> ## Content Index > Fetch the complete content index at: https://www.sanarelab.science/llms.txt > Use this file to discover other available public pages before exploring further. # Artemisinin Liposomes Suppress Breast Cancer Metastasis via TIGIT/CD155 Axis (2026 Study) - URL: https://www.sanarelab.science/artemisinin-liposomes-breast-cancer-tigit-2026/ - Published: 2026-08-11T08:46:13.000Z - Updated: 2026-08-16T07:09:03.000Z - Description: A July 2026 study in Apoptosis demonstrates that artemisinin-loaded liposomes suppress breast cancer metastasis and induce apoptosis by modulating the TIGIT/CD155 immune checkpoint axis in 4T1 cell and mouse models. - Author: Sanare Lab - Tags: #short-read, News, Research Key Takeaway A July 2026 study in *Apoptosis* reports that artemisinin-loaded liposomes suppress breast cancer metastasis and trigger apoptosis in 4T1 triple-negative breast cancer cells and mouse models. The mechanism involves disruption of the TIGIT/CD155 immune checkpoint axis, a pathway that cancer cells exploit to evade immune surveillance. This is a preclinical study; no human clinical data are available. Artemisinin, the antimalarial compound derived from the sweet wormwood plant (*Artemisia annua*), has attracted growing interest as a repurposed anticancer drug. Its endoperoxide bridge reacts with intracellular iron to generate reactive oxygen species (ROS), selectively killing cancer cells while sparing normal tissue. A new July 2026 study published in *Apoptosis* takes this research further by encapsulating artemisinin in liposomes and demonstrating a novel mechanism of action in breast cancer. The study, conducted by researchers in China and Turkey, evaluated the effects of artemisinin liposomes on 4T1 triple-negative breast cancer cells—a highly aggressive model that closely mimics human metastatic breast cancer. For patients researching how repurposed drugs are incorporated into cancer protocols, our [dosing calculator](https://www.sanarelab.science/protocol-dosing-workspace/) provides additional context on metabolic-targeting strategies. ## Table of Contents - [Study Design and Liposome Characterization](#study-design-and-liposome-characterization) - [In Vitro and In Vivo Results](#in-vitro-and-in-vivo-results) - [Mechanism: TIGIT/CD155 Axis](#mechanism-tigitcd155-axis) - [Evidence Level and Limitations](#evidence-level-and-limitations) - [Frequently Asked Questions](#faq) ## Study Design and Liposome Characterization The researchers synthesized artemisinin-loaded liposomes using the thin film dispersion method. The resulting nanoparticles had the following characteristics: - **Average size** — approximately 130 nm for artemisinin liposomes (80 nm for empty liposomes) - **Polydispersity index** — 0.287 (indicating a relatively uniform particle size distribution) - **Encapsulation efficiency** — 90.11% ± 0.88% - **Cumulative release** — 32.8% at pH 5.5 (tumor-like acidic environment) The acidic pH-triggered release is clinically relevant because the tumor microenvironment is typically more acidic than healthy tissue, which could allow for selective drug delivery. ## In Vitro and In Vivo Results The study evaluated three experimental arms in vitro and in vivo: saline control, free artemisinin, empty liposomes, and artemisinin liposomes. Key findings included: | Endpoint | Artemisinin Liposomes Result | | -------------------------- | -------------------------------------------------------- | | Cytotoxicity (4T1 cells) | Significantly greater than free artemisinin (lower IC₅₀) | | Migration (scratch assay) | Markedly suppressed compared to control and free drug | | Invasion (transwell assay) | Significantly reduced | | Colony formation | Inhibited | | Apoptosis | Increased (flow cytometry) | | Mouse tumor growth | Suppressed at 100 mg/kg/d artemisinin liposomes | These results indicate that the liposomal formulation significantly enhanced artemisinin's anticancer activity compared to the free drug, likely due to improved solubility, bioavailability, and tumor-targeted delivery. ## Mechanism: TIGIT/CD155 Axis The central mechanistic finding of the study is that artemisinin liposomes modulate the TIGIT/CD155 [immune checkpoint](https://www.sanarelab.science/ivermectin-and-cancer-immunotherapy-what-the-research-shows/) axis. TIGIT (T-cell immunoreceptor with Ig and ITIM domains) is an inhibitory receptor expressed on immune cells, while CD155 is its ligand commonly overexpressed on cancer cells. This interaction suppresses immune responses, allowing tumors to evade immune surveillance. The researchers found that artemisinin liposomes downregulated the expression of key signaling molecules in this pathway, including: - **Src** — a tyrosine kinase involved in cell proliferation and survival - **Akt** — a central regulator of the PI3K/AKT/mTOR pathway - **mTOR** — a key regulator of cell growth and metabolism - **STAT3** — a transcription factor frequently activated in cancer By suppressing these molecules, artemisinin liposomes appear to disrupt the TIGIT/CD155 axis, which may contribute to both the direct cytotoxic effects on cancer cells and the restoration of anti-tumor immune activity. ## Evidence Level and Limitations This study is preclinical and carries several important limitations: - **Mouse model only** — The in vivo data were generated in a 4T1 mouse tumor model, which is useful but not equivalent to human disease. - **Single cell line** — Most in vitro data used only the B-CPAP and 4T1 cell lines; other breast cancer subtypes were not tested. - **No human data** — No clinical trials or patient data are included. - **Dosing extrapolation** — The 100 mg/kg/d dose in mice does not directly translate to human dosing. - **Liposome manufacturing** — Clinical-scale production of artemisinin liposomes would require significant pharmaceutical development. While the findings are promising, they should be viewed as early-stage research that requires further validation before any clinical application. ## Frequently Asked Questions What is the TIGIT/CD155 axis? TIGIT (T-cell immunoreceptor with Ig and ITIM domains) is an inhibitory receptor on immune cells. CD155 is its ligand, often overexpressed on cancer cells. Their interaction suppresses immune responses, allowing tumors to evade immune surveillance. Blocking this axis is an active area of immunotherapy research. Is artemisinin approved for cancer treatment? No. Artemisinin and its derivatives are approved only for malaria treatment. Their use in cancer is experimental and based on preclinical studies. No clinical trials have established artemisinin as an effective cancer therapy in humans. What are liposomes and why do they matter? Liposomes are tiny spherical vesicles made of lipids that can encapsulate drugs. They improve drug solubility, stability, and targeted delivery to tumors. In this study, liposomes increased artemisinin's encapsulation efficiency to 90% and enhanced its anticancer effects compared to the free drug. In Plain Terms Scientists wrapped an antimalarial drug (artemisinin) inside tiny fat bubbles called liposomes and tested it on breast cancer cells. The liposomes made the drug work better, slowing tumor growth and stopping cancer cells from spreading. The drug seems to work by interfering with a communication system that cancer cells use to hide from the immune system. 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Always consult a healthcare provider before using any supplement or medication. ## References 1. Feng Y, Han Z, Shao J, et al. Artemisinin liposomes regulates breast cancer metastasis and apoptosis through TIGIT/CD155 signal axis. *Apoptosis*. 2026;Jul 27\. DOI: 10.1007/s10495-026-02373-4 **Medical Disclaimer:** This article is for educational and informational purposes only and does not constitute medical advice. Artemisinin is not approved for cancer treatment in humans. All findings described are from preclinical studies. Always consult a qualified healthcare provider before making any decisions about cancer treatment or supplement use.