Scholarlink

<p>The protein phosphatase PPP4C has been implicated in oncogenic processes, but its role in thyroid carcinoma (THCA) and triple-negative breast cancer (TNBC) remains unclear. Here, we combined bioinformatic analyses with in vitro experiments to investigate the clinical and functional significance of PPP4C in these malignancies. PPP4C was significantly upregulated in both THCA and TNBC compared with normal tissues, and higher expression was associated with adverse clinicopathological features and poorer overall survival. Functional assays showed that PPP4C knockdown suppressed proliferation, migration, and invasion in TNBC and THCA cell lines, supporting a pro-tumorigenic role in vitro. Integrative analyses further suggested that elevated PPP4C expression is associated with oncogenic signaling pathways, RNA modification–related genes, and immune-related characteristics. Drug sensitivity prediction analysis indicated differential responsiveness to selected targeted agents, and experimental validation demonstrated that PPP4C depletion enhances sensitivity to specific inhibitors in vitro. Overall, PPP4C is consistently overexpressed and functionally relevant in THCA and TNBC. PPP4C may represent a candidate biomarker associated with tumor progression and therapeutic response, warranting further mechanistic and in vivo investigation.</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

PPP4C: a potential molecular marker and therapeutic target in thyroid cancer and triple-negative breast cancer

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月4日

查看全文
  • Huashui Li,
  • Yifan Chen,
  • Guodong Guo,
  • Qinghua Luo,
  • Qiang Lin,
  • Wenjun Xie,
  • Maolin Yan

摘要

The protein phosphatase PPP4C has been implicated in oncogenic processes, but its role in thyroid carcinoma (THCA) and triple-negative breast cancer (TNBC) remains unclear. Here, we combined bioinformatic analyses with in vitro experiments to investigate the clinical and functional significance of PPP4C in these malignancies. PPP4C was significantly upregulated in both THCA and TNBC compared with normal tissues, and higher expression was associated with adverse clinicopathological features and poorer overall survival. Functional assays showed that PPP4C knockdown suppressed proliferation, migration, and invasion in TNBC and THCA cell lines, supporting a pro-tumorigenic role in vitro. Integrative analyses further suggested that elevated PPP4C expression is associated with oncogenic signaling pathways, RNA modification–related genes, and immune-related characteristics. Drug sensitivity prediction analysis indicated differential responsiveness to selected targeted agents, and experimental validation demonstrated that PPP4C depletion enhances sensitivity to specific inhibitors in vitro. Overall, PPP4C is consistently overexpressed and functionally relevant in THCA and TNBC. PPP4C may represent a candidate biomarker associated with tumor progression and therapeutic response, warranting further mechanistic and in vivo investigation.