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<p>Natural bioactive compounds with anti-neoplastic effects, such as celastrol (CLS), have attracted considerable interest in recent years. The present study aimed to investigate the effect of CLS on wnt/β-catenin signaling, and its potential combination with doxorubicin (Dox) to enhance chemotherapeutic effects. After intramuscular inoculation of Ehrlich tumor cells, tumor-bearing mice received CLS (2 mg/kg<b>,</b> i.p), Dox (5 mg/kg, once/week, i.p), and their combination for 21 days. Treatment with CLS showed showing antioxidant and anti-inflammatory, as evidenced by a significant increase in glutathione content and a significant decrease in the malondialdehyde, interleukin 6, and interleukin 1β concentrations. CLS also inhibited VEGF-mediated angiogenesis. The current study revealed that CLS downregulated <i>β‐catenin</i> gene expression with subsequent downstream target genes, such as <i>cyclin-D1</i>, and <i>survivin</i>, which dampens tumor cell proliferation and triggers cell cycle arrest as well as induces apoptosis as indicated by the increased expression of p53, caspase‐3. The current study concludes that CLS exerted its anti-neoplastic activity by suppressing the wnt/β-catenin signaling pathway, and opens a new perspective for combining CLS with Dox to enhance its chemotherapeutic effects and reduce the oxidative imbalance and inflammatory responses associated with Dox treatment.</p>

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Anti-neoplastic activity of celastrol in experimentally-induced mammary adenocarcinoma in mice: targeting wnt/β-catenin signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月28日

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  • Mohamed M. Salama,
  • Randa A. Zaghloul,
  • Rania M. Khalil,
  • Mamdouh M. El-Shishtawy

摘要

Natural bioactive compounds with anti-neoplastic effects, such as celastrol (CLS), have attracted considerable interest in recent years. The present study aimed to investigate the effect of CLS on wnt/β-catenin signaling, and its potential combination with doxorubicin (Dox) to enhance chemotherapeutic effects. After intramuscular inoculation of Ehrlich tumor cells, tumor-bearing mice received CLS (2 mg/kg, i.p), Dox (5 mg/kg, once/week, i.p), and their combination for 21 days. Treatment with CLS showed showing antioxidant and anti-inflammatory, as evidenced by a significant increase in glutathione content and a significant decrease in the malondialdehyde, interleukin 6, and interleukin 1β concentrations. CLS also inhibited VEGF-mediated angiogenesis. The current study revealed that CLS downregulated β‐catenin gene expression with subsequent downstream target genes, such as cyclin-D1, and survivin, which dampens tumor cell proliferation and triggers cell cycle arrest as well as induces apoptosis as indicated by the increased expression of p53, caspase‐3. The current study concludes that CLS exerted its anti-neoplastic activity by suppressing the wnt/β-catenin signaling pathway, and opens a new perspective for combining CLS with Dox to enhance its chemotherapeutic effects and reduce the oxidative imbalance and inflammatory responses associated with Dox treatment.