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Updated: Mar 27, 2026

Transplantation Into the Mouse Ovarian Fat Pad
Published on: September 7, 2016
PFTK1 regulates cell proliferation, migration and invasion in epithelial ovarian cancer
Weiwei Zhang1, Rong Liu2, Chunhui Tang1
1Department of Obstetrics and Gynecology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, People's Republic of China.
Abstract:
PFTK1, also named Cyclin-Dependent Kinase 14 (CDK14), is a member of the cell division cycle 2 (CDC2)-related protein kinase family. It is a serine/threonine-protein kinase involved in the regulation of cell cycle progression and cell proliferation. In this study, we investigated the role of PFTK1 in epithelial ovarian cancer (EOC) development. The expression of PFTK1 was detected by Western blot and immunohistochemistry staining, both of which demonstrated that PFTK1 was overexpressed in EOC tissues and cells. Statistical analysis showed the expression of PFTK1 was associated with multiple clinicopathological factors, including tumor grade, FIGO stage, lymph node metastatis, Ki-67 expression and predicted a poor prognosis of EOC patients. With in vitro studies we found that PFTK1 expression was decreased in serum-starved ovarian cancer cells, and progressively increased after serum-re-feeding. Knocking PFTK1 down by small interfering RNA (siRNA) significantly inhibited ovarian cancer cell proliferation, migration and invasion. Taken together, our study suggested that PFTK1 played an important role in ovarian cancer development.
Insights
Cyclin-Dependent Kinase 14 (PFTK1) is overexpressed in epithelial ovarian cancer (EOC), promoting tumor growth and progression. Inhibiting PFTK1 significantly reduced cancer cell proliferation, migration, and invasion, suggesting its role as a therapeutic target.
Area of Science:
- Molecular Biology
- Oncology
- Cell Biology
Background:
- Cyclin-Dependent Kinase 14 (PFTK1) is a serine/threonine-protein kinase involved in cell cycle regulation.
- Its role in epithelial ovarian cancer (EOC) development requires further investigation.
Purpose of the Study:
- To investigate the role of PFTK1 in the development and progression of epithelial ovarian cancer (EOC).
Main Methods:
- Western blot and immunohistochemistry were used to detect PFTK1 expression in EOC tissues and cells.
- Statistical analysis correlated PFTK1 expression with clinicopathological factors.
- In vitro studies utilized serum starvation and re-feeding models.
- Small interfering RNA (siRNA) was used to knock down PFTK1 expression.
Main Results:
- PFTK1 was significantly overexpressed in EOC tissues and cells compared to normal controls.
- High PFTK1 expression correlated with advanced tumor grade, FIGO stage, lymph node metastasis, and Ki-67 expression.
- PFTK1 expression levels fluctuated with serum availability, increasing upon re-feeding.
- siRNA-mediated knockdown of PFTK1 suppressed ovarian cancer cell proliferation, migration, and invasion.
Conclusions:
- PFTK1 is upregulated in epithelial ovarian cancer and is associated with poor prognosis.
- PFTK1 plays a critical role in promoting ovarian cancer cell proliferation, migration, and invasion.
- PFTK1 represents a potential therapeutic target for epithelial ovarian cancer.
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