Transformation of human keratinocytes is characterized by quantitative and qualitative alterations of the T‐16 antigen (Trop‐2, MOv‐16)

Schön, Michael P.; Orfanos, Constantin E.

doi:10.1002/ijc.2910600113

Cited by 6 publications

(7 citation statements)

References 19 publications

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“…The pattern of deglycosylation achieved with the three enzymes was similar in all the three cell lines studied. The higher molecular weight of gp130 in SK-CO-2 cells may result from differential glycosylation (as has been described for other surface glycoproteins in some tumor cells (Schö n and Orfanos, 1995)). When the L101 mAb was used to detect the gp130 deglycosylation products, the same pattern as detected with the BT14 mAb was seen (not shown).…”

Section: Resultsmentioning

confidence: 75%

Expression of gp130 in Tumors and Inflammatory Disorders of the Skin: Formal Proof of its Identity as CD146 (MUC18, Mel-CAM)

Schön¹,

Kähne

Gollnick

et al. 2005

Journal of Investigative Dermatology

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Two antibodies, BT14 and L101, detect a tumor-associated cell surface glycoprotein (gp130) whose properties in normal and diseased skin were assessed, and whose molecular identity was determined in this study. In normal skin, gp130 was constitutively expressed on dermal blood vessels and epidermal appendages, but not in interfollicular epidermis. Marked induction was detected within benign and malignant tumors of various origins including viral warts, basal cell carcinomas, squamous cell carcinomas, metastatic melanomas, and cutaneous T cell lymphomas. In vitro studies confirmed the general upregulation of gp130 expression in malignantly transformed cells. Surprisingly, gp130 was also induced in inflammatory skin diseases including psoriasis and allergic contact dermatitis. Halting proliferation of transformed keratinocytes through cytostatic drugs or increasing the Ca2+ concentration in the medium resulted in increased gp130 expression. In addition, overexpression of Bcl-2 led to upregulation of gp130. When the protein was purified and analyzed by peptide mass fingerprinting, we could demonstrate that it is MUC18 (Mel-CAM, CD146). Sequential immunoprecipitations and western blot analyses confirmed the identity of the antigen. Thus, both expression pattern and regulation characteristics of the now-known glycoprotein gp130 extended beyond previously published data regarding MUC18, thus shedding some new light on a supposedly well-known antigen.

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Section: Resultsmentioning

confidence: 75%

Expression of gp130 in Tumors and Inflammatory Disorders of the Skin: Formal Proof of its Identity as CD146 (MUC18, Mel-CAM)

Schön¹,

Kähne

Gollnick

et al. 2005

Journal of Investigative Dermatology

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“…Based on this assumption, EpCAM with its restricted spatial and temporal expression is relevant to morphogenesis. Further support for the role of EpCAM in morphogenesis comes from mechanistic studies showing that EpCAM expression is indeed associated with cell proliferation and differentiation during organogenesis (7)(8)(9)11,24).…”

Section: Discussionmentioning

confidence: 99%

“…Reversely, EpCAM might be an active regulator of cell differentiation. Circumstantial evidence for such a role comes from ectopic overexpression of EpCAM, which induces redifferentiation in terminally differentiated cells, such as keratynocytes (7,8). However, the debate on EpCAM as active regulator of differentiation or as a "passive" player in this process is still wide open.…”

Section: Epcam In Early Embryogenesismentioning

confidence: 99%

“…However, from these initial studies research on EpCAM has progressed to studies dedicated to its role in normal cellular behavior, which has yielded interesting new insights in EpCAM biology (for review see 1). It has by now been well established that EpCAM is also expressed in developing and normal, mature epithelia, where it participates not only in cell adhesion, but also in proliferation, migration and differentiation (1,(7)(8)(9)(10)(11). All of these processes are known to be fundamental for correct execution of morphogenesis, including embryo-and organogenesis, as well as tissue regeneration.…”

Section: Introductionmentioning

confidence: 99%

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EpCAM in morphogenesis

Trzpis

Bremer

McLaughlin³

et al. 2008

Front Biosci

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Embryonic development is one of the most complex biological phenomena that involves the appropriate expression and synchronized interactions of a plethora of proteins, including cell adhesion molecules (CAMs). Many members of the diverse family of CAMs have been shown to be critically involved in the correct execution of embryonic development. The Epithelial Cell Adhesion Molecule (EpCAM) is an atypical cell adhesion molecule originally identified as a marker for carcinoma. However, recent insights have revealed that EpCAM participates in not only cell adhesion, but also in proliferation, migration and differentiation of cells. All of these processes are known to be fundamental for morphogenesis. Here, we review the current literature that establishes EpCAM as a protein involved in morphogenesis, starting from the earliest stages of embryogenesis and ending in organogenesis. In addition, we provide directions for further elucidation of the role of EpCAM in embryogenesis.

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“…A defect in receptor glycosylation is supported by a reported defect in N-linked glycosylation in HaCat cells as well as other transformed keratinocyte cell lines. 49 However, PGE 2coupled receptors may exhibit other posttranslational modifications including isoprenylation and phosphorylation. 48,50 We have previously demonstrated that EP 2 receptor activation stimulates growth in PHKs.…”

Section: Discussionmentioning

confidence: 99%

Loss of the EP2 Prostaglandin E2 Receptor in Immortalized Human Keratinocytes Results in Increased Invasiveness and Decreased Paxillin Expression

Konger

Scott

Landt

et al. 2002

The American Journal of Pathology

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Prostaglandin E(2) (PGE(2)) receptor subtype EP(2), which is coupled to cAMP metabolism, is known to mediate proliferation of primary human keratinocytes in vitro. The effect of gain or loss of EP(2) receptors in immortalized human keratinocytes (HaCat cells) was examined. HaCat keratinocytes were transfected with sense or anti-sense constructs of the EP(2) receptor. Loss or gain of EP(2) expression was documented by immunoblot and associated changes in agonist-stimulated cAMP production. Loss or gain of EP(2) receptor expression correlated with alterations in plating efficiencies but with modest affects on growth. When cell lines were studied in an organ culture model, anti-sense clones were highly invasive compared with vector controls and sense transfectants. A marked increase in prostaglandin production is commonly seen in malignant lesions. Because prostaglandin receptors are known to undergo ligand-induced receptor down-regulation, we sought to determine whether EP(2) receptor down-regulation results in increased invasiveness. In vector controls, invasiveness was reproduced by ligand-dependent EP(2) receptor down-regulation as assessed by immunohistochemistry. In addition, loss of EP(2) receptor expression was associated with decreased paxillin expression, a critical component of focal adhesion assembly. Thus, down-regulation of EP(2) receptors represents a potential mechanism for neoplastic progression to an invasive phenotype.

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Transformation of human keratinocytes is characterized by quantitative and qualitative alterations of the T‐16 antigen (Trop‐2, MOv‐16)

Cited by 6 publications

References 19 publications

Expression of gp130 in Tumors and Inflammatory Disorders of the Skin: Formal Proof of its Identity as CD146 (MUC18, Mel-CAM)

Expression of gp130 in Tumors and Inflammatory Disorders of the Skin: Formal Proof of its Identity as CD146 (MUC18, Mel-CAM)

EpCAM in morphogenesis

Loss of the EP2 Prostaglandin E2 Receptor in Immortalized Human Keratinocytes Results in Increased Invasiveness and Decreased Paxillin Expression

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