Scholarlink

<p>AdipoRon, a small adiponectin receptor (AdipoR) agonist, has the advantages of a low molecular weight, high stability, and long half-life. Preliminary data indicate that it also has anti-cancer effects. However, the investigation of AdipoRon in the context of ovarian cancer is limited. Further research is required to explore the underlying mechanisms. Cell function assays were performed to determine the effects of AdipoRon on the proliferation, apoptosis, migration, and autophagy of ovarian cancer cells. RNA sequencing was conducted on ovarian cancer cells treated with or without AdipoRon to identify dysregulated signaling pathways and targets. The effects of AdipoRon on AdipoR1/2, AMPK, its downstream genes, and autophagy in ovarian cancer cells were examined in the presence or absence of autophagy or AMPK inhibitors. Immunocompetent mice were used to establish an ovarian cancer metastasis model to evaluate the anti-tumor effects of AdipoRon. AdipoRon inhibited the proliferation and migration, promoted cell apoptosis, and induced autophagy in ovarian cancer cells in vitro<i>.</i> High-throughput transcriptome sequencing revealed a close correlation between autophagy and anti-tumor effects of AdipoRon. Mechanistically, AdipoRon induced autophagy by acting on the AdipoR1/2-AMPK-mTOR pathway, thereby inhibiting the progression of ovarian cancer. Blockade of AdipoR via shRNA, inhibition of autophagy or AMPK effectively rescued cells from AdipoRon-induced cellular phenotypes. Moreover, AdipoRon inhibited the malignant progression of ovarian cancer without noticeable loss of weight or organ side effects in an intraperitoneal transplant mouse tumor model. AdipoRon inhibited the malignant progression of ovarian cancer by inducing autophagy through the AdipoR1/2-AMPK-mTOR signaling pathway, suggesting its potential therapeutic value.</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

Adiponectin receptor agonist AdipoRon induces autophagy via AdipoR1/2-AMPK pathway and suppresses tumor progression in ovarian cancer

  • 期刊论文

  • 发表日期：

    2026年7月8日

查看全文
  • Hengwei Du,
  • Xueyuan Liu,
  • Ruiqi Hu,
  • Xinjing Wang,
  • Bingjie Cui,
  • Weiwei Chen,
  • Fei Wang,
  • Hongliang Dong,
  • Yi Wang,
  • Cuilan Liu,
  • Jing Du

摘要

AdipoRon, a small adiponectin receptor (AdipoR) agonist, has the advantages of a low molecular weight, high stability, and long half-life. Preliminary data indicate that it also has anti-cancer effects. However, the investigation of AdipoRon in the context of ovarian cancer is limited. Further research is required to explore the underlying mechanisms. Cell function assays were performed to determine the effects of AdipoRon on the proliferation, apoptosis, migration, and autophagy of ovarian cancer cells. RNA sequencing was conducted on ovarian cancer cells treated with or without AdipoRon to identify dysregulated signaling pathways and targets. The effects of AdipoRon on AdipoR1/2, AMPK, its downstream genes, and autophagy in ovarian cancer cells were examined in the presence or absence of autophagy or AMPK inhibitors. Immunocompetent mice were used to establish an ovarian cancer metastasis model to evaluate the anti-tumor effects of AdipoRon. AdipoRon inhibited the proliferation and migration, promoted cell apoptosis, and induced autophagy in ovarian cancer cells in vitro. High-throughput transcriptome sequencing revealed a close correlation between autophagy and anti-tumor effects of AdipoRon. Mechanistically, AdipoRon induced autophagy by acting on the AdipoR1/2-AMPK-mTOR pathway, thereby inhibiting the progression of ovarian cancer. Blockade of AdipoR via shRNA, inhibition of autophagy or AMPK effectively rescued cells from AdipoRon-induced cellular phenotypes. Moreover, AdipoRon inhibited the malignant progression of ovarian cancer without noticeable loss of weight or organ side effects in an intraperitoneal transplant mouse tumor model. AdipoRon inhibited the malignant progression of ovarian cancer by inducing autophagy through the AdipoR1/2-AMPK-mTOR signaling pathway, suggesting its potential therapeutic value.