1. Academic Validation
  2. Role of ADAM33 short isoform as a tumor suppressor in the pathogenesis of thyroid cancer via oncogenic function disruption of full-length ADAM33

Role of ADAM33 short isoform as a tumor suppressor in the pathogenesis of thyroid cancer via oncogenic function disruption of full-length ADAM33

  • Hum Cell. 2023 Mar 28. doi: 10.1007/s13577-023-00898-3.
Jing Lan # 1 Yehui Zhou # 1 Yang Liu 1 Yu Xia 1 Yuqiu Wan 2 Jianbo Cao 3
Affiliations

Affiliations

  • 1 Department of General Surgery, The first affiliated hospital of Soochow University, 188 Shizi Street, Suzhou, 215000, People's Republic of China.
  • 2 Department of General Surgery, The first affiliated hospital of Soochow University, 188 Shizi Street, Suzhou, 215000, People's Republic of China. lanjing20082022@163.com.
  • 3 Department of General Surgery, The first affiliated hospital of Soochow University, 188 Shizi Street, Suzhou, 215000, People's Republic of China. 598442626@qq.com.
  • # Contributed equally.
Abstract

Thyroid Cancer is the most prevalent endocrine malignancy globally; however, its underlying pathogenesis remains unclarified. Reportedly, alternative splicing is involved in processes such as embryonic stem and precursor cell differentiation, cell lineage reprogramming, and epithelial-mesenchymal transitions. ADAM33-n, an alternative splicing isoform of ADAM33, encodes a small protein containing 138 Amino acids of the N-terminal of full-length ADAM33, which constructs a chaperone-like domain that was previously reported to bind and block the proteolysis activity of ADAM33. In this study, we reported for the first time that ADAM33-n was downregulated in thyroid Cancer. The results of cell counting kit-8 and colony formation assays showed that ectopic ADAM33-n in papillary thyroid Cancer cell lines restricted cell proliferation and colony formation. Moreover, we demonstrated that ectopic ADAM33-n reversed the oncogenic function of full-length ADAM33 in cell growth and colony formation in the MDA-T32 and BCPAP cells. These findings indicate the tumor suppressor ability of ADAM33-n. Altogether, our study findings present a potential explanatory model of how the downregulation of the oncogenic gene ADAM33 promotes the pathogenesis of thyroid Cancer.

Keywords

ADAM33; Alternative splicing; Thyroid cancer.

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