Matrix Metalloproteinases Shape the Tumor Microenvironment in Cancer Progression

Niland, Stephan; Riscanevo, Andrea Ximena; Eble, Johannes A.

doi:10.3390/ijms23010146

Cited by 183 publications

(150 citation statements)

References 511 publications

(676 reference statements)

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“…They do this by using MMP that degrade the ECM. Especially considering that MMPs are inflammation markers, their effect on the cancerization process is inevitable 12 . Metformin, which is used as a type 2 diabetes treatment agent, has been known to slow down and sometimes stop carcinogenesis in recent years 13 .…”

Section: Discussionmentioning

confidence: 99%

A direct bridge to metformin and matrix metalloproteinase relationship in prostate cancer model: oxidative stress

Aydın

2022

Cukurova Medical Journal

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Öz Purpose:The purpose of the study was to evaluate the effect of metformin as well as the possible role of Matrix metalloproteinase2 (MMP2) and oxidative stress parameters on the prostate cancer model. Materials and Methods: Male Copenhagen rats were divided into three groups. Control group, cancer group, cancer+metformin (CM) group. 2x104 Mat-LyLu cells were inoculated subcutaneously to generate prostate cancer. Metformin treatment was administered daily by gavage following inoculation of the Mat-Lylu cells. The experiment was terminated on the 14th day following Mat-LyLu cell injection. Serum glutathione (GSH), prostatespecific antigen (PSA), and malondialdehyde (MDA) levels were determined by employing the Enzyme-Linked ImmunoSorbent Assay (ELISA) method. In addition, the serum matrix metalloproteinase (MMP) 2 activities were determined via ELISA. Results: GSH was significantly increased in the CM group than in the cancer group. PSA, MDA and MMP2 were significantly lower in the CM group than in the cancer group. Oxidative stress parameters were significantly higher in the cancer group. Metformin reversed cancer's effect in GSH, PSA, MDA, and MMP2 parameters. Conclusion: Prostate cancer model caused a detrimental effect on MMP and oxidative stress parameters, and metformin administration ameliorated the changes caused by cancer. Metformin showed its mechanism of action by inhibiting free radical products originating from prostate cancer and changing the antioxidant capacity. Metformin is a candidate to be a potential anticancer drug in the therapeutic cancer treatment process.

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Section: Discussionmentioning

confidence: 99%

A direct bridge to metformin and matrix metalloproteinase relationship in prostate cancer model: oxidative stress

Aydın

2022

Cukurova Medical Journal

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“…Biologically, tumor cells, CAFs, macrophages (TAM and M2), and CAAs are involved in the degradation of the ECM by MMP secretion [ 37 , 108 , 109 , 110 , 112 , 113 , 114 , 115 ]. MMPs are proteolytic enzymes that destroy the ECM surrounding the tumor, allowing tumor cells to escape the primary tumor and invade the surrounding tissue, thus enhancing metastases [ 84 , 113 , 116 , 117 ]. MMPs are normally secreted as zymogens (inactive) and activated in the extracellular space [ 118 ].…”

Section: Degradation Of Ecm and Metastasesmentioning

confidence: 99%

“…In addition, within the tumor’s protective cells, macrophages are converted to immunosuppressive macrophages of TAM type M2. The different phenotypes of these two macrophages depend on their different markers, gene expression profiles of metabolic properties and microbial signals that represent macrophage polarization [ 113 , 114 , 115 , 182 , 185 , 217 , 225 , 226 , 227 , 228 , 229 , 230 , 231 ]. Well-stimulated macrophages can kill tumor cells.…”

Section: Macrophage Polarizationmentioning

confidence: 99%

“…TAM improves vascular angiogenesis and metastasis [ 14 , 15 , 89 , 90 , 280 ]. It is also involved in the degradation of ECM by the secretion of MMP-2 and MMP-9 [ 113 , 114 , 115 ] ( Table 1 ), which depicts the importance of ECM and macrophages in the progression of cancer [ 281 , 282 ]. TAM has several partially conflicting activities, both inflammatory and anti-inflammatory, immunostimulatory, anti-immunosuppressive, and tissue-destroying anti-anabolic effects [ 19 , 283 , 284 , 285 , 286 , 287 , 288 , 289 , 290 , 291 , 292 , 293 ].…”

Section: Macrophage Polarizationmentioning

confidence: 99%

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The Impact of Obesity, Adipose Tissue, and Tumor Microenvironment on Macrophage Polarization and Metastasis

