Magnetic Reprogramming of Macrophages Stimulates Phagocytosis of Breast Cancer Cells via a TRPC1-STING Inflammatory Axis

Abstract

The reprogramming of tumor-associated macrophages (TAMs) from a pro-tumoral M2 to an anti-tumoral M1 phenotype is an attractive therapeutic strategy whose clinical translation is undermined by the systemic toxicity of currently available pharmacological approaches. Here, we demonstrate that non-invasive and localizable pulsed electromagnetic fields (PEMFs) induce macrophage reprogramming downstream of transient receptor potential canonical 1 (TRPC1) channel activation. Brief (10 min) PEMF exposure polarized macrophages toward an M1 phenotype by activating Stimulator of Interferon Genes (STING)-dependent NF-κB inflammatory pathways that were abolished by TRPC1 knockdown or inhibition. PEMF exposure directly enhanced the immunogenicity of breast cancer cells and modified macrophage-cancer crosstalk to promote M1 macrophage polarization and the attraction of STING-activated macrophages to the cancer cells. In co-cultures, PEMF exposure stimulated macrophage-mediated phagocytosis of cancer cells in a STING- and TRPC1-dependent manner. In spheroids, PEMFs induced the reprogramming of TAMs to an M1 status and selectively enhanced infiltration of M1 macrophages, resulting in STING-mediated phagocytosis of cancer cells. In mice, 2 weeks of twice-weekly PEMF exposure resorbed engrafted tumors and selectively eliminated cancer cells within tumors while promoting immune cell recruitment. PEMFs offer a non-invasive manner to locally reprogram TAMs within the tumor microenvironment to preferentially eliminate cancer cells.

Keywords

adaptive antitumor immunity / cyclic GMP-AMP synthase (cGAS) / immunotherapy / interferons / NF-κB / pulsed electromagnetic field (PEMF) / tumor microenvironment (TME) / tumor-associated macrophages (TAMs)

References

[1] A. Shapouri-Moghaddam, S. Mohammadian, H. Vazini, et al., “Macrophage Plasticity, Polarization, and Function in Health and Disease,” Journal of Cellular Physiology 233 (2018): 6425–6440.

[2] P. J. Murray, “Macrophage Polarization,” Annual Review of Physiology 79 (2017): 541–566.

[3] A. T. Gharavi, N. A. Hanjani, E. Movahed, and M. Doroudian, “The Role of Macrophage Subtypes and Exosomes in Immunomodulation,” Cellular & Molecular Biology Letters 27 (2022): 83.

[4] Q. Zong, H. Zhang, F. Liu, et al., “Activation of the cGAS-STING Pathway by Viral dsDNA Leading to M1 Polarization of Macrophages Mediates Antiviral Activity Against Hepatitis B Virus,” Immunobiology 229 (2024): 152810.

[5] M. T. Zdrenghea, H. Makrinioti, A. Muresan, S. L. Johnston, and L. A. Stanciu, “The Role of Macrophage IL-10/Innate IFN Interplay During Virus-Induced Asthma,” Reviews in Medical Virology 25 (2015): 33–49.

[6] Y. Pan, Y. Yu, X. Wang, and T. Zhang, “Tumor-Associated Macrophages in Tumor Immunity,” Frontiers in Immunology 11 (2020): 583084.

[7] S. U. Khan, M. U. Khan, M. Azhar Ud Din, et al., “Reprogramming Tumor-Associated Macrophages as a Unique Approach to Target Tumor Immunotherapy,” Frontiers in Immunology 14 (2023): 1166487.

[8] Y. Kawaguchi, Y. Ohshio, A. Watanabe, et al., “Depletion of Tumor-Associated Macrophages Inhibits Lung Cancer Growth and Enhances the Antitumor Effect of Cisplatin,” Cancer Science 114 (2023): 750–763.

[9] M. Rakaee, L. R. Busund, S. Jamaly, et al., “Prognostic Value of Macrophage Phenotypes in Resectable Non-Small Cell Lung Cancer Assessed by Multiplex Immunohistochemistry,” Neoplasia 21 (2019): 282–293.

[10] I. Larionova, G. Tuguzbaeva, A. Ponomaryova, et al., “Tumor-Associated Macrophages in Human Breast, Colorectal, Lung, Ovarian and Prostate Cancers,” Frontiers in Oncology 10 (2020): 566511.

