ArticleIntegrative cancer therapies
Mechanism Study of Bufalin Reversal of Drug Resistance by Inhibiting Hypoxic Colon Cancer Cell-Induced Polarization of M2 Macrophages.
Article in Integrative cancer therapies. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Bufalin-Loaded Multifunctional Nanodrugs for Cancer Therapy: Mechanisms, Delivery Strategies, and Translational Perspectives.Biomolecules · 2026Review
- Targeting tumor-associated macrophages through phytochemicals: a promising strategy for cold tumor therapy.Chinese medicine · 2026Review
- Traditional Chinese medicine remodels the immune microenvironment of colorectal cancer: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Recent advances in drug repurposing for cancer immunomodulation emerging strategies, mechanistic insights, and clinical translation.Frontiers in oncology · 2026Review
- Targeting steroid receptor coactivators for the treatment of benign female reproductive disorders.Endocrine connections · 2025Review
- Unveiling the tumor microenvironment in colorectal cancer therapeutic resistance.Frontiers in cell and developmental biology · 2025Review
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7 authors.
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Abstract
Chemoresistance is still an important factor affecting the efficacy of treatment in colorectal cancer (CRC) patients. Hypoxia is related to poor prognosis and treatment resistance in cancer. Relevant studies have shown that a hypoxic microenvironment can promote the polarization of M2 macrophages and thus promote tumor development. Previous research has found that bufalin has a wide range of antitumor effects, but whether bufalin can reverse tumor resistance by improving the hypoxic tumor microenvironment is still unclear. In present research, it was found that high expression of SRC-3 in CRC cells under hypoxic conditions promoted the polarization of M2 and caused chemotherapy resistance, while bufalin, a monomeric drug used in Chinese medicine, reduced the level of SRC-3 and HIF-1α, thereby reversing chemoresistance. In addition, overexpression of SRC-3 reduced the hypoxia-mitigating effect of bufalin on CRC cells to promote the polarization of M2. Bufalin also inhibits the polarization of M2 caused by hypoxic CRC cells. Therefore, bufalin has the potential to become a new adjuvant therapy that can be further explored in future studies on its treatment of CRC.
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