Novel thrombospondin-1 transcript exhibits distinctive expression and activity in thyroid tumorigenesis
- Authors
- Hong, Yukyung; Kim, Ilju; Moon, Hyunjin; Lee, Jaehak; Lertpatipanpong, Pattawika; Ryu, Chang Hwan; Jung, Yuh-Seog; Seok, Jungirl; Kim, Yonghwan; Ryu, Junsun; Baek, Seung Joon
- Issue Date
- 2-Jun-2023
- Publisher
- SPRINGERNATURE
- Citation
- ONCOGENE, v.42, no.22, pp 1832 - 1842
- Pages
- 11
- Journal Title
- ONCOGENE
- Volume
- 42
- Number
- 22
- Start Page
- 1832
- End Page
- 1842
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/151740
- DOI
- 10.1038/s41388-023-02692-9
- ISSN
- 0950-9232
1476-5594
- Abstract
- Thrombospondin 1 (TSP1) is known for its cell-specific functions in cancer progression, such as proliferation and migration. It contains 22 exons that may potentially produce several different transcripts. Here, we identified TSP1V as a novel TSP1-splicing variant produced by intron retention (IR) in human thyroid cancer cells and tissues. We observed that TSP1V functionally inhibited tumorigenesis contrary to TSP1 wild-type, as identified in vivo and in vitro. These activities of TSP1V are caused by inhibiting phospho-Smad and phospho-focal adhesion kinase. Reverse transcription polymerase chain reaction and minigene experiments revealed that some phytochemicals/non-steroidal anti-inflammatory drugs enhanced IR. We further found that RNA-binding motif protein 5 (RBM5) suppressed IR induced by sulindac sulfide treatment. Additionally, sulindac sulfide reduced phospho-RBM5 levels in a time-dependent manner. Furthermore, trans-chalcone demethylated TSP1V, thereby preventing methyl-CpG-binding protein 2 binding to TSP1V gene. In addition, TSP1V levels were significantly lower in patients with differentiated thyroid carcinoma than in those with benign thyroid nodule, indicating its potential application as a diagnostic biomarker in tumor progression.
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