[11] S. Chen, A. Saeed, Q. Liu, et al., “Macrophages in Immunoregulation and Therapeutics,” Signal Transduction and Targeted Therapy 8 (2023): 207.

[12] J. H. Rannikko and M. Hollmen, “Clinical Landscape of Macrophage-Reprogramming Cancer Immunotherapies,” British Journal of Cancer 131 (2024): 627–640.

[13] A. Chauhan, Y. Sun, P. Sukumaran, et al., “M1 Macrophage Polarization Is Dependent on TRPC1-Mediated Calcium Entry,” iScience 8 (2018): 85–102.

[14] A. Franco-Obregón, “Harmonizing Magnetic Mitohormetic Regenerative Strategies: Developmental Implications of a Calcium-Mitochondrial Axis Invoked by Magnetic Field Exposure,” Bioengineering 10 (2023): 1176.

[15] J. L. Y. Yap, Y. K. Tai, J. Fröhlich, et al., “Ambient and Supplemental Magnetic Fields Promote Myogenesis via a TRPC1-Mitochondrial Axis: Evidence of a Magnetic Mitohormetic Mechanism,” FASEB Journal 33 (2019): 12853–12872.

[16] O. M. Elzamzamy, R. Penner, and L. A. Hazlehurst, “The Role of TRPC1 in Modulating Cancer Progression,” Cells 9 (2020): 388.

[17] S. P. Gravel, “Deciphering the Dichotomous Effects of PGC-1 α on Tumorigenesis and Metastasis,” Frontiers Oncology 8 (2018): 75.

[18] X. Zhang, Y. Chen, X. Liu, et al., “STING in Cancer Immunoediting: Modeling Tumor-Immune Dynamics Throughout Cancer Development,” Cancer Letters 612 (2025): 217410.

[19] N. Natarajan, J. Florentin, E. Johny, et al., “Aberrant Mitochondrial DNA Synthesis in Macrophages Exacerbates Inflammation and Atherosclerosis,” Nature Communications 15 (2024): 7337.

[20] S. Crocetti, C. Beyer, G. Schade, M. Egli, J. Fröhlich, and A. Franco-Obregón, “Low Intensity and Frequency Pulsed Electromagnetic Fields Selectively Impair Breast Cancer Cell Viability,” PLoS One 8 (2013): e72944.

[21] Y. K. Tai, K. K. W. Chan, C. H. H. Fong, et al., “Modulated TRPC1 Expression Predicts Sensitivity of Breast Cancer to Doxorubicin and Magnetic Field Therapy: Segue Towards a Precision Medicine Approach,” Frontiers in Oncology 11 (2021): 783803.

[22] V. K. Sukumar, Y. K. Tai, C. W. Chan, et al., “Brief Magnetic Field Exposure Stimulates Doxorubicin Uptake Into Breast Cancer Cells in Association With TRPC1 Expression: A Precision Oncology Methodology to Enhance Chemotherapeutic Outcome,” Cancers 16 (2024): 3860.

[23] L. Wu, K. Chen, J. Xiao, et al., “Angiotensin II Induces RAW264.7 Macrophage Polarization to the M1-Type Through the Connexin 43/NF-κB Pathway,” Molecular Medicine Reports 21 (2020): 2103–2112.

[24] L. Liu, S. Peng, M. Duan, et al., “The Role of C/EBP Homologous Protein (CHOP) in Regulating Macrophage Polarization in RAW264.7 Cells,” Microbiology and Immunology 65 (2021): 531–541.

[25] T. D. Smith, M. J. Tse, E. L. Read, and W. F. Liu, “Regulation of Macrophage Polarization and Plasticity by Complex Activation Signals,” Integrative Biology 8 (2016): 946–955.

[26] S. Yum, M. Li, Y. Fang, and Z. J. Chen, “TBK1 Recruitment to STING Activates Both IRF3 and NF-κB That Mediate Immune Defense Against Tumors and Viral Infections,” Proceedings of the National Academy of Sciences 118 (2021): e2100225118.

[27] R. C. Coll, J. R. Hill, C. J. Day, et al., “MCC950 Directly Targets the NLRP3 ATP-Hydrolysis Motif for Inflammasome Inhibition,” Nature Chemical Biology 15 (2019): 556–559.

[28] Z. Yang, Z. Min, and B. Yu, “Reactive Oxygen Species and Immune Regulation,” International Reviews of Immunology 39 (2020): 292–298.

