TSLC1 expression discriminates cutaneous melanomas from dysplastic nevi

Abstract

Cutaneous melanoma is a malignant tumor of melanocytes that causes the majority of skin cancer-related deaths. However, sometimes, discrimination between dysplastic nevi and early melanomas is difficult, even for experienced pathologists. Besides histology, the silencing of tumor suppressor genes aids in the diagnosis of melanoma. We have shown previously that tumor suppressor in lung cancer 1 (TSLC1) is a tumor suppressor gene, and its silencing through aberrant promoter methylation is associated with the generation of cutaneous melanoma. To examine TSLC1 expression in melanocytic skin lesions to determine whether it can serve as a diagnostic marker in histologically questionable lesions. Cytoplasmic localization of the expression of the TSLC1 gene was detected by immunohistochemistry; the levels of TSLC1 mRNA and protein were detected by quantitative real-time reverse transcription-PCR and western blot, respectively. Using immunohistochemistry, the average TSLC1 expression levels in cutaneous melanomas decreased approximately 3.6-fold (n=20) as compared with dysplastic nevi (n=30) and 3.7-fold as compared with normal skin (n=25). The average expression levels of TSLC1 mRNA and protein in dysplastic nevi lesions and normal skin were significantly higher than the levels in cutaneous melanomas. No significant changes in TSLC1 mRNA and protein expressions were found between normal skin and dysplastic nevi. Our results show that a loss of TSLC1 frequently occurs in cutaneous melanoma, and indicate that it could serve as a diagnostic marker for cutaneous melanoma in histologically questionable lesions.

Tumor Suppressor in Lung Cancer-1 Is a Prognostic Predictor for the Recurrence and Progression of Non-Muscle-Invasive Bladder Cancer

“…Our results showed that TSLC1 expression was low in NMIBC tissues, in agreement with the reported low expression of TSLC1 in other tumors [10,11,12,13,14,15,16,17,18,19,20,21]. The function of TSLC1 is to participate in calcium-independent cell-cell adhesion and signal transduction, similar to E-cadherin [7].…”

“…Previous studies have shown that TSLC1 is ubiquitously expressed in a wide range of human tissues, such as the lung, brain, testes as well as most epithelial and neuronal tissues [9]. Recently, TSLC1 protein expression was found to be lost or downregulated in a variety of human cancers, including lung, breast, nasopharyngeal, cervical, liver and colon cancer, meningioma, cutaneous melanoma and T-cell leukemia/lymphoma [10,11,12,13,14,15,16,17,18,19,20,21]. Furthermore, experimental studies have shown that reconstitution of TSLC1 expression inhibited esophageal carcinoma in vitro and in vivo [22,23,24].…”

Tumor Necrosis Factor α Regulates Endothelial Progenitor Cell Migration via CADM1 and NF-kB

“…Cell Adhesion Molecule 1 is a protein that has been found to be strongly expressed in neurons, [71][72][73][74][75] spermatogenic cells, [52,[76][77][78] immune cells, [79][80][81][82][83][84][85][86][87] and endothelial cells [88,89]. Functionally, CADM1 has been shown to participate in homophilic binding, and paradoxically, tumor suppression.…”