Melanoma cells produce multiple laminin isoforms and strongly migrate on α5 laminin(s) via several integrin receptors

Oikawa, Yuko; Hansson, Johan; Sasaki, Takako; Rousselle, Patricia; Domogatskaya, Anna; Rodin, Sergey; Tryggvason, Karl; Patarroyo, Manuel Elkín

doi:10.1016/j.yexcr.2010.12.019

Cited by 51 publications

(54 citation statements)

References 49 publications

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“…Consistent with a previous report that laminin-332 is able to promote melanoma cell migration, as shown in a chemotaxis assay with soluble laminin-332 and a haptotaxis assay with laminin-332-coated membranes (27,28), we herein show that laminin-332 stimulates the migration of melanoma cells (Fig. 7).…”

Section: Discussionsupporting

confidence: 93%

“…5). Because integrin ␣6␤4 is known to be down-regulated in melanoma cells (27), it is likely that integrin ␣6␤1 mediates the laminin-332-mediated adhesion of melanoma cells. Oikawa et al (27) demonstrated that laminin-332 stimulated migration of melanoma cells through integrin ␣3␤1 and ␣6␤1, and Tsuji et al (28) reported that integrin ␣3 mediated laminin-332-mediated melanoma cell migration and invasion on laminin-332-coated membrane.…”

Section: Discussionmentioning

confidence: 99%

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Keratinocyte-derived Laminin-332 Promotes Adhesion and Migration in Melanocytes and Melanoma

Chung

Suh

Han

et al. 2011

Journal of Biological Chemistry

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Melanocytes are highly motile cells that play an integral role in basic skin physiological processes such as wound healing and proper skin pigmentation. It has been postulated that surrounding keratinocytes contribute to melanocyte migration, but underlying mechanisms remain rather vague so far. In this study, we set out to analyze the specific potential contribution of keratinocyte components to melanocytes and melanoma cell migration-related processes. Our studies revealed that A375 human melanoma cell attachment, spreading, and migration are interestingly better supported by HaCaT keratinocyte extracellular matrix (ECM) than by self-derived A375 ECM. Moreover, HaCaT ECM caused increased integrin ␣6 expression, adhesion-mediated focal adhesion kinase phosphorylation, and focal adhesion formations. Similar effects were confirmed in human melanocytes. Furthermore, we found that keratinocyte-derived soluble factors did not appear to significantly contribute to these processes. Specific extrinsic factors that promoted melanoma migration were attributed to keratinocyte-derived laminin-332, whereas alternative ECM component such as laminin-111 and fibronectin functions appeared to have insignificant contributions. Taken together, these studies implicate extrinsic laminin-332 in promoting the high mobility property and perhaps invasiveness inherently characteristic of, and that are the menace of, melanocytes and melanomas, respectively.Melanocytes, which are present in the skin, hair, eyes, and ears, synthesize melanin via a process known as melanogenesis (1), and thus play a key role in the pigmentary system of the skin in the body. These cells are located in the bottom layer of the skin (basal epidermis), where they comprise 5-10% of the total cells. The major cells comprising the epidermis are keratinocytes, which are organized into the basal cell layer, spinous cell layer, granular cell layer, and keratinized squames (2). The keratinocytes in the basal cell layer gradually differentiate, proliferate, and migrate upward to form the primary protection of the body from the outside environment.There is a close and important functional association between melanocytes and keratinocytes. Melanocytes transfer mature melanosomes to neighboring keratinocytes, resulting in visible skin pigmentation (3) and protecting the keratinocytes from the deleterious effects of UV light (4). Therefore, melanocytes play an important role in keratinocyte functions. Reciprocally, keratinocytes mediate melanocyte functions via several pathways, including cell-cell adhesion, cell-matrix adhesion, and paracrine signaling (5). Normal melanocytes maintain cellcell adhesion with keratinocytes by expressing cell-cell adhesion proteins such as E-cadherin, desmoglein 1, and connexins (6). In turn, keratinocytes secrete many paracrine factors to melanocytes, including ␣-melanocyte-stimulating hormone (␣-MSH), 2 adrenocorticotrophic hormone, endothelin-1, -2, and -3, FGF-2, and hepatocyte growth factor, all of which regulate the proliferation and di...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Keratinocyte-derived Laminin-332 Promotes Adhesion and Migration in Melanocytes and Melanoma

Chung

Suh

Han

et al. 2011

Journal of Biological Chemistry

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“…Laminin, a major structural component of the basement membrane, drives cell proliferation, differentiation, adhesion and migration via integrins and other cell surface receptors (1)(2)(3)(4)(5)(6)(7)(8). Increased laminin expression was also observed in melanoma cell lines and led to increased melanoma cell proliferation and metastatic potential (1-7).…”

Section: Discussionmentioning

confidence: 99%

“…The proteins laminin and type-IV collagen are major structural constituents of the basement membrane, and serve as promoters of cell proliferation, differentiation, adhesion and migration via integrins and other cell surface receptors (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). Increased expression of laminin and type-IV (1-7) collagen (6,7,(9)(10)(11) has also been demonstrated in melanoma cell lines with increased proliferation and metastatic potential (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

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Clinical significance of serum laminin and type-IV collagen levels in cutaneous melanoma patients

Taş

Bilgin

Karabulut

et al. 2016

Molecular and Clinical Oncology

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Prolyl 4‐hydroxylase subunit alpha 1 (P4HA1) is a biomarker of poor prognosis in primary melanomas, and its depletion inhibits melanoma cell invasion and disrupts tumor blood vessel walls

et al. 2020

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Melanoma is an unpredictable, highly metastatic malignancy, and treatment of advanced melanoma remains challenging. Novel molecular markers based on the alterations in gene expression and the molecular pathways activated or deactivated during melanoma progression are needed for predicting the course of the disease already in primary tumors and for providing new targets for therapy. Here, we sought to identify genes whose expression in primary melanomas correlate with patient disease‐specific survival using global gene expression profiling. Many of the identified potential markers of poor prognosis were associated with the epithelial–mesenchymal transition, extracellular matrix formation, and angiogenesis. We studied further the significance of one of the genes, prolyl 4‐hydroxylase subunit alpha 1 (P4HA1), in melanoma progression. P4HA1 depletion in melanoma cells reduced cell adhesion, invasion, and viability in vitro. In melanoma xenograft assays, we found that P4HA1 knockdown reduced melanoma tumor invasion as well as the deposition of collagens, particularly type IV collagen, in the interstitial extracellular matrix and in the basement membranes of tumor blood vessels, leading to vessel wall rupture and hemorrhages. Further, P4HA1 knockdown reduced the secretion of collagen triple helix repeat containing 1 (CTHRC1), an important mediator of melanoma cell migration and invasion, in vitro and its deposition around tumor blood vessels in vivo. Taken together, P4HA1 is an interesting potential prognostic marker and therapeutic target in primary melanomas, influencing many aspects of melanoma tumor progression.

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Melanoma cells produce multiple laminin isoforms and strongly migrate on α5 laminin(s) via several integrin receptors

Cited by 51 publications

References 49 publications

Keratinocyte-derived Laminin-332 Promotes Adhesion and Migration in Melanocytes and Melanoma

Keratinocyte-derived Laminin-332 Promotes Adhesion and Migration in Melanocytes and Melanoma

Clinical significance of serum laminin and type-IV collagen levels in cutaneous melanoma patients

Prolyl 4‐hydroxylase subunit alpha 1 (P4HA1) is a biomarker of poor prognosis in primary melanomas, and its depletion inhibits melanoma cell invasion and disrupts tumor blood vessel walls

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