Habanjar

Diab‐Assaf

Caldefie-Chézet

et al. 2022

Biology

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Tumor metastasis is a major cause of death in cancer patients. It involves not only the intrinsic alterations within tumor cells, but also crosstalk between these cells and components of the tumor microenvironment (TME). Tumorigenesis is a complex and dynamic process, involving the following three main stages: initiation, progression, and metastasis. The transition between these stages depends on the changes within the extracellular matrix (ECM), in which tumor and stromal cells reside. This matrix, under the effect of growth factors, cytokines, and adipokines, can be morphologically altered, degraded, or reorganized. Many cancers evolve to form an immunosuppressive TME locally and create a pre-metastatic niche in other tissue sites. TME and pre-metastatic niches include myofibroblasts, immuno-inflammatory cells (macrophages), adipocytes, blood, and lymphatic vascular networks. Several studies have highlighted the adipocyte-macrophage interaction as a key driver of cancer progression and dissemination. The following two main classes of macrophages are distinguished: M1 (pro-inflammatory/anti-tumor) and M2 (anti-inflammatory/pro-tumor). These cells exhibit distinct microenvironment-dependent phenotypes that can promote or inhibit metastasis. On the other hand, obesity in cancer patients has been linked to a poor prognosis. In this regard, tumor-associated adipocytes modulate TME through the secretion of inflammatory mediators, which modulate and recruit tumor-associated macrophages (TAM). Hereby, this review describes the cellular and molecular mechanisms that link inflammation, obesity, and cancer. It provides a comprehensive overview of adipocytes and macrophages in the ECM as they control cancer initiation, progression, and invasion. In addition, it addresses the mechanisms of tumor anchoring and recruitment for M1, M2, and TAM macrophages, specifically highlighting their origin, classification, polarization, and regulatory networks, as well as their roles in the regulation of angiogenesis, invasion, metastasis, and immunosuppression, specifically highlighting the role of adipocytes in this process.

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“…The degradation of basement membrane and extracellular matrix (ECM) structures are essential features of invasion and metastasis in gastric cancer. In this regard, heparanase activity plays a decisive role in tumor cell dissemination associated with the metastatic process and promotes tumor growth, angiogenesis, and metastasis [ 5 , 6 , 7 , 8 ]. Additionally, several matrix metalloproteinases (MMPs) participate in the proteolytic degradation of the ECM during the cancer invasion processes [ 2 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Decreases the Invasion Potential of Gastric Cancer Cells

et al. 2022

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The cancer-preventive agent Resveratrol (RSV) [3,5,4′-trihydroxytrans-stilbene] is a widely recognized antioxidant molecule with antitumoral potential against several types of cancers, including prostate, hepatic, breast, skin, colorectal, and pancreatic. Herein, we studied the effect of RSV on the cell viability and invasion potential of gastric cancer cells. AGS and MKN45 cells were treated with different doses of RSV (0–200 μM) for 24 h. Cell viability was determined using the Sulphorhodamine B dye (SRB) assay. For invasion assays, gastric cells were pre-treated with RSV (5–25 μM) for 24 h and then seeded in a Transwell chamber with coating Matrigel. The results obtained showed that RSV inhibited invasion potential in both cell lines. Moreover, to elucidate the mechanism implicated in this process, we analyzed the effects of RSV on SOD, heparanase, and NF-κB transcriptional activity. The results indicated that RSV increased SOD activity in a dose-dependent manner. Conversely, RSV significantly reduced the DNA-binding activity of NF-κB and the enzymatic activity of heparanase in similar conditions, which was determined using ELISA-like assays. In summary, these results show that RSV increases SOD activity but decreases NF-kB transcriptional activity and heparanase enzymatic activity, which correlates with the attenuation of invasion potential in gastric cancer cells. To our knowledge, no previous study has described the effect of RSV on heparanase activity. This article proposes that heparanase could be a key effector in the invasive events occurring during gastric cancer metastasis.

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Matrix Metalloproteinases Shape the Tumor Microenvironment in Cancer Progression

Cited by 183 publications

References 511 publications

A direct bridge to metformin and matrix metalloproteinase relationship in prostate cancer model: oxidative stress

A direct bridge to metformin and matrix metalloproteinase relationship in prostate cancer model: oxidative stress

The Impact of Obesity, Adipose Tissue, and Tumor Microenvironment on Macrophage Polarization and Metastasis

Resveratrol Decreases the Invasion Potential of Gastric Cancer Cells

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