Tetraspanin8 expression predicts an increased metastatic risk and is associated with cancer-related death in human cutaneous melanoma

Berthier‐Vergnes, Odile; Barbollat-Boutrand, Laetitia; Pommier, Roxane M.; Fouchardière, Arnaud de la; Combemale, P.; Grimont, Maxime; Lopez-Ramirez, Noémie; Caramel, Julie; Dalle, Stéphane; Perrot, Jean‐Luc; Gaudy‐Marqueste, C.; Macagno, Nicolas; Mansard, Sandrine; Bouquet, Fanny; Masse, Ingrid

doi:10.1186/s12943-021-01429-0

Cited by 3 publications

(6 citation statements)

References 18 publications

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“…TSPAN31 and TSPAN7 can promote migration of hepatocellular carcinoma and myeloma cells respectively, but do not affect cell proliferation [ 30 , 66 ]. More interestingly, TSPAN12 could inhibit the growth of breast cancer cells, but facilitate metastasis [ 44 ]. These results showed the complex roles of TSPAN members in cancer metastasis.…”

Section: Discussionmentioning

confidence: 99%

“…TSPAN8 is reported to be highly expressed in colorectal cancer, pancreatic cancer tissues and melanoma [41][42][43][44]. TSPAN8 promotes the proliferation, migration and EMT process of colorectal cancer cells [41].…”

Section: Tspans In Cancer Invasion and Metastasismentioning

confidence: 99%

“…Meanwhile, TSPAN8 could induce the EMT process and enhance cell–cell adhesion of breast cancer cells via interacting with p120 [ 19 ]. TSPAN8 is more frequently expressed in metastatic melanoma species and correlates with the presence of a BRAF-V600E mutation, a higher propensity to form distant metastases and an increased risk of death [ 44 ]. TSPAN8 stabilizes β-catenin, which in turn directly triggers the transcription of TSPAN8, leading to melanoma invasion [ 43 ].…”

Section: Introductionmentioning

confidence: 99%

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The versatile roles of testrapanins in cancer from intracellular signaling to cell–cell communication: cell membrane proteins without ligands

et al. 2023

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The tetraspanins (TSPANs) are a family of four-transmembrane proteins with 33 members in mammals. They are variably expressed on the cell surface, various intracellular organelles and vesicles in nearly all cell types. Different from the majority of cell membrane proteins, TSPANs do not have natural ligands. TSPANs typically organize laterally with other membrane proteins to form tetraspanin-enriched microdomains (TEMs) to influence cell adhesion, migration, invasion, survival and induce downstream signaling. Emerging evidence shows that TSPANs can regulate not only cancer cell growth, metastasis, stemness, drug resistance, but also biogenesis of extracellular vesicles (exosomes and migrasomes), and immunomicroenvironment. This review summarizes recent studies that have shown the versatile function of TSPANs in cancer development and progression, or the molecular mechanism of TSPANs. These findings support the potential of TSPANs as novel therapeutic targets against cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Tspans In Cancer Invasion and Metastasismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The versatile roles of testrapanins in cancer from intracellular signaling to cell–cell communication: cell membrane proteins without ligands

et al. 2023

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Section: Remodeling Of Epidermal Microenvironment During Melanoma Ons...mentioning

confidence: 99%

“…The mechanism of Tspan8-dependent dissolution of dermo-epidermal junction depends on the presence of keratinocytes and specifically on their capacity to produce MMPs and TIMPs [211]. Due to the tight correlation between Tspan8 expression and invasive capacity, Tspan8 has been proposed to predict metastasis risk in individual patients [212]. Melanoma cells lose the capacity to form gap junction communication with keratinocytes but still use these structures to communicate with themselves and with dermal fibroblasts [141].…”

Section: Alteration Of Melanocyte-keratinocyte Physical Interaction D...mentioning

confidence: 99%

The Keratinocyte in the Picture Cutaneous Melanoma Microenvironment

Marrapodi,

Bellei

2024

Cancers

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Melanoma progression is a multistep evolution from a common melanocytic nevus through a radial superficial growth phase, the invasive vertical growth phase finally leading to metastatic dissemination into distant organs. Melanoma aggressiveness largely depends on the propensity to metastasize, which means the capacity to escape from the physiological microenvironment since tissue damage due to primary melanoma lesions is generally modest. Physiologically, epidermal melanocytes are attached to the basement membrane, and their adhesion/migration is under the control of surrounding keratinocytes. Thus, the epidermal compartment represents the first microenvironment responsible for melanoma spread. This complex process involves cell–cell contact and a broad range of secreted bioactive molecules. Invasion, or at the beginning of the microinvasion, implies the breakdown of the dermo-epidermal basement membrane followed by the migration of neoplastic melanocytic cells in the superficial papillary dermis. Correspondingly, several experimental evidences documented the structural and functional rearrangement of the entire tissue surrounding neoplasm that in some way reflects the atypia of tumor cells. Lastly, the microenvironment must support the proliferation and survival of melanocytes outside the normal epidermal–melanin units. This task presumably is mostly delegated to fibroblasts and ultimately to the self-autonomous capacity of melanoma cells. This review will discuss remodeling that occurs in the epidermis during melanoma formation as well as skin changes that occur independently of melanocytic hyperproliferation having possible pro-tumoral features.

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Cancer Cell Biomechanical Properties Accompany Tspan8-Dependent Cutaneous Melanoma Invasion

Runel,

Lopez-Ramirez,

Barbollat-Boutrand

et al. 2024

Cancers

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The intrinsic biomechanical properties of cancer cells remain poorly understood. To decipher whether cell stiffness modulation could increase melanoma cells’ invasive capacity, we performed both in vitro and in vivo experiments exploring cell stiffness by atomic force microscopy (AFM). We correlated stiffness properties with cell morphology adaptation and the molecular mechanisms underlying epithelial-to-mesenchymal (EMT)-like phenotype switching. We found that melanoma cell stiffness reduction was systematically associated with the acquisition of invasive properties in cutaneous melanoma cell lines, human skin reconstructs, and Medaka fish developing spontaneous MAP-kinase-induced melanomas. We observed a systematic correlation of stiffness modulation with cell morphological changes towards mesenchymal characteristic gains. We accordingly found that inducing melanoma EMT switching by overexpressing the ZEB1 transcription factor, a major regulator of melanoma cell plasticity, was sufficient to decrease cell stiffness and transcriptionally induce tetraspanin-8-mediated dermal invasion. Moreover, ZEB1 expression correlated with Tspan8 expression in patient melanoma lesions. Our data suggest that intrinsic cell stiffness could be a highly relevant marker for human cutaneous melanoma development.

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Tetraspanin8 expression predicts an increased metastatic risk and is associated with cancer-related death in human cutaneous melanoma

Cited by 3 publications

References 18 publications

The versatile roles of testrapanins in cancer from intracellular signaling to cell–cell communication: cell membrane proteins without ligands

The versatile roles of testrapanins in cancer from intracellular signaling to cell–cell communication: cell membrane proteins without ligands

The Keratinocyte in the Picture Cutaneous Melanoma Microenvironment

Cancer Cell Biomechanical Properties Accompany Tspan8-Dependent Cutaneous Melanoma Invasion

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