[29] Z. Wang, Y. Wang, Z. He, and C. Liu, “Emerging cGAS-STING Agonist-Based Nanotherapeutics: Mechanistic Insights and Applications in Cancer Combination Therapy,” Advanced Science 12 (2025): e09890.

[30] J. N. Iversen, Y. K. Tai, K. Y. Wu, C. J. K. Wong, H. Y. Lim, and A. Franco-Obregón, “Magnetically Stimulated Myogenesis Recruits a CRY2-TRPC1 Photosensitive Signaling Axis,” Cells 14 (2025): 231.

[31] F. Kurth, Y. K. Tai, D. Parate, et al., “Cell-Derived Vesicles as TRPC1 Channel Delivery Systems for the Recovery of Cellular Respiratory and Proliferative Capacities,” Advanced Biosystems 4 (2020): 2000146.

[32] A. Kougioumoutzakis, J. G. Pelletier, I. Laplante, A. Khlaifia, and J. C. Lacaille, “TRPC1 Mediates Slow Excitatory Synaptic Transmission in Hippocampal Oriens/Alveus Interneurons,” Molecular Brain 13 (2020): 12.

[33] P. Sukumaran, Y. Sun, N. Antonson, and B. B. Singh, “Dopaminergic Neurotoxins Induce Cell Death by Attenuating NF-κB-Mediated Regulation of TRPC1 Expression and Autophagy,” FASEB Journal 32 (2018): 1640–1652.

[34] P. Sukumaran, Y. Sun, M. Vyas, and B. B. Singh, “TRPC1-Mediated Ca²⁺ Entry Is Essential for the Regulation of Hypoxia and Nutrient Depletion-Dependent Autophagy,” Cell Death & Disease 6 (2015): e1674.

[35] N. Tang, W. Tian, G. Y. Ma, et al., “TRPC Channels Blockade Abolishes Endotoxemic Cardiac Dysfunction by Hampering Intracellular Inflammation and Ca²⁺ Leakage,” Nature Communications 13 (2022): 7455.

[36] C. Y. Matsumura, A. P. Taniguti, A. Pertille, H. S. Neto, and M. J. Marques, “Stretch-Activated Calcium Channel Protein TRPC1 Is Correlated With the Different Degrees of the Dystrophic Phenotype in Mdx Mice,” American Journal of Physiology-Cell Physiology 301 (2011): C1344–C1350.

[37] A. K. Singh, K. Saotome, L. L. McGoldrick, and A. I. Sobolevsky, “Structural Bases of TRP Channel TRPV6 Allosteric Modulation by 2-APB,” Nature Communications 9 (2018): 2465.

[38] C. K. Colton and M. X. Zhu, “2-Aminoethoxydiphenyl Borate as a Common Activator of TRPV1, TRPV2, and TRPV3 Channels,” in Transient Receptor Potential (TRP) Channels, ed. V. Flockerzi and B. Nilius (Springer, 2007), 173–187.

[39] A. Schaar, P. Sukumaran, Y. Sun, A. Dhasarathy, and B. B. Singh, “TRPC1-STIM1 Activation Modulates Transforming Growth Factor β-Induced Epithelial-to-Mesenchymal Transition,” Oncotarget 7 (2016): 80554–80567.

[40] S. Srikanth, J. S. Woo, B. Wu, et al., “The Ca²⁺ Sensor STIM1 Regulates the Type I Interferon Response by Retaining the Signaling Adaptor STING at the Endoplasmic Reticulum,” Nature Immunology 20 (2019): 152–162.

[41] J. Wu, Z. Li, Y. Deng, et al., “Function of TRP Channels in monocytes/macrophages,” Frontiers in Immunology 14 (2023): 1187890.

[42] K. Yao, B. Dou, Y. Zhang, et al., “Inflammation-The Role of TRPA1 Channel,” Frontiers in Physiology 14 (2023): 1093925.

[43] K. J. Racacho, Y. P. Shiau, R. Villa, et al., “The Tumor Immune Microenvironment: Implications for Cancer Immunotherapy, Treatment Strategies, and Monitoring Approaches,” Frontiers in Immunology 16 (2025): 1621812.

