Interleukin-18 enhances breast cancer cell migration via down-regulation of claudin-12 and induction of the p38 MAPK pathway

Yang, Yoolhee; Cheon, Soyoung; Jung, M.; Song, Seung‐Wan; Kim, Daejin; Kim, Hee Jung; Park, Hyun-Jeong; Bang, Sa Ik; Cho, Daeho

doi:10.1016/j.bbrc.2015.02.108

Cited by 71 publications

(53 citation statements)

References 26 publications

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“…Our studies are also in agreement with the previous studies demonstrating that Ang-(1-7) decreases the ERK signal transduction pathway in lung and prostate cancer cell growth arrest (10,16). A growing number of studies have shown that p38 MAPK-mediated cell migration and invasion (38)(39)(40)(41) pathways are involved in Ang II-stimulated migration of vascular adventitial fibroblasts in spontaneously hypertensive rats (42). A recent study demonstrated that the antimigration and anti-invasion effect of Ang-(1-7) was mediated through inactivation of the PI3K-Akt, p38 MAPK, and JNK signaling pathways (43).…”

Section: Discussionsupporting

confidence: 82%

Angiotensin-(1-7) Decreases Cell Growth and Angiogenesis of Human Nasopharyngeal Carcinoma Xenografts

Pei

Wan

Chen

et al. 2016

Molecular Cancer Therapeutics

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Angiotensin-(1-7) [Ang-(1-7)] is an endogenous, heptapeptide hormone acting through the Mas receptor (MasR), with antiproliferative and antiangiogenic properties. Recent studies have shown that Ang-(1-7) has an antiproliferative action on lung adenocarcinoma cells and prostate cancer cells. In this study, we report that MasR levels were significantly upregulated in nasopharyngeal carcinoma (NPC) specimens and NPC cell lines. Viral vector–mediated expression of Ang-(1-7) dramatically suppressed NPC cell proliferation and migration in vitro. These effects were completely blocked by the specific Ang-(1-7) receptor antagonist A-779, suggesting that they are mediated by the Ang-(1-7) receptor Mas. In this study, Ang-(1-7) not only caused a significant reduction in the growth of human nasopharyngeal xenografts, but also markedly decreased vessel density, suggesting that the heptapeptide inhibits angiogenesis to reduce tumor size. Mechanistic investigations revealed that Ang-(1-7) inhibited the expression of the proangiogenic factors VEGF and PlGF. Taken together, the data suggest that upregulation of MasR could be used as a diagnostic marker of NPC and Ang-(1-7) may be a novel therapeutic agent for nasopharyngeal cancer therapy because it exerts significant antiangiogenic activity. Mol Cancer Ther; 15(1); 37–47. ©2015 AACR.

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Section: Discussionsupporting

confidence: 82%

Angiotensin-(1-7) Decreases Cell Growth and Angiogenesis of Human Nasopharyngeal Carcinoma Xenografts

Pei

Wan

Chen

et al. 2016

Molecular Cancer Therapeutics

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“…46 Inhibition of ERK phosphorylation by PD98059, a specific inhibitor of the upstream kinase MEK, blocked cell migration in a concentration-dependent manner. 39,47 …”

Section: Resultsmentioning

confidence: 99%

Phytochemicals potently inhibit migration of metastatic breast cancer cells

et al. 2015

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Cell migration is a major process that drives metastatic progression of cancers, the major cause of cancer death. Existing chemotherapeutic drugs have limited efficacy to prevent and/or treat metastasis, emphasizing the need for new treatments. We focus on triple negative breast cancer (TNBC), the subtype of breast cancer with worst prognosis and no standard chemotherapy protocols. Here we demonstrate that a group of natural compounds, known as phytochemicals, effectively block migration of metastatic TNBC cells. Using a novel cell micropatterning technology, we generate consistent migration niches in standard 96-well plates where each well contains a cell-excluded gap within a uniform monolayer of cells. Over time, cells migrate into and occupy the gap. Treating TNBC cells with non-toxic concentrations of phytochemicals significantly blocks motility of cells. Using a molecular analysis approach, we show that anti-migratory property of phytochemicals is partly due to their inhibitory effects on phosphorylation of ERK1/2. This study provides a framework for future studies to understand molecular targets of phytochemicals and evaluate their effectiveness in inhibiting metastasis in animal models of cancer.

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“…Another study suggests that IL-18 enhances breast cancer cell migration (Yang et al 2015). Due to a potential role of IL-18 in cancer progression and metastasis, an IL18BP-Fc has been developed to antagonize the effects of IL-18 (Cao et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Physical Confirmation and Comparative Genomics of the RatMammary carcinoma susceptibility 3Quantitative Trait Locus

Martin

Samuelson

2017

G3 Genes|Genomes|Genetics

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Human breast and rat mammary cancer susceptibility are complex phenotypes where complete sets of risk associated loci remain to be identified for both species. We tested multiple congenic rat strains to physically confirm and positionally map rat Mammary carcinoma susceptibility 3 (Mcs3)—a mammary cancer resistance allele previously predicted at Rattus norvegicus chromosome 1 (RNO1). The mammary cancer susceptible Wistar Furth (WF) strain was the recipient, and the mammary cancer resistant Copenhagen (Cop) strain was the RNO1-segment donor for congenics. Inbred WF females averaged 6.3 carcinogen-induced mammary carcinomas per rat. Two WF.Cop congenic strains averaged 2.8 and 3.4 mammary carcinomas per rat, which confirmed Mcs3 as an independently acting allele. Two other WF.Cop congenic strains averaged 6.6 and 8.1 mammary carcinomas per rat, and, thus, did not contain Mcs3. Rat Mcs3 was delimited to 27.8 Mb of RNO1 from rs8149408 to rs105131702 (RNO1:143700228-171517317 of RGSC 6.0/rn6). Human genetic variants with p values for association to breast cancer risk below 10−7 had not been reported for Mcs3 orthologous loci; however, human variants located in Mcs3-orthologous regions with potential association to risk (10−7 < p < 10−3) were listed in some population-based studies. Further, rat Mcs3 contains sequence orthologous to human 11q13/14—a region frequently amplified in female breast cancer. We conclude that Mcs3 is an independently acting mammary carcinoma resistance allele. Human population-based, genome-targeted association studies interrogating Mcs3 orthologous loci may yield novel breast cancer risk associated variants and genes.

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Interleukin-18 enhances breast cancer cell migration via down-regulation of claudin-12 and induction of the p38 MAPK pathway

Cited by 71 publications

References 26 publications

Angiotensin-(1-7) Decreases Cell Growth and Angiogenesis of Human Nasopharyngeal Carcinoma Xenografts

Angiotensin-(1-7) Decreases Cell Growth and Angiogenesis of Human Nasopharyngeal Carcinoma Xenografts

Phytochemicals potently inhibit migration of metastatic breast cancer cells

Physical Confirmation and Comparative Genomics of the RatMammary carcinoma susceptibility 3Quantitative Trait Locus

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