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AHNAK 通过 Wnt/β-catenin 信号通路抑制卵巢癌细胞的进展。

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

机构信息

Department of Gynecology and Obstetrics, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.

Department of Obstetrics and Gynecology, Nanfang Hospital of Southern Medical University, Guangzhou, Guangdong, China.

出版信息

Aging (Albany NY). 2021 Oct 23;13(20):23579-23587. doi: 10.18632/aging.203473.

DOI:10.18632/aging.203473
PMID:34689136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8580348/
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.

摘要

在全球范围内,卵巢癌是女性妇科相关癌症死亡的第二大常见原因。其预后不良。有必要阐明卵巢癌进展中涉及的机制,并确定新的癌症靶点。我们研究并验证了卵巢癌组织和相应的正常组织中 AHNAK 的含量。然后,我们在体外和体内过表达 AHNAK,以确定 AHNAK 在卵巢癌细胞增殖和转移中的作用。最后,我们评估了可能的潜在分子机制。我们发现,卵巢癌中 AHNAK 的表达下调。卵巢癌细胞系中 AHNAK 含量的升高显著抑制了卵巢癌细胞的生长以及体外和体内的转移。此外,AHNAK 通过抑制经典 Wnt 级联反应部分抑制了卵巢癌的进展。因此,AHNAK 可能是卵巢癌的生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/fef3e79c969e/aging-13-203473-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/94c501cb0254/aging-13-203473-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/1bc70cd27d7f/aging-13-203473-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/eafe1b51c5cc/aging-13-203473-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/fef3e79c969e/aging-13-203473-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/94c501cb0254/aging-13-203473-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/1bc70cd27d7f/aging-13-203473-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/eafe1b51c5cc/aging-13-203473-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/779d/8580348/fef3e79c969e/aging-13-203473-g004.jpg

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