Extracellular Matrix Protein Laminin Induces Matrix Metalloproteinase-9 in Human Breast Cancer Cell Line MCF-7

Pal, Samares; Moulik, Shuvojit; Dutta, Anindita; Chatterjee, Amitava

doi:10.1007/s12307-014-0146-6

Cited by 23 publications

(18 citation statements)

References 33 publications

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“…The extracellular matrix can be destroyed by matrix metalloproteinases, which is the key process of cancer metastasis (25). In pancreatic cancer, Glut1 may promote the expression of MMP2 and enhance MIAPaCa-2 and PANC-1 cell invasion (26).…”

Section: Discussionmentioning

confidence: 99%

High-concentration glucose enhances invasion in invasive ductal breast carcinoma by promoting Glut1/MMP2/MMP9 axis expression

et al. 2017

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Abstract. Type 2 diabetes mellitus (T2DM) has been considered to be a risk factor for numerous human cancers. Hyperglycemia is one of the most direct internal environmental changes for patients with T2DM. Increasing evidence reveals that a high concentration of glucose can promote tumor progression, while its role for migration and invasion of invasive ductal breast carcinoma (IDBC) cells remains unclear. In the present study, it was demonstrated that IDBC patients with T2DM suffered an increased tumor size and more frequent lymphatic and distant metastasis compared with those without T2DM (P<0.05). MCF-7 breast carcinoma cells, which were cultured in a high glucose concentration medium (25.00 mM), exhibited increased invasion (P<0.05). In addition, the expression of glucose transporters (Gluts), matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9) in IDBC tissues with T2DM was significantly higher compared to those without T2DM. Downregulation of glucose transporter 1 (Glut1) by small interfering RNA may markedly suppress MCF-7 cell invasion as well as the expression of MMP2 and MMP9. These results suggest that T2DM can affect the malignant features of tumors in IDBC. The high glucose concentration in the tumor microenvironment may enhance IDBC invasion via upregulating Glut1/MMP2/MMP9 axis expression.

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Section: Discussionmentioning

confidence: 99%

High-concentration glucose enhances invasion in invasive ductal breast carcinoma by promoting Glut1/MMP2/MMP9 axis expression

et al. 2017

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“…Upregulation of ERK signaling has been identified to contribute to the development and progression of various human malignancies including gastric cancer (23)(24)(25)(26). MMP-9 additionally serves a critical role in the regulation of cancer cell invasion through degradation of the extracellular matrix and promotion of cancer metastasis (27)(28)(29).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-29a inhibits cell migration and invasion via targeting Roundabout homolog 1 in gastric cancer cells

Liu

Cai

Sun

et al. 2015

Molecular Medicine Reports

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Abstract. Deregulation of Roundabout homolog 1 (Robo1) has been demonstrated to be associated with several types of human cancer, including gastric cancer. However, the detailed role of Robo1 and its regulatory mechanism in gastric cancer remain largely unclear. In the current study, it was demonstrated that the expression of microRNA (miR)-29a was frequently reduced in gastric cancer tissues, compared with their matched normal adjacent tissues. Similar results were additionally observed in AGS and SGC-7901 human gastric cancer cells. Overexpression of miR-29a led to reduced migration and invasion of AGS cells. To explore the targets of miR-29a in gastric cancer, bioinformatics analysis was conducted and Robo1 was identified as a putative target of miR-29a. Further western blotting and luciferase activity assay data confirmed that miR-29a was able to negatively regulate the protein expression of Robo1, through directly binding to the 3'-untranslated region of Robo1 mRNA in gastric cancer cells. In addition, it was demonstrated that Robo1 was frequently upregulated in gastric cancer tissues compared with their matched adjacent normal tissues, and a significant inverse correlation was identified between miR-29a and Robo1 expression. In addition, knockdown of Robo1 by small interfering RNA markedly inhibited the migratory and invasive capabilities of AGS cells, which the results obtained with overexpression of miR-29a. In conclusion, to the best of our knowledge the current study suggested for the first time, that miR-29a inhibits migration and invasion in part via direct inhibition of Robo1 in gastric cancer cells. Therefore, Robo1 and miR-29a may serve as diagnostic or therapeutic targets for gastric cancer.

