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Updated: Jan 31, 2026
Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
Published on: May 3, 2018
Cyclin-dependent kinase 7 is a potential therapeutic target in papillary thyroid carcinoma
1Department of Thyroid and Parathyroid Surgery Center, Sichuan University West China Hospital, China.
Abstract:
Given the pathological incidence of metastases or radioiodine-refractory papillary thyroid carcinoma (PTC) is increasing worldwide, patients have little alternatives when choosing effective drugs. Therefore, it is necessary to develop new therapeutic targets for PTC treatment. CDK7 is a member of the cyclindependent protein kinase (CDK) family, which plays an important role in various types of cancers. In this study, we found CDK7 were upregulated in PTC cell lines compared to normal thyroid cells using qRT-PCR and Western blot. Furthermore, using cell counting kit-8 (CCK-8) assay and 5-ethynyl-2-deoxyuridine (EdU) assay, we discovered cell growth ratio was positively correlated to the expression level of CDK7. Cell cycle analysis showed that the cells with higher CDK7 expression levels were prone to be in S phase. More importantly, we tested the inhibitory effects of BS-181 on CDK7 both in vitro and in vivo. Results obtained from this study indicated that BS-181 not only suppressed the cell proliferation in vitro, but also inhibited the tumor growth in nude mouse without changing mRNA and protein levels of CDK7. In conclusion, our study might provide a novel potential target for PTC therapy.
Insights
Cyclin-dependent kinase 7 (CDK7) is upregulated in papillary thyroid carcinoma (PTC). Inhibiting CDK7 with BS-181 suppressed tumor growth in vitro and in vivo, suggesting CDK7 as a potential therapeutic target for PTC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Papillary thyroid carcinoma (PTC) with metastases or radioiodine-refractory disease presents limited therapeutic options.
- Cyclin-dependent kinase 7 (CDK7), a cell cycle regulator, is implicated in various cancers.
- CDK7 upregulation in PTC suggests its potential role in tumorigenesis.
Purpose of the Study:
- To investigate the role of CDK7 in papillary thyroid carcinoma (PTC) pathogenesis.
- To evaluate the therapeutic potential of CDK7 inhibition in PTC treatment.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) and Western blot to assess CDK7 expression in PTC cells.
- Cell counting kit-8 (CCK-8) and 5-ethynyl-2-deoxyuridine (EdU) assays to evaluate cell proliferation.
- Cell cycle analysis to determine the effect of CDK7 on cell cycle progression.
- In vitro and in vivo studies using the CDK7 inhibitor BS-181 in a nude mouse model.
Main Results:
- CDK7 expression was significantly upregulated in PTC cell lines compared to normal thyroid cells.
- Higher CDK7 expression correlated positively with increased cell growth and S-phase progression.
- BS-181 treatment inhibited PTC cell proliferation in vitro.
- BS-181 suppressed tumor growth in vivo without altering CDK7 mRNA or protein levels.
Conclusions:
- CDK7 plays a crucial role in PTC cell proliferation and cell cycle progression.
- CDK7 inhibition by BS-181 demonstrates therapeutic potential for PTC.
- CDK7 represents a promising novel therapeutic target for papillary thyroid carcinoma treatment.
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