[44] L. A. Moraes, S. Kar, S. L. Foo, et al., “Annexin-A1 Enhances Breast Cancer Growth and Migration by Promoting Alternative Macrophage Polarization in the Tumour Microenvironment,” Scientific Reports 7 (2017): 17925.

[45] Y. Hong, Y. Fu, and Q. Long, “Post-Translational Governance of NF-κB in Cancer Immunity: Mechanisms and Therapeutic Horizons,” Frontiers in Immunology 16 (2025): 1627084.

[46] V. Pandey, A. Fleming-Martinez, L. Bastea, et al., “CXCL10/CXCR3 Signaling Contributes to an Inflammatory Microenvironment and Its Blockade Enhances Progression of Murine Pancreatic Precancerous Lesions,” eLife 10 (2021): e60646.

[47] C. L. Langrish, B. S. McKenzie, N. J. Wilson, R. de Waal Malefyt, R. A. Kastelein, and D. J. Cua, “IL-12 and IL-23: Master Regulators of Innate and Adaptive Immunity,” Immunological Reviews 202 (2004): 96–105.

[48] J. Liu, X. Geng, J. Hou, and G. Wu, “New Insights into M1/M2 Macrophages: Key Modulators in Cancer Progression,” Cancer Cell International 21 (2021): 389.

[49] S. E. Malawista, J. B. Gee, and K. G. Bensch, “Cytochalasin B Reversibly Inhibits Phagocytosis: Functional, Metabolic, and Ultrastructural Effects in Human Blood Leukocytes and Rabbit Alveolar Macrophages,” Yale Journal of Biology and Medicine 44 (1971): 286–300.

[50] H. Ahvati, R. Roudi, N. Sobhani, and F. Safari, “CD47 as a Potent Target in Cancer Immunotherapy: A Review,” Biochimica et Biophysica Acta (BBA)—Reviews on Cancer 1880 (2025): 189294.

[51] A. Wang, L. A. Madden, and V. N. Paunov, “Advanced Biomedical Applications Based on Emerging 3D Cell Culturing Platforms,” Journal of Materials Chemistry B 8 (2020): 10487–10501.

[52] G. M. Weir, R. S. Liwski, and M. Mansour, “Immune Modulation by Chemotherapy or Immunotherapy to Enhance Cancer Vaccines,” Cancers 3 (2011): 3114–3142.

[53] U. Anand, A. Dey, A. K. S. Chandel, et al., “Cancer Chemotherapy and Beyond: Current Status, Drug Candidates, Associated Risks and Progress in Targeted Therapeutics,” Genes & Diseases 10 (2023): 1367–1401.

[54] M. Xiao, J. He, L. Yin, X. Chen, X. Zu, and Y. Shen, “Tumor-Associated Macrophages: Critical Players in Drug Resistance of Breast Cancer,” Frontiers in Immunology 12 (2021): 799428.

[55] V. Salemme, G. Centonze, L. Avalle, et al., “The Role of Tumor Microenvironment in Drug Resistance: Emerging Technologies to Unravel Breast Cancer Heterogeneity,” Frontiers in Oncology 13 (2023): 1170264.

[56] D. A. Yardley, “Drug Resistance and the Role of Combination Chemotherapy in Improving Patient Outcomes,” International Journal of Breast Cancer 2013 (2013): 137414.

[57] K. Fenech, I. Micallef, and B. Baron, “5-Fluorouracil Dose Escalation Generated Desensitized Colorectal Cancer Cells With Reduced Expression of Protein Methyltransferases and No Epithelial-to-Mesenchymal Transition Potential,” Oncology Research 32 (2024): 1047–1061.

[58] Y. Wang, N. Li, X. Zhang, and T. Horng, “Mitochondrial Metabolism Regulates Macrophage Biology,” Journal of Biological Chemistry 297 (2021): 100904.

[59] I. Golovynska, Y. V. Stepanov, S. Golovynskyi, et al., “Macrophages Modulated by Red/NIR Light: Phagocytosis, Cytokines, Mitochondrial Activity, Ca²⁺ Influx, Membrane Depolarization and Viability,” Photochemistry and Photobiology 98 (2022): 484–497.

[60] Y. Chen, M. M. Menger, B. J. Braun, et al., “Modulation of Macrophage Activity by Pulsed Electromagnetic Fields in the Context of Fracture Healing,” Bioengineering 8 (2021): 167.

