2013
DOI: 10.1371/journal.pone.0062823
|View full text |Cite
|
Sign up to set email alerts
|

Simvastatin Inhibits Renal Cancer Cell Growth and Metastasis via AKT/mTOR, ERK and JAK2/STAT3 Pathway

Abstract: Renal cell carcinoma (RCC) is the most lethal type of genitourinary cancer due to its occult onset and resistance to chemotherapy and radiation. Recently, accumulating evidence has suggested stains, inhibitors of 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase, were associated with the risk reduction of cancer. In the present study, we aimed to investigate the potential effects of simvastatin on RCC cells and the underlying mechanisms by which simvastatin exerted its actions. With cell viability, co… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
2

Citation Types

8
98
1
1

Year Published

2013
2013
2024
2024

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 125 publications
(110 citation statements)
references
References 55 publications
8
98
1
1
Order By: Relevance
“…In addition, our results showed that simvastatin decreased CCL17-induced HT-29 cell migration without any concomitant effects on cell proliferation of apoptosis, indicating a direct effect of simvastatin on colon cancer cell migration, which might be of beneficial value. Although this is the first report to show that simvastatin inhibits colon cancer cell migration in response to chemokine signaling, other investigations 11 have found that simvastatin can inhibit migration of breast [21], hepatic [22], renal [17] and prostate [23] cancer cells, supporting the concept that simvastatin is an effective inhibitor of tumor cell migration.…”
Section: Role Of Hmg-coa Reductase and Geranygeranylation In Cell Migsupporting
confidence: 58%
See 1 more Smart Citation
“…In addition, our results showed that simvastatin decreased CCL17-induced HT-29 cell migration without any concomitant effects on cell proliferation of apoptosis, indicating a direct effect of simvastatin on colon cancer cell migration, which might be of beneficial value. Although this is the first report to show that simvastatin inhibits colon cancer cell migration in response to chemokine signaling, other investigations 11 have found that simvastatin can inhibit migration of breast [21], hepatic [22], renal [17] and prostate [23] cancer cells, supporting the concept that simvastatin is an effective inhibitor of tumor cell migration.…”
Section: Role Of Hmg-coa Reductase and Geranygeranylation In Cell Migsupporting
confidence: 58%
“…4). anti-tumoral effects [17]. For example, previous studies have shown that statins, such as simvastatin, are powerful inhibitors of colon cancer cell proliferation [18].…”
Section: Role Of Hmg-coa Reductase and Geranygeranylation In Cell Migmentioning
confidence: 99%
“…In addition, JNK is selectively activated in ccRCC specimens and, induces epithelial-mesenchymal transition, suggesting that JNK represents a novel molecular target that is selectively activated in and drives the growth of ccRCCs (46). In addition to previously reported anticancer effects of combined sorafenib and ERK inhibitor or simvastatin treatment suppressing Akt or ERK signaling pathway (47,48), our findings can serve as the preclinical foundation for a combination targeting both the Tpl2/MEK/ERK and JNK pathways and the Ras/Raf/MEK/ERK pathway may lead to new therapeutic intervention strategies for ccRCC.…”
Section: Discussionmentioning
confidence: 84%
“…However, one recent metaanalysis suggested that there was no association between statin use and the risk of renal cancer (33). Regarding the mechanisms underlying the anticancer effects of simvastatin in renal cancer in vitro, Fang et al reported that simvastatin inhibited the protein kinase B (AKT)/mammalian target of rapamycin (mTOR), extracellular signal-regulated kinase (ERK), and Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathways (7). In the present study, we confirmed that simvastatin inhibited Caki-1 cell proliferation in vitro.…”
Section: Discussionmentioning
confidence: 99%