{"title":"NUF2 Promotes Breast Cancer Metastasis via Activating Wnt/β-Catenin Pathways.","authors":"Nijiati AiErken, Xidi Wang, Jiamei Wang, Weisen Ma, Lingfei Cui, Mingxia Zhang, Weifeng Ma, Dongwei Liu","doi":"10.31083/j.fbl2911371","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is the most common malignancy and the leading cause of cancer death among women. NDC80 kinetochore complex component (NUF2) is demonstrated to implicate the progression of human cancer. But the role of NUF2 in breast cancer progression is unclear. Here, we aimed to study the role and regulatory mechanisms of NUF2 in breast cancer metastasis.</p><p><strong>Methods: </strong>Immunohistochemistry was used to determine UNF2 expression in clinical samples. Transwell assas were used to determine the role of NUF2 in breast cancer migration and invasion. Animal model <i>in vivo</i> was used to determine the rold of NUF2 in breast cancer metastasis.</p><p><strong>Results: </strong>NUF2 was upregulated significantly in breast cancer tissues and cells. Worse prognosis was noted in patients with high NUF2 levels compared with that in patients with low NUF2 levels. NUF2 overexpression markedly enhanced, while NUF2 knockdown inhibited, breast cancer cell invasion and migration. Mechanistically, NUF2 was observed to upregulate Wnt/β-catenin signaling pathway activity. The promoting effect of NUF2 on cell migration and invasion were blocked by inhibition of the Wnt/β-catenin pathway.</p><p><strong>Conclusions: </strong>We revealed that NUF2 promotes breast cancer progression via activating Wnt/β-catenin signaling, suggesting that NUF2 might be a new potential target for breast cancer treatment.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"371"},"PeriodicalIF":3.3000,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in bioscience (Landmark edition)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31083/j.fbl2911371","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Breast cancer is the most common malignancy and the leading cause of cancer death among women. NDC80 kinetochore complex component (NUF2) is demonstrated to implicate the progression of human cancer. But the role of NUF2 in breast cancer progression is unclear. Here, we aimed to study the role and regulatory mechanisms of NUF2 in breast cancer metastasis.
Methods: Immunohistochemistry was used to determine UNF2 expression in clinical samples. Transwell assas were used to determine the role of NUF2 in breast cancer migration and invasion. Animal model in vivo was used to determine the rold of NUF2 in breast cancer metastasis.
Results: NUF2 was upregulated significantly in breast cancer tissues and cells. Worse prognosis was noted in patients with high NUF2 levels compared with that in patients with low NUF2 levels. NUF2 overexpression markedly enhanced, while NUF2 knockdown inhibited, breast cancer cell invasion and migration. Mechanistically, NUF2 was observed to upregulate Wnt/β-catenin signaling pathway activity. The promoting effect of NUF2 on cell migration and invasion were blocked by inhibition of the Wnt/β-catenin pathway.
Conclusions: We revealed that NUF2 promotes breast cancer progression via activating Wnt/β-catenin signaling, suggesting that NUF2 might be a new potential target for breast cancer treatment.
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