Insulin Promotes Proliferation and Migration of Breast Cancer Cells through the Extracellular Regulated Kinase Pathway

Pan, Feng; Hong, Li-quan

doi:10.7314/apjcp.2014.15.15.6349

Cited by 22 publications

(14 citation statements)

References 28 publications

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“…MAPK is one of the protein kinases which can be stimulated in many kinds of cancer cells and related to tumorigenesis [10][11][12][13]. Smallmolecule inhibitors targeted MAPK have been wildly used for cancer therapeutics as a biologically viable model.…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that ERK1/2 acts as nearly 180 different molecules targets and regulates several diverse cellular functions such as cell growth, cell cycle, proliferation, cell death, cell apoptosis, cell adhesion and transcription [9]. In fact, the ERK1/2 plays the above roles in various cancers, such as breast cancer [10], colorectal cancer [11], prostate cancer [12] and lung cancer [13]. However, not all references support the role of activated ERKs in promoting tumorigenesis, and result consistent with the role in tumor suppression has been reported as well [14].…”

Section: Introductionmentioning

confidence: 99%

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ERK1/2 promoted proliferation and inhibited apoptosis of human cervical cancer cells and regulated the expression of c-Fos and c-Jun proteins

et al. 2015

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Small-molecule inhibitors targeted MAPK have been wildly used for some cancer therapeutics as a biologically viable model, but no one has been used for cervical caner. ERK1/2, one of MAPK kinases, is expressed high in cervical cancer tissue. The aim of the present study was to evaluate the effects of ERK1/2 inhibitor U0126 on proliferation and apoptosis of cervical cancer cells and appraise the correlated mechanism of the effects. In this study, the cell proliferation of Hela and C33A cervical cancer cells was tested by Cell Counting Kit-8 (CCK8) assay and cell counting after treated with ERK1/2 inhibitor U0126. The cell cycle and apoptosis were evaluated by flow cytometry (FCM). The protein levels of ERK1/2 and c-Fos and c-Jun were detected by Western blot. The results indicated that after down-regulating ERK1/2 proteins with the inhibitor U0126, Hela and C33A cells proliferation was inhibited, cell apoptosis was promoted, the proportions of G0/G1 stage in cell cycle increased, and G2/M stages decreased. After down-regulating ERK1/2 proteins of Hela and C33A cells, the expression levels of p-c-Fos protein decreased, while p-c-Jun protein increased. The results of this study indicated that ERK1/2 may promote the development of cervical cancer cells, suggesting ERK1/2 inhibitor may be used as an effective target for cervical cancer therapies working for. It might inhibit cervical cancer cells growth via regulating the transcription factors expression of c-Fos and c-Jun.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ERK1/2 promoted proliferation and inhibited apoptosis of human cervical cancer cells and regulated the expression of c-Fos and c-Jun proteins

et al. 2015

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“…By binding to IRs, insulin enhances the proliferation and migration of MCF-7 via extracellular signal-regulated kinase (ERK) signaling in vivo and in vitro (14,15). Consistent with this, the present results showed that the level of phosphorylated IRs was increased in MSC-pretreated human breast cancer MDA-MB-231 cells, without significant alteration in the level of phosphorylated insulin-like growth factor 1 receptors (IGF-1Rs) and the subsequent c-Jun N-terminal kinase (JNK) activation, thus enhancing cell proliferative and migratory abilities.…”

Section: Discussionmentioning

confidence: 99%

Mesenchymal stem cell-conditioned medium promotes MDA-MB-231 cell migration and inhibits A549 cell migration by regulating insulin receptor and human epidermal growth factor receptor 3 phosphorylation

Li¹,

Zhou²,

Di³

et al. 2017

Oncology Letters

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Various in vitro and in vivo studies have linked mesenchymal stem cells (MSCs) with cancer, but little is known about the effect of MSCs on tumor progression. The present study aimed to analyze the role of the MSCs from different tissues, consisting of human bone marrow, adipose and the umbilical cord tissues, and the heterogeneity of tumors in tumor progression. By collecting the culture supernatants of MSCs as MSC-conditioned media (CMs), the present study found that MSC-CM produces no significant effect on the proliferation of MDA-MB-231 and A549 tumor cells. The migration of MDA-MB-231 cells was enhanced upon incubation with MSC-CM, while that of A549 cells was inhibited. Furthermore, the phosphorylation of insulin receptors (IRs) was upregulated in MSC-CM-treated MDA-MB-231 cells, while in MSC-CM-treated A549 cells, the phosphorylation of human epidermal growth factor receptor 3 (Her3) was downregulated. Taken together, the findings suggest that the phosphorylation of IR and Her3 may contribute to the discrepant effects of MSC-CM on the migration of the 2 cell lines.

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“…Besides, there exist other studies revealing the crosstalk between MLCK and ERK1/2 in the process of cell migration (Zhou et al, 2008). ERK1/2, one of MAPKs signal cascade, is known as a prominent signal pathway in cell proliferation and differentiation (Pan et al, 2014;Zhu et al, 2014a). Whereas the detailed mechanisms of ERK1/2 together with MLCK in cell migration are unclear.…”

Section: Discussionmentioning

confidence: 99%

A Novel All-trans Retinoid Acid Derivative N-(3-trifluoromethyl-phenyl)-Retinamide Inhibits Lung Adenocarcinoma A549 Cell Migration through Down-regulating Expression of Myosin Light Chain Kinase

Fan

Cheng²,

Wang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Insulin Promotes Proliferation and Migration of Breast Cancer Cells through the Extracellular Regulated Kinase Pathway

Abstract: The present study was undertaken to determine the roles of insulin in the growth of transplanted breast cancer in nude mice, and the proliferation and migration of MCF-7 human breast cancer cells and assess its influence on downstream signaling pathways.

Cited by 22 publications

References 28 publications

ERK1/2 promoted proliferation and inhibited apoptosis of human cervical cancer cells and regulated the expression of c-Fos and c-Jun proteins

ERK1/2 promoted proliferation and inhibited apoptosis of human cervical cancer cells and regulated the expression of c-Fos and c-Jun proteins

Mesenchymal stem cell-conditioned medium promotes MDA-MB-231 cell migration and inhibits A549 cell migration by regulating insulin receptor and human epidermal growth factor receptor 3 phosphorylation

A Novel All-trans Retinoid Acid Derivative N-(3-trifluoromethyl-phenyl)-Retinamide Inhibits Lung Adenocarcinoma A549 Cell Migration through Down-regulating Expression of Myosin Light Chain Kinase

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