| Autor: |
Meiqin Liu, Shile Gao, Xingjun Xu, Huan Ma, Dongmei Wang, Xueqin Cai, Yang Wang |
| Zdroj: |
European Journal of Gynaecological Oncology; Oct2024, Vol. 45 Issue 5, p146-151, 6p |
| Abstrakt: |
Cervical cancer is the 4th leading cause of tumor-related deaths among women, primarily due to high-risk Human Papillomavirus (HPV). The role of Collapsin Response Mediator Protein 4 (CRMP4) in cervical cancer remains poorly understood, despite its variable expression across various cancers. This study aimed to investigate the mechanisms by which CRMP4 regulates cervical cancer cell growth as well as Epithelial-Mesenchymal Transition (EMT). Based on transcriptome data from The Cancer Genome Atlas (TCGA), CRMP4 is significantly downregulated in cervical cancer tissues compared to normal tissues. Immunoblot assays revealed lower CRMP4 expression in cervical cancer cell lines. Cell Counting Kit-8 (CCK-8), colony formation and flowcytometry demonstrated that CRMP4 overexpression inhibited cell growth as well as stimulated apoptosis in HeLa as well as SiHa cells. In addition, CRMP4 overexpression increased Epithelial cadherin (E-cadherin) levels and decreased Neural cadherin (N-cadherin) and alpha-Smooth Muscle Actin (α-SMA) levels, indicating EMT suppression. CRMP4 overexpression downregulated the Wnt/β-catenin axis by reducing expressions of β- catenin, Wnt family member 3A (Wnt3a), c-Myc and cyclin D1. In summary, CRMP4 inhibits cervical cancer cell proliferation as well as EMT by mediating the Wnt/β-catenin axis. CRMP4 may therefore be a potential therapeutic target of cervical cancer. [ABSTRACT FROM AUTHOR] |
| Databáze: |
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