Differential expression of Low density lipoprotein Receptor–related Protein 1 (LRP-1) and matrix metalloproteinase-9 (MMP-9) in prostate gland: From normal to malignant lesions

Gilardoni, Mónica Beatriz; Remedi, María Mónica; Oviedo, Mabel; Dellavedova, Tristán; Sarria, Juan Pablo; Racca, Laura; Dominguez, Mariana; Pellizas, Claudia G.; Donadío, Ana Carolina

doi:10.1016/j.prp.2016.11.008

Cited by 11 publications

(15 citation statements)

References 33 publications

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“…In addition, the increased expression of MMP2 in tumor and stromal cells was also related to tumor progression and metastasis in prostate cancer (34). In agreement, we also reported a higher and significant proMMP9 activity in human whole prostate cancer tissues compared with proMMP9 activity in benign prostatic hyperplasia (35).…”

Section: Discussionsupporting

confidence: 87%

Thyroid tumor cells-fibroblasts crosstalk: role of extracellular vesicles

Bravo-Miana

Vedova

Paul

et al. 2020

Endocrine Connections

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Tumor-stroma crosstalk leads to a tumor-promoting microenvironment. In this milieu, extracellular vesicles (EVs) are protagonists in cell-cell communication. Despite thyroid cancer being the most common endocrine malignancy, the contribution of the tumor microenvironment to thyroid cancer progression is still largely underexplored. We focused on the role of thyroid tumor cell-fibroblast interaction and EVs as mediators of tumor-stroma interplay, in the promotion of thyroid tumor aggressiveness. Thyroid tumor (TPC-1, 8505c) or non-tumor thyroid cells (NThyOri) were co-cultured with human fibroblasts (Fb). Thyroid cell migration was investigated by the wound-healing assay and actin-network staining. Cell-CD147 expression was characterized by flow cytometry. EVs, obtained by ultracentrifugation of conditioned media (CMs), were characterized by transmission electron-microscopy and CD81 and CD147 expression. Metalloproteinases (MMPs) were evaluated by zymography in CMs. A migratory phenotype was triggered in thyroid tumor cells treated with CMs from Fb or from Fb-thyroid tumor cell co-cultures. Fb-thyroid cell co-cultures induced the secretion of proMMP9 and proMMP2 and led to a significant MMP2 activation in CMs. Fb, thyroid cells and Fb-thyroid cell co-cultures released EVs, and remarkably, EVs released by Fb-thyroid tumor cell co-cultures induced the secretion of proMMP2 and the expression of MMP2 from normal Fb. A significant CD147 expression was demonstrated in Fb-thyroid tumor cell-derived EVs. These findings reveal the role of Fb and thyroid tumor cell-Fb interaction in the promotion of a microenvironment suitable for thyroid tumor progression. Moreover, they highlight, for the first time, the role of thyroid tumor cell-Fb interaction in the production of specialized EVs.

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Section: Discussionsupporting

confidence: 87%

Thyroid tumor cells-fibroblasts crosstalk: role of extracellular vesicles

Bravo-Miana

Vedova

Paul

et al. 2020

Endocrine Connections

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“…These results also support the notion that TβR-V acts as a tumor suppressor gene which causes cancer when it is inactivated or turned off (7). This notion is also supported by the recent findings that primary tumors from a few hundred human patients with liver, prostate and colon cancers in China, Argentina and France, respectively, exhibit loss or very low levels of LRP-1 (TβR-V) expression (16)(17)(18). Understanding of the mechanisms whereby the TβR-V mediates growth inhibition (tumor suppressor) signaling stimulated by IGFBP-3 and TGF-β should be important to elucidate the molecular basis of IGFBP-3 and TGF-β actions and to understand their roles in human cancers (19,20).…”

Section: Accepted Articlesupporting

confidence: 83%

IGFBP‐3 and TGF‐β inhibit growth in epithelial cells by stimulating type V TGF‐β receptor (TβR‐V)‐mediated tumor suppressor signaling

