Related Experiment Video
Updated: Sep 25, 2025
An Orthotopic Endometrial Cancer Model with Retroperitoneal Lymphadenopathy Made From In Vivo Propagated and Cultured VX2 Cells
Published on: September 12, 2019
SPOP Inhibition of Endometrial Carcinoma and Its Clinicopathological Relationship
Qing Zhu1,2, Guanghui Zhang3, Mingyang Tang4
1Department of Pathology, The First Affiliated Hospital of Bengbu Medical College, Bengbu, 233399 Anhui, China.
Objective:
Endometrial carcinoma (EC) ranks first in the incidence of female genital malignancies in developed countries. SPOP (speckle-type POZ protein) has changed in EC with a statistically high frequency. This research may play a crucial role in the initiation and progression of EC, ultimately leading to fresh therapeutic targets. Explore the expression of SPOP in EC; observe its effect on the proliferation, invasion, and migration of EC cells after upregulating the expression of SPOP through RNA activation.
Methods:
The expression levels of SPOP protein in 150 EC tissues and 45 normal endometrial tissues were detected by immunohistochemistry and Western blotting. Analyze the relationship between SPOP expression and clinicopathological characteristics. The differences of the proliferation, migration, and invasion abilities between before and after transfection were analyzed using CCK-8 and Transwell assays.
Results:
The results of immunohistochemistry and Western blotting showed the expression level of SPOP in EC tissue significantly reduced or even missed compared with normal endometrial tissue. The results of CCK-8 showed that the growth of EC significantly slowed down after the upregulating of SPOP expression. The results of the Transwell assay showed the migration and invasion abilities of EC cells were weakened after the level of SPOP was upregulated.
Conclusions:
The expression level of SPOP in EC tissues is lower and related to the clinicopathological features compared with normal endometrial tissues. After upregulating the SPOP expression by RNA activation in EC cell lines, the abilities of proliferation, migration, and invasion of cells were significantly inhibited.
Insights
Speckle-type POZ protein (SPOP) is significantly reduced in endometrial carcinoma (EC) tissues. Restoring SPOP expression in EC cells inhibits their proliferation, migration, and invasion, suggesting SPOP as a potential therapeutic target for EC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Endometrial carcinoma (EC) is a leading cause of female genital malignancies.
- Alterations in Speckle-type POZ protein (SPOP) expression are frequently observed in EC.
- SPOP may influence EC initiation and progression, presenting potential therapeutic targets.
Purpose of the Study:
- To investigate SPOP expression levels in EC tissues.
- To determine the impact of upregulated SPOP on EC cell proliferation, invasion, and migration.
Main Methods:
- Immunohistochemistry and Western blotting were used to assess SPOP protein levels in EC and normal endometrial tissues.
- CCK-8 and Transwell assays were employed to evaluate EC cell proliferation, migration, and invasion after SPOP upregulation via RNA activation.
Main Results:
- SPOP expression was significantly reduced or absent in EC tissues compared to normal tissues.
- Upregulating SPOP expression via RNA activation markedly inhibited EC cell proliferation.
- The migration and invasion capabilities of EC cells were significantly weakened following SPOP upregulation.
Conclusions:
- Reduced SPOP expression in EC is linked to clinicopathological features.
- Restoring SPOP expression in EC cell lines inhibits proliferation, migration, and invasion.
- SPOP represents a promising therapeutic target for endometrial carcinoma.