[61] J. Gu, X. He, X. Chen, L. Dong, W. Weng, and K. Cheng, “Effects of Electrical Stimulation on Cytokine-Induced Macrophage Polarization,” Journal of Tissue Engineering and Regenerative Medicine 16 (2022): 448–459.

[62] T. A. Henderson and L. D. Morries, “Near-Infrared Photonic Energy Penetration: Can Infrared Phototherapy Effectively Reach the Human Brain?,” Neuropsychiatric Disease and Treatment 11 (2015): 2191–2208.

[63] C. Lee, J. J. Polari, K. E. Kramer, and S. C. Wang, “Near-Infrared (NIR) Spectrometry as a Fast and Reliable Tool for Fat and Moisture Analyses in Olives,” ACS Omega 3 (2018): 16081–16088.

[64] K. Nosaka, A. Aldayel, M. Jubeau, and T. C. Chen, “Muscle Damage Induced by Electrical Stimulation,” European Journal of Applied Physiology 111 (2011): 2427–2437.

[65] D. R. Dolbow, A. S. Gorgey, T. W. Sutor, V. Bochkezanian, and K. Musselman, “Invasive and Non-Invasive Approaches of Electrical Stimulation to Improve Physical Functioning After Spinal Cord Injury,” Journal of Clinical Medicine 10 (2021): 5356.

[66] M. Mansourian and A. Shanei, “Evaluation of Pulsed Electromagnetic Field Effects: A Systematic Review and Meta-Analysis on Highlights of Two Decades of Research In Vitro Studies,” Biomed Research International 2021 (2021): 6647497.

[67] M. Bedder and A. Abd-Elsayed, “Mechanisms of Action of Low-Frequency Pulsed Magnetic Fields in Pain Control,” Bioengineering 13 (2026): 407.

[68] M. M. Rosado, M. Simkó, M. O. Mattsson, and C. Pioli, “Immune-Modulating Perspectives for Low Frequency Electromagnetic Fields in Innate Immunity,” Frontiers in Public Health 6 (2018): 85.

[69] F. Guerriero and G. Ricevuti, “Extremely Low Frequency Electromagnetic Fields Stimulation Modulates Autoimmunity and Immune Responses: A Possible Immuno-Modulatory Therapeutic Effect in Neurodegenerative Diseases,” Neural Regeneration Research 11 (2016): 1888–1895.

[70] M. Ristow and K. Zarse, “How Increased Oxidative Stress Promotes Longevity and Metabolic Health: The Concept of Mitochondrial Hormesis (Mitohormesis),” Experimental Gerontology 45 (2010): 410–418.

[71] J. Ouyang, B. Zhang, L. Kuang, et al., “Pulsed Electromagnetic Field Inhibits Synovitis via Enhancing the Efferocytosis of Macrophages,” Biomed Research International 2020 (2020): 4307385.

[72] D. E. Clapham, “TRP Channels as Cellular Sensors,” Nature 426 (2003): 517–524.

[73] Y. Jang, Y. Lee, S. M. Kim, Y. D. Yang, J. Jung, and U. Oh, “Quantitative Analysis of TRP Channel Genes in Mouse Organs,” Archives of Pharmacal Research 35 (2012): 1823–1830.

[74] C. Van den Eynde, J. Vriens, and K. De Clercq, “Transient Receptor Potential Channel Regulation by Growth Factors,” Biochimica et Biophysica Acta (BBA)—Molecular Cell Research 1868 (2021): 118950.

[75] A. Minard, C. C. Bauer, D. J. Wright, et al., “Remarkable Progress With Small-Molecule Modulation of TRPC1/4/5 Channels: Implications for Understanding the Channels in Health and Disease,” Cells 7 (2018): 52.

[76] X. Pan, W. Zhang, H. Guo, et al., “Strategies Involving STING Pathway Activation for Cancer Immunotherapy: Mechanism and Agonists,” Biochemical Pharmacology 213 (2023): 115596.

[77] Y. Liu, P. Xu, S. Rivara, et al., “Clathrin-Associated AP-1 Controls Termination of STING Signalling,” Nature 610 (2022): 761–767.

[78] J. Kwon and S. F. Bakhoum, “The Cytosolic DNA-Sensing cGAS-STING Pathway in Cancer,” Cancer Discovery 10 (2020): 26–39.

[79] T. Stylianopoulos, L. L. Munn, and R. K. Jain, “Reengineering the Tumor Vasculature: Improving Drug Delivery and Efficacy,” Trends in Cancer 4 (2018): 258–259.