Chen

Huang

et al. 2021

FASEB BioAdvances

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A549 cells -human Caucasian lung carcinoma cells β 1 25 (41-65) -TGF-β peptide antagonist containing amino acid residues 41 st to 65 th of human TGF-β 1 CDK -cyclin-dependent kinase CHO cells -Chinese hamster ovary epithelial cells D32 cells -murine 32D myeloid cells EMT -epithelial mesenchymal transition IGF-1 -insulin-like growth factor-1 IGF-2 -insulin-like growth factor-1 IGFBP-3 -insulin-like growth factor binding protein-3 IR -insulin receptor IRS-1/2 -insulin receptor substrate-1/2 LRP-1 -low density lipoprotein receptor-related protein-1 Mv1Lu cells -mink lung epithelial cells OA -okadaic acid p107, p130 -pRb-related proteins PAI-1 -plasminogen activator inhibitor-1 PPase -protein phosphatase PP1 -protein phosphatase 1 PP1 c -36-kDa PP1 catalytic subunt PP2A -protein phosphatase 2A PP2A c -37-kDa PP2A catalytic subunit PP2A-B56 -a 56-kDa substrate-recognition B subunit of PP2A pRb -retinoblastoma protein (p105) RAP -receptor-associated protein siRNA -small interfering RNA TGF-β -transforming growth factor-β TβR-I -type I TGF-β receptor TβR-II -type II TGF-β receptor

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“…In the extracellular compartment, MMP-9 protein levels are effectively reduced by low-density lipoprotein receptors-related proteins, which complex MMP-9 and cause its uptake and intracellular degradation by macrophages, fibroblasts, hepatocytes and other cell types ( Figure 1 ) [ 40 , 41 ]. In addition, MMP-9 can be counteracted by endogenous inhibitors including serum α2-macroglobulin or TIMPs ( Figure 1 ) [ 6 , 42 ].…”

Section: Mmp-9 Production or Activity Is Regulated At Multiple Levmentioning

confidence: 99%

“…Interestingly, MMP-9 clearance by low-density lipoprotein, receptor-related proteins is reduced in tumors compared to normal tissues ( Figure 2 ) [ 40 ]. Furthermore, tumor-infiltrating neutrophils produce enzymes, such as trypsin and chymotrypsin, which degrade local, preexistent TIMPs ( Figure 2 and Table 1 ) [ 67 ].…”

Section: Mmp-9 Production or Activity Is Regulated At Multiple Levmentioning

confidence: 99%

The Impact of Matrix Metalloproteinase-9 on the Sequential Steps of the Metastatic Process

Barillari

2020

IJMS

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In industrialized countries, cancer is the second leading cause of death after cardiovascular disease. Most cancer patients die because of metastases, which consist of the self-transplantation of malignant cells in anatomical sites other than the one from where the tumor arose. Disseminated cancer cells retain the phenotypic features of the primary tumor, and display very poor differentiation indices and functional regulation. Upon arrival at the target organ, they replace preexisting, normal cells, thereby permanently compromising the patient’s health; the metastasis can, in turn, metastasize. The spread of cancer cells implies the degradation of the extracellular matrix by a variety of enzymes, among which the matrix metalloproteinase (MMP)-9 is particularly effective. This article reviews the available published literature concerning the important role that MMP-9 has in the metastatic process. Additionally, information is provided on therapeutic approaches aimed at counteracting, or even preventing, the development of metastasis via the use of MMP-9 antagonists.

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Differential expression of Low density lipoprotein Receptor–related Protein 1 (LRP-1) and matrix metalloproteinase-9 (MMP-9) in prostate gland: From normal to malignant lesions

Cited by 11 publications

References 33 publications

Thyroid tumor cells-fibroblasts crosstalk: role of extracellular vesicles

Thyroid tumor cells-fibroblasts crosstalk: role of extracellular vesicles

IGFBP‐3 and TGF‐β inhibit growth in epithelial cells by stimulating type V TGF‐β receptor (TβR‐V)‐mediated tumor suppressor signaling

The Impact of Matrix Metalloproteinase-9 on the Sequential Steps of the Metastatic Process

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