Scholarlink

Introduction <p>The discovery and identification of novel diagnostic markers and effective therapeutic targets for ovarian cancer are urgently required. Recent studies have demonstrated that SOX30 suppresses tumor metastasis and serves as a prognostic and chemotherapeutic marker in advanced-stage ovarian cancer. In this study, we aim to investigate the expression patterns, regulatory mechanisms, and diagnostic potential of SOX30, as well as its SOX30 in tumor growth and the underlying mechanisms in ovarian cancer.</p> Methods <p>Using data from The Cancer Genome Atlas (TCGA) database, we comprehensively analyzed the association between SOX30 expression levels and copy number variations (CNVs) as well as DNA methylation in ovarian cancer. The functional role of SOX30 in tumor growth was evaluated through MTS assays, colony formation assays, rescue experiments, and xenograft models. Flow cytometry, western blotting, and confocal microscopy were employed to explore the effects of SOX30 on apoptosis and autophagy. Additionally, co-expression analysis of SOX30-related genes and functional enrichment analysis were performed to uncover potential biological pathways.</p> Results <p>SOX30 was frequently overexpressed in ovarian cancer, closely associated with copy number amplification, and effectively distinguished tumor tissues from normal tissues. Functionally, SOX30 significantly inhibited cancer cell proliferation in vitro and suppressed tumor growth in vivo, inducting slight cell apoptosis but marked autophagy in ovarian cancer cells. Mechanistically, the inhibitory effect of SOX30 on cancer cell proliferation was dependent on the regulation of autophagy. At the molecular level, SOX30 modulated biological processes and signaling pathways related to autophagy rather than apoptosis in ovarian cancer. Furthermore, SOX30 showed a strong positive correlation with key autophagy-related genes in ovarian cancer.</p> Conclusions <p>Our findings identify SOX30 as a promising diagnostic marker and therapeutic target in ovarian cancer, and highlight the previously underappreciated role of SOX30 in suppressing cancer cell proliferation and tumor growth primarily through an autophagy-mediated mechanism, offering new insights into the pathogenesis and treatment of ovarian cancer.</p> Graphical Abstract <p></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

SOX30 is a diagnostic biomarker that suppresses ovarian cancer progression through an autophagy mediated mechanism

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月21日

查看全文
  • Qian Li,
  • Peng Guo,
  • Keying Chen,
  • Jing Gu,
  • Na Sun,
  • Yating Deng,
  • Fei Wang,
  • Jun Ding,
  • Jinyi Liu,
  • Fei Han

摘要

Introduction

The discovery and identification of novel diagnostic markers and effective therapeutic targets for ovarian cancer are urgently required. Recent studies have demonstrated that SOX30 suppresses tumor metastasis and serves as a prognostic and chemotherapeutic marker in advanced-stage ovarian cancer. In this study, we aim to investigate the expression patterns, regulatory mechanisms, and diagnostic potential of SOX30, as well as its SOX30 in tumor growth and the underlying mechanisms in ovarian cancer.

Methods

Using data from The Cancer Genome Atlas (TCGA) database, we comprehensively analyzed the association between SOX30 expression levels and copy number variations (CNVs) as well as DNA methylation in ovarian cancer. The functional role of SOX30 in tumor growth was evaluated through MTS assays, colony formation assays, rescue experiments, and xenograft models. Flow cytometry, western blotting, and confocal microscopy were employed to explore the effects of SOX30 on apoptosis and autophagy. Additionally, co-expression analysis of SOX30-related genes and functional enrichment analysis were performed to uncover potential biological pathways.

Results

SOX30 was frequently overexpressed in ovarian cancer, closely associated with copy number amplification, and effectively distinguished tumor tissues from normal tissues. Functionally, SOX30 significantly inhibited cancer cell proliferation in vitro and suppressed tumor growth in vivo, inducting slight cell apoptosis but marked autophagy in ovarian cancer cells. Mechanistically, the inhibitory effect of SOX30 on cancer cell proliferation was dependent on the regulation of autophagy. At the molecular level, SOX30 modulated biological processes and signaling pathways related to autophagy rather than apoptosis in ovarian cancer. Furthermore, SOX30 showed a strong positive correlation with key autophagy-related genes in ovarian cancer.

Conclusions

Our findings identify SOX30 as a promising diagnostic marker and therapeutic target in ovarian cancer, and highlight the previously underappreciated role of SOX30 in suppressing cancer cell proliferation and tumor growth primarily through an autophagy-mediated mechanism, offering new insights into the pathogenesis and treatment of ovarian cancer.

Graphical Abstract