Research Paper Volume 13, Issue 20 pp 23579—23587

AHNAK suppresses ovarian cancer progression through the Wnt/β-catenin signaling pathway

Yanlin Cai1, , Yi Hu1, , Furong Yu1, , Wenjuan Tong1, , Shufen Wang1, , Shunliang Sheng1, , Jiayu Zhu2, ,

  • 1 Department of Gynecology and Obstetrics, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China
  • 2 Department of Obstetrics and Gynecology, Nanfang Hospital of Southern Medical University, Guangzhou, Guangdong, China

Received: September 17, 2020       Accepted: June 18, 2021       Published: October 23, 2021
How to Cite

Copyright: © 2021 Cai et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Globally, ovarian cancer is the 2nd most frequent cause of gynecologic-associated cancer fatalities among women. It has an unfavorable prognosis. There is a need to elucidate on the mechanisms involved in ovarian cancer progression and to identify novel cancer targets. We investigated and verified AHNAK contents in ovarian cancer tissues and corresponding healthy tissues. Then, we overexpressed AHNAK in vitro and in vivo to establish the roles of AHNAK in ovarian cancer cell proliferation and metastasis. Finally, we evaluated the possible molecular mechanisms underlying. We established that AHNAK was downregulated in ovarian cancer. Elevated AHNAK contents in ovarian cancer cell lines remarkably repressed ovarian cancer cell growth, along with metastasis in vitro, as well as in vivo. Moreover, AHNAK suppressed the progress of ovarian cancer partly via dampening the Canonical Wnt cascade. Therefore, AHNAK may be a biomarker and treatment target for ovarian cancer.


CCK-8: cell counting kit-8; qRT-PCR: quantitative RT-PCR; HE: hematoxylin and eosin; EMT: epithelial-mesenchymal transition; MET: mesenchymal-epithelial transition.