Kallikrein-related peptidase 7 overexpression in melanoma cells modulates cell adhesion leading to a malignant phenotype

Haddada, Meriem; Draoui, Hend; Deschamps, Lydia; Walker, Francine; Delaunay, Tiphaine; Brattsand, Maria; Magdolen, Viktor; Darmoul, Dalila

doi:10.1515/hsz-2017-0339

Cited by 10 publications

(12 citation statements)

References 40 publications

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“…These cells showed a higher capacity for invasion than control cells, with, in parallel, a decrease in adhesion to fibronectin and vitronectin and a decrease in expression of α5β1 and αvβ3 integrins 54,55 . Moreover, these integrins were down regulated in melanoma cells modulating cell adhesion 56 . Together these data demonstrate that KLK5 could have opposite effects depending on cancerous or non‐cancerous cell characteristics.…”

Section: Discussionmentioning

confidence: 80%

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Kallikrein‐related peptidase 5 contributes to the remodeling and repair of bronchial epithelium

et al. 2021

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Inflammation, oxidative stress, and protease/protease inhibitor imbalance with excessive production of proteases are factors associated with pathogenesis of the chronic obstructive pulmonary disease (COPD). In this study, we report that kallikrein-related peptidase 5 (KLK5) is a crucial protease involved in extracellular matrix (ECM) remodeling and bronchial epithelial repair after injury. First, we showed that KLK5 degrades the basal layer formed by culture of primary bronchial epithelial cells from COPD or non-COPD patients. Also, exogenous KLK5 acted differently on BEAS-2B cells already engaged in epithelial-to-mesenchymal transition (EMT) or on 16HBE 14o-cells harboring epithelial characteristics. Indeed, by inducing EMT, KLK5 reduced BEAS-2B cell adherence to the ECM. This effect, neutralized by tissue factor pathway inhibitor 2, a kunitz-type serine protease inhibitor, was due to a direct proteolytic activity of KLK5 on E-cadherin, β-catenin, fibronectin, and α5β1 integrin. Thus, KLK5 may strengthen EMT mechanisms and promote the migration of cells by activating the mitogen-activated protein kinase signaling pathway required for this function. In contrast, knockdown of endogenous KLK5 in 16HBE14o-cells, accelerated wound healing repair after injury, and exogenous KLK5 addition delayed the closure repair. These data suggest that among proteases, KLK5 could play a critical role in airway remodeling events

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Section: Discussionmentioning

confidence: 80%

“…54,55 Moreover, these integrins were down regulated in melanoma cells modulating cell adhesion. 56 Together these data demonstrate that KLK5 could have opposite effects depending on cancerous or non-cancerous cell characteristics.…”

Section: Discussionmentioning

confidence: 85%

Kallikrein‐related peptidase 5 contributes to the remodeling and repair of bronchial epithelium

et al. 2021

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“…This suggests that hKLKs have specific roles in the epithelial-mesenchymal transition. In fact, hKLK7 overexpression induces the production of CD146 (cluster of differentiation 146) ( 79 ), also known as melanoma cell adhesion molecule (MCAM), a surface glycoprotein that functions as a receptor for laminin subunit alpha 4, a matrix protein expressed in vascular walls, which could be related to melanoma metastasis ( 80 ). KLK6 −/− mice induced with carcinogenesis developed fewer tumors compared to wild-type animals, suggesting that KLK6 has a role in skin tumor development and progression ( 81 ).…”

Section: Skin Diseases and Their Relationship With Hklksmentioning

confidence: 99%

Human Tissue Kallikreins-Related Peptidases Are Targets for the Treatment of Skin Desquamation Diseases

et al. 2022

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Human tissue Kallikrein-related peptidases (hKLKs) are serine proteases distributed in several tissues that are involved in several biological processes. In skin, many are responsible for skin desquamation in the Stratum Corneum (SC) of the epidermis, specially hKLK5, hKLK7, hKLK6, hKLK8, and hKLK14. In SC, hKLKs cleave proteins of corneodesmosomes, an important structure responsible to maintain corneocytes attached. As part of skin desquamation, hKLKs are also involved in skin diseases with abnormal desquamation and inflammation, such as Atopic Dermatitis (AD), psoriasis, and the rare disease Netherton Syndrome (NS). Many studies point to hKLK overexpression or overactive in skin diseases, and they are also part of the natural skin inflammation process, through the PAR2 cleavage pathway. Therefore, the control of hKLK activity may offer successful treatments for skin diseases, improving the quality of life in patients. Diseases like AD, Psoriasis, and NS have an impact on social life, causing pain, itchy and mental disorders. In this review, we address the molecular mechanisms of skin desquamation, emphasizing the roles of human tissue Kallikrein-related peptidases, and the promising therapies targeting the inhibition of hKLKs.

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“…We found that kallikreinrelated peptidase 7 (KLK7) and keratin 7 (KRT7) were the most related genes in melanoma and renal cancer separately (Supplementary Figure 2). Aberrant expression of KLK7 has found to be related to melanoma aggressiveness by stimulating cell migration and adhesion (Delaunay et al, 2017;Haddada et al, 2018). KRT7 could distinguish the precursor lesions of papillary renal cell tumors, mucinous tubular and spindle cell carcinomas (Szponar and Kovacs, 2012).…”

Section: Gene Expression Analysis Of Cystatin E/m In the Merged Microarray-acquired Datasetsmentioning

confidence: 99%

A Pan-Cancer Analysis of Cystatin E/M Reveals Its Dual Functional Effects and Positive Regulation of Epithelial Cell in Human Tumors

Ding

Cao

et al. 2021

Front. Genet.

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Cystatin E/M (CST6), a representative cysteine protease inhibitor, plays both tumor-promoting and tumor-suppressing functions and is pursued as an epigenetically therapeutic target in special cancer types. However, a comprehensive and systematic analysis for CST6 in pan-cancer level is still lacking. In the present study, we explored the expression pattern of CST6 in multiple cancer types across ∼10,000 samples from TCGA (The Cancer Genome Atlas) and ∼8,000 samples from MMDs (Merged Microarray-acquired Datasets). We found that the dynamic expression alteration of CST6 was consistent with dual function in different types of cancer. In addition, we observed that the expression of CST6 was globally regulated by the DNA methylation in its promoter region. CST6 expression was positively correlated with the epithelial cell infiltration involved in epithelial-to-mesenchymal transition (EMT) and proliferation. The relationship between CST6 and tumor microenvironment was also explored. In particular, we found that CST6 serves a protective function in the process of melanoma metastasis. Finally, the clinical association analysis further revealed the dual function of CST6 in cancer, and a combination of the epithelial cell infiltration and CST6 expression could predict the prognosis for SKCM patients. In summary, this first CST6 pan-cancer study improves the understanding of the dual functional effects on CST6 in different types of human cancer.

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Kallikrein-related peptidase 7 overexpression in melanoma cells modulates cell adhesion leading to a malignant phenotype

Cited by 10 publications

References 40 publications

Kallikrein‐related peptidase 5 contributes to the remodeling and repair of bronchial epithelium

Kallikrein‐related peptidase 5 contributes to the remodeling and repair of bronchial epithelium

Human Tissue Kallikreins-Related Peptidases Are Targets for the Treatment of Skin Desquamation Diseases

A Pan-Cancer Analysis of Cystatin E/M Reveals Its Dual Functional Effects and Positive Regulation of Epithelial Cell in Human Tumors

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