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“…Specific ECM proteins have been reported to induce morphological changes in MCF-7 cells, triggering EMT [12,13,23,[29][30][31]. The time of treatment has been reported to be critical for inducing EMT, varying with the stimulus.…”

Section: Interaction With Mda-ecm Induced Emt-associated Changes In Mmentioning

confidence: 99%

Extracellular Matrix Derived from High Metastatic Human Breast Cancer Triggers Epithelial-Mesenchymal Transition in Epithelial Breast Cancer Cells through αvβ3 Integrin

Brandão-Costa

Helal-Neto

Vieira

et al. 2020

IJMS

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Alterations in the composition and architecture of the extracellular matrix (ECM) can influence cancer growth and dissemination. During epithelial-mesenchymal transition (EMT), epithelial cells assume a mesenchymal cell phenotype, changing their adhesion profiles from cell-cell contacts to cell-matrix interactions, contributing to metastasis. Breast cancer cells present at different stages of differentiation, producing distinct ECMs in the same tumor mass. However, the contribution of ECM derived from metastatic tumor cells to EMT is unclear. Here, we showed the mechanisms involved in the interaction of MCF-7, a low-metastatic, epithelial breast cancer cell line, with the ECM produced by a high metastatic breast tumor cell, MDA-MB-231 (MDA-ECM). MDA-ECM induced morphological changes in MCF-7 cells, decreased the levels of E-cadherin, up-regulated mesenchymal markers, and augmented cell migration. These changes were accompanied by the activation of integrin-associated signaling, with increased phosphorylation of FAK, ERK, and AKT and activation canonical TGF-β receptor signaling, enhancing phosphorylation of SMAD2 and SMAD4 nuclear translocation in MCF-7 cells. Treatment with Kistrin (Kr), a specific ligand of integrin αvβ3 EMT induced by MDA-ECM, inhibited TGF-β receptor signaling in treated MCF-7 cells. Our results revealed that after interaction with the ECM produced by a high metastatic breast cancer cell, MCF-7 cells lost their characteristic epithelial phenotype undergoing EMT, an effect modulated by integrin signaling in crosstalk with TGF-β receptor signaling pathway. The data evidenced novel potential targets for antimetastatic breast cancer therapies.During metastasis, tumor epithelial cells must acquire a migratory profile assuming a mesenchymal phenotype. The epithelial to mesenchymal transition (EMT) encompasses a well-coordinated series of molecular changes that lead epithelial cells to lose E-cadherin expression, acquire increased vimentin, fibronectin, and N-cadherin expression, and rearrange cortical actin structures, increasing their migratory capacity, characteristics of mesenchymal cells [5,6]. Considered the main inductor of EMT in tumor cells, TGF-β-through the activation of their receptors-regulates two different pathways. The non-canonical pathway is related to the activation of focal adhesion kinase (FAK), ERK/MAPK, and AKT signaling. While the canonical pathway is initiated by the phosphorylation of the cytoplasmic signaling molecules, SMAD2 is followed by recruitment and activation of R-SMAD (SMAD3 associated with SMAD2). This complex is phosphorylated and then associates with SMAD4 through the MH2 domain, triggering its translocation to the nucleus. These two signaling pathways regulate the transcription of different genes that culminate in the characteristic morphological and functional changes of EMT [7,8].The crosstalk between TGF-β receptors and other receptors, such as integrin, can modulate EMT in different cell types [9]. Integrins are transmembrane adhesive receptors that are ab...

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Extracellular Matrix Protein Laminin Induces Matrix Metalloproteinase-9 in Human Breast Cancer Cell Line MCF-7

Cited by 23 publications

References 33 publications

High-concentration glucose enhances invasion in invasive ductal breast carcinoma by promoting Glut1/MMP2/MMP9 axis expression

High-concentration glucose enhances invasion in invasive ductal breast carcinoma by promoting Glut1/MMP2/MMP9 axis expression

MicroRNA-29a inhibits cell migration and invasion via targeting Roundabout homolog 1 in gastric cancer cells

Extracellular Matrix Derived from High Metastatic Human Breast Cancer Triggers Epithelial-Mesenchymal Transition in Epithelial Breast Cancer Cells through αvβ3 Integrin

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