Scholarlink

<p>The Hippo pathway is a tumor suppressor pathway, and most related studies have indicated that its inhibition leads to tumorigenesis. However, recent studies have suggested that the activated Hippo pathway can promote tumorigenesis in certain contexts. Here, we demonstrate that the activated Hippo pathway induces non-cell-autonomous tumorigenesis, characterized by tumor markers in the <i>Drosophila</i> wing epithelium. This suggests that Hippo-activated cells behave similarly to “oncogenic niche cells.” We find that Hippo-activated cells induce Dronc-Wingless/Spitz signaling in the hinge/ventral notum region, which causes tumorigenesis. Moreover, we identify the amino acid transporters Sat1/2, which are implicated in amino acid incorporation and function redundantly with the growth factors Wingless and Spitz to facilitate non-cell-autonomous tumorigenesis.</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

The Hippo tumor suppressor pathway triggers non-cell autonomous tumorigenesis in Drosophila

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月1日

查看全文
  • Daichi Honda,
  • Misako Okumura,
  • Ayano Oi,
  • Chisako Sakuma,
  • Fumiaki Obata,
  • Toshinori Ando,
  • Masayuki Miura,
  • Takahiro Chihara

摘要

The Hippo pathway is a tumor suppressor pathway, and most related studies have indicated that its inhibition leads to tumorigenesis. However, recent studies have suggested that the activated Hippo pathway can promote tumorigenesis in certain contexts. Here, we demonstrate that the activated Hippo pathway induces non-cell-autonomous tumorigenesis, characterized by tumor markers in the Drosophila wing epithelium. This suggests that Hippo-activated cells behave similarly to “oncogenic niche cells.” We find that Hippo-activated cells induce Dronc-Wingless/Spitz signaling in the hinge/ventral notum region, which causes tumorigenesis. Moreover, we identify the amino acid transporters Sat1/2, which are implicated in amino acid incorporation and function redundantly with the growth factors Wingless and Spitz to facilitate non-cell-autonomous tumorigenesis.