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Original Papers

Beclin 1 is Highly Expressed in Papillary Thyroid Carcinoma and Correlates with Lymph Node Metastasis

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Pages 175-181 | Published online: 11 Mar 2016
 

Abstract

Background : Autophagy is believed to be important in tumorigenesis and tumor progression. The human beclin-1 gene, a key regulator of autophagy formation, located on chromosome 17q21, has been identified as the mammalian orthologue of Atg6 (autophagy-related gene) and may be a haploinsufficient tumor suppressor gene. Loss of expression or point mutation could serve as a mechanism of loss of beclin-1 tumor suppressor function in cancers. However, our recent study revealed that point mutation of the beclin-1 gene is a rare event in papillary thyroid carcinoma (PTC).

Methods : We investigated the expression of beclin-1 in human PTC. Tissue samples from 86 cases of papillary thyroid carcinoma were used for the present study. 57 cases of papillary thyroid carcinoma were with lymph node metastasis. The expression of beclin-1 in tumor, normal tissue adjacent to tumor, distant normal tissue, metastatic lymph node and normal lymph node was examined with immunohistochemistry. The beclin-1 expression between tumor and normal tissue, metastatic and normal lymph node was also analyzed.

Results : The expression of beclin-1 was detected in 88.4% (76/86) of the tumors and 98.2% (56/57) of metastatic lymph nodes. In contrast, normal tissues adjacent to tumor, distant normal tissues and normal lymph nodes showed no or very weak expression of beclin-1. Beclin-1 was significantly correlated with tumorigenesis and lymph node metastasis in human PTC.

Conclusions : High expression of beclin-1 in PTC and metastatic lymph node suggest that neo-expression of beclin-1 may play a role in tumorigenesis and lymph node metastasis in human PTC.

Additional information

Notes on contributors

H. Ma

H. Ma Department of Thyroid Surgery Shandong Provincial Hospital Shandong University Jinan, 250021, P.R.China Tel.: +86 531–85186940 Fax: +86 531–85186940 E-mail: [email protected]

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