Scholarlink

Background <p>Breast cancer (BCa) is a major contributor to female mortality worldwide. Treatment resistance and tumor heterogeneity contribute to the lack of effective therapeutic targets, posing a significant challenge in BCa management. CENPI, a core centromere protein involved in chromosome segregation, has emerging evidence implicating it in oncogenesis across diverse malignancies. However, its functional and molecular mechanisms in BCa remain unclear.</p> Methods <p>We analyzed CENPI expression and its clinical significance by using the BCa dataset from the Cancer Genome Atlas (TCGA) and immunohistochemical staining of 3 human BCa tissue samples. Cellular functional assays and mice xenograft models were utilized to assess the effects of CENPI on BCa growth. RNA sequencing combined with bioinformatics analysis was conducted to elucidate the molecular mechanisms underlying CENPI function, with further validation through Western blotting, immunofluorescence, and TOP/FOP flash assays.</p> Results <p>CENPI was aberrantly overexpressed in BCa, with elevated expression levels strongly associated with disease progression and poor prognosis. Functional assays demonstrated that CENPI significantly promoted breast carcinogenesis in both cellular and animal models. Mechanistically, CENPI increased BCa progression and malignant phenotypes by modulating the Wnt/β-catenin axis.</p> Conclusions <p>CENPI is a critical oncogene in BCa, driving tumorigenesis and disease progression via the Wnt/β-catenin axis, which represents a promising biomarker and therapeutic target for BCa.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Centromere protein I facilitates breast cancer tumorigenesis and disease progression through modulation of Wnt/β-Catenin signaling

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月10日

查看全文
  • Chaoshen Wu,
  • Yibing Zhou,
  • Yuxiao Mu,
  • Yijie Cheng,
  • Wenqian Xu,
  • Mengna Huang,
  • Jingyuan Xu,
  • Ming Li,
  • Jianfeng Gu,
  • Xuli Meng,
  • Da Qian

摘要

Background

Breast cancer (BCa) is a major contributor to female mortality worldwide. Treatment resistance and tumor heterogeneity contribute to the lack of effective therapeutic targets, posing a significant challenge in BCa management. CENPI, a core centromere protein involved in chromosome segregation, has emerging evidence implicating it in oncogenesis across diverse malignancies. However, its functional and molecular mechanisms in BCa remain unclear.

Methods

We analyzed CENPI expression and its clinical significance by using the BCa dataset from the Cancer Genome Atlas (TCGA) and immunohistochemical staining of 3 human BCa tissue samples. Cellular functional assays and mice xenograft models were utilized to assess the effects of CENPI on BCa growth. RNA sequencing combined with bioinformatics analysis was conducted to elucidate the molecular mechanisms underlying CENPI function, with further validation through Western blotting, immunofluorescence, and TOP/FOP flash assays.

Results

CENPI was aberrantly overexpressed in BCa, with elevated expression levels strongly associated with disease progression and poor prognosis. Functional assays demonstrated that CENPI significantly promoted breast carcinogenesis in both cellular and animal models. Mechanistically, CENPI increased BCa progression and malignant phenotypes by modulating the Wnt/β-catenin axis.

Conclusions

CENPI is a critical oncogene in BCa, driving tumorigenesis and disease progression via the Wnt/β-catenin axis, which represents a promising biomarker and therapeutic target for BCa.