Tetraspanins in Cell Migration

Jiang, Xupin; Zhang, Jiaping; Huang, Yuesheng

doi:10.1080/19336918.2015.1005465

Cited by 59 publications

(52 citation statements)

References 134 publications

(118 reference statements)

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“…Since we recently identified that FRCs exhibit a type of apical to basolateral polarity, in order to secrete matrix components unilaterally into conduit structures (43), this may explain the lack of front to back polarity which would be required for cell migration. Although CD9 is important in other cell types for migration (65), our data indicate that in FRCs, CD9 is involved in cellcell connections, thereby contributing to the formation and preservation of the FRC network.…”

Section: Discussionmentioning

confidence: 69%

Fibroblastic Reticular Cell Response to Dendritic Cells Requires Coordinated Activity of Podoplanin, CD44 and CD9

Winde

Makris

Millward

et al. 2019

Preprint

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Lymph node expansion is pivotal during immune activation. It is controlled by interactions between CLEC-2 hi migratory dendritic cells and podoplanin + fibroblastic reticular cells (FRCs) resulting in rapid loss of actomyosin contractility permitting FRC spreading. Podoplanin is an inflammatory marker in many pathologies, reported to facilitate both contractility and cell protrusions. However, how podoplanin expression is regulated, and how this one membrane protein can elicit these opposing phenotypes is unknown. We report that CLEC-2 binding to FRCs induces transcriptional upregulation of podoplanin, increasing surface protein expression. Further, we find that tetraspanin CD82 is required for trafficking of podoplanin to the plasma membrane. At the cell surface, podoplanin elicits multiple functions, balanced by its membrane binding partners hyaluronan receptor CD44 and tetraspanin CD9. FRCs lacking expression of both CD44 and CD9 are hypercontractile, and upon binding to CLEC-2 hi dendritic cells, both CD44 KO and CD9 KO FRCs exhibit defective protrusion formation and fail to spread. Podoplanin co-localises with CD44 or CD9 in distinct membrane domains, and both CD44 and CD9 are required for FRCs to spread in response to dendritic cells, however they control formation of cell protrusions via different and complimentary mechanisms. In vivo, surface expression levels of podoplanin, CD44 and CD9 are upregulated on T-cell zone FRCs in the early phase of lymph node expansion. Our data support a model whereby podoplanin resides in distinct plasma membrane domains, and that CLEC-2 binding serves as a molecular switch to change podoplanin function. Podoplanin | CD44 | CD9 | CD82 | Tetraspanins | Fibroblastic reticular cell | Lymph node Correspondence: s.acton@ucl.ac.uk de Winde et al. | bioRχiv | October 3, 2019 | 1-2

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Section: Discussionmentioning

confidence: 69%

Fibroblastic Reticular Cell Response to Dendritic Cells Requires Coordinated Activity of Podoplanin, CD44 and CD9

Winde

Makris

Millward

et al. 2019

Preprint

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“…Previous studies have indicated that tetraspanins can regulate the function of proteins involved in all aspects of cell migration 11 . For example, tetraspanins can directly interact with integrins and modulate their downstream signalling in response to migratory signals 54, 55 .…”

Section: Discussionmentioning

confidence: 99%

The cancer-associated cell migration protein TSPAN1 is under control of androgens and its upregulation increases prostate cancer cell migration

Munkley

McClurg

Livermore

et al. 2017

Sci Rep

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Cell migration drives cell invasion and metastatic progression in prostate cancer and is a major cause of mortality and morbidity. However the mechanisms driving cell migration in prostate cancer patients are not fully understood. We previously identified the cancer-associated cell migration protein Tetraspanin 1 (TSPAN1) as a clinically relevant androgen regulated target in prostate cancer. Here we find that TSPAN1 is acutely induced by androgens, and is significantly upregulated in prostate cancer relative to both normal prostate tissue and benign prostate hyperplasia (BPH). We also show for the first time, that TSPAN1 expression in prostate cancer cells controls the expression of key proteins involved in cell migration. Stable upregulation of TSPAN1 in both DU145 and PC3 cells significantly increased cell migration and induced the expression of the mesenchymal markers SLUG and ARF6. Our data suggest TSPAN1 is an androgen-driven contributor to cell survival and motility in prostate cancer.Cancer, in its most aggressive form, is not only a disease of uncontrolled cell growth, but also a disease of inappropriate cell migration. Activating invasion and metastasis is a hallmark of cancer progression 1, 2 and is the leading cause of mortality among cancer patients 3 . Metastasis involves cancer cells detaching from the primary tumour, and travelling as circulating tumour cells through the bloodstream or lymphatic system to other parts of the body. Prostate cancer is the most common male cancer in Europe, with around 50,000 new cases in the UK each year 4 . At initial diagnosis 37-43% of men have late stage disease and 17-34% of prostate cancer patients have metastasis (http://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/ prostate-cancer/incidence#ref-8). The development of prostate cancer is initially driven by androgen steroid hormones via the androgen receptor (AR) transcription factor. The first line treatment for prostate cancer that is no longer organ confined is androgen deprivation therapy (ADT). However, after 2-3 years many patients develop

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“…2B). The ability of cells to migrate strongly depends on a dynamic actin assembly [9] and the protein superfamily of tetraspanins such as CD63 was shown to be involved in cell migration and adhesion [10]. Other dynamic entities which co-cluster in the membrane with CD63-YFP can also be studied with this new method.…”

Section: Resultsmentioning

confidence: 99%

Easy and cost-effective stable positioning of suspension cells during live-cell imaging

2017

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Dynamic processes of cells can be best monitored when living cells are analyzed by imaging. While it is easy to observe adherent living cells it has been extremely challenging to analyze suspension cells. This cell type floats freely in the culture dish, and it is only a question of time when the focus or the observation field is lost. In order to keep the cells in focus, an easy and inexpensive method allowing the observation of living suspension cells during confocal laser scanning microscope imaging was developed.

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Tetraspanins in Cell Migration

Cited by 59 publications

References 134 publications

Fibroblastic Reticular Cell Response to Dendritic Cells Requires Coordinated Activity of Podoplanin, CD44 and CD9

Fibroblastic Reticular Cell Response to Dendritic Cells Requires Coordinated Activity of Podoplanin, CD44 and CD9

The cancer-associated cell migration protein TSPAN1 is under control of androgens and its upregulation increases prostate cancer cell migration

Easy and cost-effective stable positioning of suspension cells during live-cell imaging

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