WNT6 promotes choriocarcinoma progression by driving proliferation, invasion, and metastasis

WNT6通过促进增殖、侵袭和转移来促进绒毛膜癌的进展。

阅读:1

Abstract

OBJECTIVE: Choriocarcinoma has a high propensity for distant metastasis, imposing a substantial psychological burden on patients. Unveiling the molecular mechanisms underlying tumor invasion and metastasis holds great clinical significance. METHODS: Immunohistochemistry was employed to detect WNT6 expression in normal early pregnancy villi, regressive hydatidiform moles, malignant hydatidiform moles and gestational trophoblastic neoplasia. Quantitation of mRNA expression by real-time PCR and Western blotting were utilized to quantify WNT6 expression in human chorionic trophoblastic cells and choriocarcinoma cells. Lentiviruses were used to construct stable cell models with either overexpressed or knocked-down WNT6, aiming to explore the impact of WNT6 expression on cell proliferation, migration, and invasion. RESULTS: The expression of WNT6 was significantly higher in malignant tissues and cells compared to normal counterparts. In the malignant hydatidiform mole group, WNT6 expression was correlated with tumor metastasis and the FIGO anatomical stage. Kaplan-Meier survival curve analysis indicated that the disease progression time of the high-WNT6-expression subgroup in the malignant hydatidiform mole group was notably shorter than that of the low-expression subgroup. CCK-8 assay, wound healing assay, and Transwell assays demonstrated that overexpression of WNT6 could enhance the proliferation, migration, and invasion of HTR-8 cells. Conversely, interfering with WNT6 expression led to opposite outcomes. CONCLUSION: High WNT6 expression is associated with tumor progression and poor prognosis. WNT6 is involved in the development of gestational trophoblastic diseases and can serve as a reference biomarker for disease progression and prognosis assessment.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。