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CD82, and CD63 in thyroid cancer
Zhouxun Chen1, Tarek Mustafa, Bogusz Trojanowicz
1Department of General, Visceral and Vascular Surgery, Martin-Luther-University Halle-Wittenberg, Magdeburger Strasse 18, D-06097 Halle, Germany.
Abstract:
CD82 (KAI1) and CD63 (ME491) are highly glycosylated proteins which belong to the transmembrane 4 superfamily (TM4SF). CD82 has been implicated as a possible prostate cancer metastasis suppressor gene, whereas CD63 is involved in the progression of human melanoma cancer. Down-regulation of both CD82 and CD63 expression has been associated with the metastatic potential of several solid tumors. Currently, information is lacking on the role of CD82 and CD63 during thyroid carcinogenesis. The aim of this study was to determine whether the expression of CD82 and CD63 is a useful prognostic indicator in patients with thyroid carcinoma. The expression of CD82 and CD63 was analysed by reverse transcriptase-PCR (RT-PCR) and immunohistochemistry in benign goiter (n=12) and 75 primary thyroid carcinoma tissue specimens (PTC: 33, FTC: 24, UTC: 18) out of which 36 were non-metastasized primary tumors and 39 were metastasized tumors (regional lymph node and/or distant metastases). All of the benign goiter tissues showed CD82 expression. By contrast, a significant decrease in CD82 mRNA and protein levels was detected in carcinoma tissues as compared to benign goiter tissues (p<0.001). A similar down-regulation was observed in metastasized tumor tissues when compared with non-metastasized tumors (all p<0.05). CD82 expression was correlated with pTNM status of differentiated and undifferentiated thyroid tumor and the pathologic stage of differentiated thyroid tumor. In contrast to CD82, CD63 mRNA and protein expression was unchanged in all thyroid carcinomas. Benign goiter tissues showed weak expression of CD63. There were no significant correlation between CD63 mRNA/protein expression and any clinical/pathological parameters. Our results support the hypothesis that down-regulation of CD82 expression may reflect an increased in vivo metastatic potential of thyroid cancer cells. CD82 may serve as a prognostic marker of metastasis in thyroid cancer. Constitutive expression of CD63 may indicate that this factor does not play a direct role in thyroid carcinogenesis.
Insights
Down-regulation of CD82 (KAI1) protein expression is linked to increased thyroid cancer metastasis. CD82 may serve as a prognostic marker for thyroid cancer, while CD63 (ME491) shows no significant role in thyroid carcinogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- CD82 (KAI1) and CD63 (ME491) are transmembrane 4 superfamily proteins implicated in cancer progression.
- CD82 is a potential prostate cancer metastasis suppressor, and CD63 is involved in melanoma progression.
- Down-regulation of CD82 and CD63 is associated with metastatic potential in various solid tumors, but their role in thyroid carcinogenesis is unclear.
Purpose of the Study:
- To investigate the expression of CD82 and CD63 in thyroid carcinoma.
- To determine if CD82 and CD63 expression can serve as prognostic indicators for thyroid cancer metastasis.
Main Methods:
- Reverse transcriptase-PCR (RT-PCR) and immunohistochemistry were used to analyze CD82 and CD63 expression.
- Tissues from benign goiter (n=12) and 75 primary thyroid carcinoma specimens (PTC, FTC, UTC) were analyzed.
- Specimens included non-metastasized (n=36) and metastasized (n=39) tumors.
Main Results:
- CD82 expression was present in all benign goiter tissues but significantly decreased in thyroid carcinoma tissues (p<0.001).
- Down-regulation of CD82 was also observed in metastasized tumors compared to non-metastasized tumors (p<0.05).
- CD82 expression correlated with pTNM status and pathological stage. CD63 expression was unchanged and showed no correlation with clinical or pathological parameters.
Conclusions:
- Down-regulation of CD82 expression correlates with increased metastatic potential in thyroid cancer.
- CD82 may function as a prognostic marker for metastasis in thyroid cancer.
- CD63 does not appear to play a direct role in thyroid carcinogenesis.
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