ArticleMolecular therapy oncolytics2022
Metabolic remodeling in tumor-associated macrophages contributing to antitumor activity of cryptotanshinone by regulating TRAF6-ASK1 axis.
Article in Molecular therapy oncolytics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 22 citations in OpenAlex.
- Ubiquitin signaling in tumor-associated macrophage reprogramming: mechanisms and therapeutic opportunities in cancers.Biomarker research · 2026Review
- Targeting the tumor microenvironment: a new strategy for natural products in breast cancer therapy.Natural products and bioprospecting · 2026Review
- Targeting tumor-associated macrophages through phytochemicals: a promising strategy for cold tumor therapy.Chinese medicine · 2026Review
- Autophagy modulation in gynaecologic oncology: insights into immune regulation and therapeutic potential.Frontiers in immunology · 2026Review
- Article
- Global research status and frontiers on autophagy in triple negative breast cancer (TNBC): a comprehensive bibliometric and visualized analysis.Discover oncology · 2025Article
- Autophagy in tumor immune escape and immunotherapy.Molecular cancer · 2025Review
- Natural Products as Novel Therapeutic Agents for Triple-Negative Breast Cancer: Current Evidence, Mechanisms, Challenges, and Opportunities.Molecules (Basel, Switzerland) · 2025Review
- Sweet regulation - The emerging immunoregulatory roles of hexoses.Journal of advanced research · 2025Review
- The ubiquitination-autophagy axis in cancer therapy resistance: mechanistic insights and therapeutic opportunities.Frontiers in pharmacology · 2025Review
- CLG promotes mTOR/ULK1 pathway-mediated autophagy to inhibit OS development by inhibiting TRAF6-mediated FLT3 ubiquitination.Cancer science · 2024Article
- Progress in the Regulation of Immune Cells in the Tumor Microenvironment by Bioactive Compounds of Traditional Chinese Medicine.Molecules (Basel, Switzerland) · 2024Review
- Pharmacological Mechanisms of Cryptotanshinone: Recent Advances in Cardiovascular, Cancer, and Neurological Disease Applications.Drug design, development and therapy · 2024Review
- A new perspective on the therapeutic potential of tumor metastasis: targeting the metabolic interactions between TAMs and tumor cells.International journal of biological sciences · 2024Review
- Tumour-associated macrophages: versatile players in the tumour microenvironment.Frontiers in cell and developmental biology · 2023Review
- The promise of targeting heme and mitochondrial respiration in normalizing tumor microenvironment and potentiating immunotherapy.Frontiers in oncology · 2022Review
- Progress of Traditional Chinese Medicine in Regulating Immune Cell in the Tumor Microenvironment of Triple-Negative Breast Cancer.Integrative cancer therapiesReview
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dampening tumor growth by converting tumor-associated macrophages (TAMs) from M2/repair-types to M1/kill-types is of high interest. Here, we show that cryptotanshinone (CPT) can function as an antitumor immune modulator that switches TAMs from an M2 to an M1 phenotype, leading to tumor regression. An orthotopic triple-negative breast cancer (TNBC) implantation model was used to determine the role and mechanism of CPT in suppressing M1-to-M2 repolarization of TAMs. Co-culturing TNBC cells with CPT-treated macrophages reduced TNBC proliferation and motility, while in TNBC orthotopic mouse models, CPT treatment inhibited breast tumor formation. Moreover, we identified that CPT inhibits mitochondrial oxidative phosphorylation and mitochondrial fusion via autophagy and transcriptional activation of the apoptosis signal-regulating kinase 1 (ASK1) pathway. Suppression of ASK1 downregulates autophagy and abolishes CPT-induced effects upon TAMs. In addition, CPT inhibits M2 macrophage differentiation and causes TRAF6 auto-ubiquitination-dependent activation of the ASK1, leading to M1 polarization. On the contrary, in M1 macrophage, CPT increases interaction of ASK1 and TRAF6 which induces ASK1 ubiquitination and degradation. Intriguingly, CPT plays opposite roles in the M1 and M2 phenotype. Our findings help to illuminate a previously unrecognized antitumor mechanism of CPT and suggest that this natural compound offers a macrophage-based approach for cancer immunotherapy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.