Volume 49, Issue 8 pp. 687-694

Expression of sonic hedgehog signal transducers, patched and smoothened, in human basal cell carcinoma

Michiko Tojo

Michiko Tojo

Department of Cell Science, Institute of Biomedical Sciences,

Department of Dermatology, Fukushima Medical University School of Medicine, Fukushima, Japan

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Tetsuji Mori

Tetsuji Mori

Department of Cell Science, Institute of Biomedical Sciences,

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Hidenori Kiyosawa

Hidenori Kiyosawa

Department of Cell Science, Institute of Biomedical Sciences,

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Yutaka Honma

Yutaka Honma

Department of Cell Science, Institute of Biomedical Sciences,

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Yoshihiro Tanno

Yoshihiro Tanno

Department of Cell Science, Institute of Biomedical Sciences,

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Ken-ya Kanazawa

Ken-ya Kanazawa

Department of Cell Science, Institute of Biomedical Sciences,

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Sachihiko Yokoya

Sachihiko Yokoya

Department of Cell Science, Institute of Biomedical Sciences,

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Fumio Kaneko

Fumio Kaneko

Department of Dermatology, Fukushima Medical University School of Medicine, Fukushima, Japan

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Akio Wanaka

Akio Wanaka

Department of Cell Science, Institute of Biomedical Sciences,

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First published: 04 January 2002
Citations: 42
Correspondence: MichikoTojo MD. Department of Cell Science, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima City, Fukushima 960-1295, Japan. Email address: [email protected]

Abstract

In basal cell nevus syndrome (BCNS) patients, mutations of a gene, patched (ptc), which encodes a putative signal transducer of sonic hedgehog protein (SHH), were found and are thought to be one of the major causes of BCNS. The SHH signaling pathway is an important developmental pathway, and ptc protein (PTC) is a suppressive component serving as a receptor for the secreted SHH. Another transmembrane protein, smoothened (SMO), forms a complex with PTC and regulates this signaling pathway. Recent transgenic studies have strengthened the importance of the SHH signaling system in the etiology of basal cell carcinoma (BCC). In this study, we examined the expression patterns of mRNA for ptc and smo in two different BCC subtypes and normal skin. We found that the expressions of ptc and smo mRNA were enhanced in the tumor nests of the nodular BCC, especially at the advancing portions, but were under the detectable level in the superficial BCC cases examined, indicating that ptc and smo mRNA expressions might be associated with BCC tumor progression and divide the BCC histologic types into two subtypes, superficial and nodular types. In addition, no obvious signals for ptc and smo mRNA were detected in the normal human epidermis, appendages, or seborrheic keratosis, indicating that the abnormal proliferation of follicular epithelial cells caused by ptc, smo and/or other genetic changes, which also cause ptc and smo overexpressions, might result in BCC tumor formation.

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