Scholarlink

<p>Mitogen-activated protein kinase phosphatases (MKPs), also known as dual-specificity phosphatases (DUSPs), are key regulatory factors within the mitogen-activated protein kinase (MAPK) pathway. MKP7/DUSP16, a member of the MKP family, has been identified in vitro as a phosphatase with specificity for p38 mitogen-activated protein kinase (p38) and c-jun amino-terminal kinase (JNK), with a stronger inhibitory effect on JNK compared to other MAPKs. In recent years, MKP7/DUSP16 has recently attracted increasing interest, with accumulating evidence suggesting its dysfunction is correlated with the progression and drug resistance of various cancers, making it a potential prognostic biomarker. However, research into the specific mechanisms by which MKP7/DUSP16 regulates cancer cells remains limited. Current studies suggest that MKP7/DUSP16 may promote cancer progression through the regulation of the MAPK pathway, mitochondrial apoptosis pathways, and the induction of cancer cell proliferation by immune cells. This review summarizes the mechanisms by which MKP7/DUSP16 may promote tumor proliferation. Further studies are needed to clarify its specific regulatory roles in cancer.</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

Regulatory roles of MKP7/DUSP16 in cancer

  • 期刊论文

  • 发表日期：

    2025年12月1日

查看全文
  • Shiqi Chen,
  • Maryam Mohammed Abbas Karekad,
  • Jiaxi Yan,
  • Linfeng Qian,
  • Xuanwei Wu,
  • Xiaoai Lv,
  • Xiaohong Xu

摘要

Mitogen-activated protein kinase phosphatases (MKPs), also known as dual-specificity phosphatases (DUSPs), are key regulatory factors within the mitogen-activated protein kinase (MAPK) pathway. MKP7/DUSP16, a member of the MKP family, has been identified in vitro as a phosphatase with specificity for p38 mitogen-activated protein kinase (p38) and c-jun amino-terminal kinase (JNK), with a stronger inhibitory effect on JNK compared to other MAPKs. In recent years, MKP7/DUSP16 has recently attracted increasing interest, with accumulating evidence suggesting its dysfunction is correlated with the progression and drug resistance of various cancers, making it a potential prognostic biomarker. However, research into the specific mechanisms by which MKP7/DUSP16 regulates cancer cells remains limited. Current studies suggest that MKP7/DUSP16 may promote cancer progression through the regulation of the MAPK pathway, mitochondrial apoptosis pathways, and the induction of cancer cell proliferation by immune cells. This review summarizes the mechanisms by which MKP7/DUSP16 may promote tumor proliferation. Further studies are needed to clarify its specific regulatory roles in cancer.