Abstract

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.

Highlights

  • Ovarian cancer, which is among the most frequent gynecologic malignancies, is the second most common cause of mortality among women with gynecologic cancers [1]

  • AHNAK overexpression represses ovarian cancer cell growth and infiltration in vitro To determine the significance of AHNAK in the progression of ovarian cancer, AHNAK was overexpressed in ovarian cancer cells (Figure 2A)

  • A cell proliferation assay was conducted, and the results demonstrated that AHNAK overexpression suppressed the cell proliferation of ovarian cancer cells (Figure 2B)

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Summary

Introduction

Ovarian cancer, which is among the most frequent gynecologic malignancies, is the second most common cause of mortality among women with gynecologic cancers [1]. In 2018 alone, there were 295,414 new morbidities accompanied by 184,799 mortalities from ovarian cancer around the world [2]. The prognosis of ovarian cancer is still poor. Studies have recently found that AHNAK is pivotal in cell migration along with infiltration in an extensive range of cancers [5]. It is believed that the Canonical Wnt cascade is linked to cancer progress, especially with cell migration along with infiltration [7]. Canonical Wnt is hyper-activated in metastatic breast cancer cells [8]. The Canonical Wnt cascade participates in enhanced EMT, cell migration, and cancer cell metastasis [9]. The function of AHNAK and Canonical Wnt cascade in ovarian cancer is poorly characterized at present

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