenic effects in endometrial cancer

Stine

Schointuch

Zhou

et al. 2014

Gynecologic Oncology

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“…Notably, minocycline is also able to reduce MCP-1 secretion by glioblastoma cells, thus potentially limiting GAMs' recruitment at tumor site (as discussed above). The same inhibitory effects on MT1-MMP were displayed in vitro by the lipid lowering agent, atorvastatin [77] . In addition, propentofylline, an atypical methylxanthine with central nervous system (CNS) glial modulating and antinflammatory actions, significantly reduced tumor growth by targeting microglial production of MMP-9.…”

Section: Drugs That Interfere With Matrix Remodeling Promoted By Gam-mentioning

confidence: 56%

Glioma associated microglia/macrophages, a potential pharmacological target to promote antitumor inflammatory immune response in the treatment of glioblastoma

Russo¹,

Cappoli²

2018

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Glioma associated microglia/macrophages (GAMs) constitute the largest proportion of glioma infiltrating cells, particularly in high grade tumors (i.e., glioblastoma). Once inside the tumors, GAMs usually acquire a specific phenotype of activation that favors tumor growth, angiogenesis and promotes the invasion of normal brain parenchyma. Therefore, treatments that limit or prevent GAMs' recruitment at the tumor site or modulate their immune activation promoting antitumor activities are expected to exert beneficial effects in glioblastoma. In the present paper, we aim at the revision of pharmacological strategies that interfere with GAMs' function and are currently proposed as an alternative/additional option to current approved cytotoxic regimens.

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“…In preclinical studies, statins have shown to synergize with antineoplastic drugs in different cancer cells, including GBM 45–52. Statins also reduced invasiveness and migration in glioma cells 53. In our recent investigation, inhibition of the mevalonate cascade by simvastatin boosted TMZ-induced apoptosis in GBM tumor cells, thereby highlighting the promising potential of statins in combination with TMZ on GBM (manuscript under revision).…”

Section: Statins and Gbm Cancer Therapymentioning

confidence: 84%

Statins: A New Approach to Combat Temozolomide Chemoresistance in Glioblastoma

Shojaei

Alizadeh

Thliveris

et al. 2018

Journal of Investigative Medicine

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Patients with glioblastoma multiforme (GBM) have an average life expectancy of approximately 15 months. Recently, statins have emerged as a potential adjuvant cancer therapy due to their ability to inhibit cell proliferation and induce apoptosis in many types of cancer. The exact mechanisms that mediate the inhibitory actions of statins in cancer cells are largely unknown. The purpose of this proceeding paper is to discuss some of the known anticancer effects of statins, while focusing on GBM therapy that includes adjunct therapy of statins with chemotherapeutic agents.

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Atorvastatin suppresses glioma invasion and migration by reducing microglial MT1-MMP expression

Cited by 45 publications

References 27 publications

Simvastatin, an HMG-CoA reductase inhibitor, exhibits antimetastatic and antitumorigenic effects in endometrial cancer

Simvastatin, an HMG-CoA reductase inhibitor, exhibits antimetastatic and antitumorigenic effects in endometrial cancer

Glioma associated microglia/macrophages, a potential pharmacological target to promote antitumor inflammatory immune response in the treatment of glioblastoma

Statins: A New Approach to Combat Temozolomide Chemoresistance in Glioblastoma

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