Role of ADAM33 short isoform as a tumor suppressor in the pathogenesis of thyroid cancer via oncogenic function disruption of full-length ADAM33
© 2023. The Author(s)..
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.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2023 |
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| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:36 |
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| Enthalten in: |
Human cell - 36(2023), 4 vom: 28. Juli, Seite 1451-1463 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Lan, Jing [VerfasserIn] |
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| Links: |
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| Themen: |
ADAM Proteins |
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| Anmerkungen: |
Date Completed 23.06.2023 Date Revised 01.07.2023 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1007/s13577-023-00898-3 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM354828657 |
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| 245 | 1 | 0 | |a Role of ADAM33 short isoform as a tumor suppressor in the pathogenesis of thyroid cancer via oncogenic function disruption of full-length ADAM33 |
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| 500 | |a Date Revised 01.07.2023 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2023. The Author(s). | ||
| 520 | |a 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 | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a ADAM33 | |
| 650 | 4 | |a Alternative splicing | |
| 650 | 4 | |a Thyroid cancer | |
| 650 | 7 | |a Protein Isoforms |2 NLM | |
| 650 | 7 | |a ADAM33 protein, human |2 NLM | |
| 650 | 7 | |a EC 3.4.24.- |2 NLM | |
| 650 | 7 | |a ADAM Proteins |2 NLM | |
| 650 | 7 | |a EC 3.4.24.- |2 NLM | |
| 700 | 1 | |a Zhou, Yehui |e verfasserin |4 aut | |
| 700 | 1 | |a Liu, Yang |e verfasserin |4 aut | |
| 700 | 1 | |a Xia, Yu |e verfasserin |4 aut | |
| 700 | 1 | |a Wan, Yuqiu |e verfasserin |4 aut | |
| 700 | 1 | |a Cao, Jianbo |e verfasserin |4 aut | |
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