[80] C. B. Synn, D. K. Kim, J. H. Kim, et al., “Primary Tumor Suppression and Systemic Immune Activation of Macrophages Through the Sting Pathway in Metastatic Skin Tumor,” Yonsei Medical Journal 63 (2021): 42–55.

[81] D. Arias-Salvatierra, E. K. Silbergeld, L. C. Acosta-Saavedra, and E. S. Calderon-Aranda, “Role of Nitric Oxide Produced by iNOS Through NF-κB Pathway in Migration of Cerebellar Granule Neurons Induced by Lipopolysaccharide,” Cellular Signalling 23 (2011): 425–435.

[82] K. Jin, D. Zhao, J. Zhou, X. Zhang, Y. Wang, and Z. Wu, “Pulsed Electromagnetic Fields Inhibit IL-37 to Alleviate CD8⁺ T Cell Dysfunction and Suppress Cervical Cancer Progression,” Apoptosis 29 (2024): 2108–2127.

[83] L. Tao, A. Lemoff, G. Wang, et al., “Reactive Oxygen Species Oxidize STING and Suppress Interferon Production,” eLife 9 (2020): e57837.

[84] M. Simkó, S. Droste, R. Kriehuber, and D. G. Weiss, “Stimulation of Phagocytosis and Free Radical Production in Murine Macrophages by 50 Hz Electromagnetic Fields,” European Journal of Cell Biology 80 (2001): 562–566.

[85] M. Zhu, X. Tang, Z. Zhu, et al., “STING Activation in Macrophages by Vanillic Acid Exhibits Antineoplastic Potential,” Biochemical Pharmacology 213 (2023): 115618.

[86] B. Hoesel and J. A. Schmid, “The Complexity of NF-κB Signaling in Inflammation and Cancer,” Molecular Cancer 12 (2013): 86.

[87] J. Yoon, X. T. Le, J. Kim, et al., “Macrophage-Reprogramming Upconverting Nanoparticles for Enhanced TAM-Mediated Antitumor Therapy of Hypoxic Breast Cancer,” Journal of Controlled Release 360 (2023): 482–495.

[88] S. N. Bess, G. K. Smart, M. J. Igoe, and T. J. Muldoon, “Scaffold-Free Development of Multicellular Tumor Spheroids With Spatial Characterization of Structure and Metabolic Radial Profiles,” In Vitro Models 3 (2024): 91–108.

[89] S. S. Ho, W. Y. Zhang, N. Y. Tan, et al., “The DNA Structure-Specific Endonuclease MUS81 Mediates DNA Sensor STING-Dependent Host Rejection of Prostate Cancer Cells,” Immunity 44 (2016): 1177–1189.

[90] A. S. Almeida, M. R. Fein, and M. Egeblad, “Multi-Color Flow Cytometry for Comprehensive Analysis of the Tumor Immune Infiltrate in a Murine Model of Breast Cancer,” Bio-Protocol 11 (2021): e4012.

[91] S. E. Liyanage, P. J. Gardner, J. Ribeiro, et al., “Flow Cytometric Analysis of Inflammatory and Resident Myeloid Populations in Mouse Ocular Inflammatory Models,” Experimental Eye Research 151 (2016): 160–170.

[92] W. Yang, Z. Guo, H. Ju, et al., “IL-4-STAT6-induced High Siglec-G/10 Expression Aggravates the Severe Immune Suppressive Tumor Microenvironment and Impedes the Efficacy of Immunotherapy in Head and Neck Squamous Cell Carcinoma,” Journal for ImmunoTherapy of Cancer 13 (2025): e011474.

[93] S. Rose, A. Misharin, and H. Perlman, “A Novel Ly6C/Ly6G-Based Strategy to Analyze the Mouse Splenic Myeloid Compartment,” Cytometry, Part A 81 (2012): 343–350.

[94] C. Xu, H. Wu, Y. Liu, F. Li, R. K. Manne, and H. K. Lin, “Protocol for Detecting Macrophage-Mediated Cancer Cell Phagocytosis In Vitro and In Vivo,” STAR Protocols 4 (2023): 101940.

Rights & permissions

2026 The Author(s). Smart Medicine published by Wiley-VCH GmbH on behalf of Wenzhou Institute, University of Chinese Academy of Sciences.