Artemisinin and Cancer: A Natural Compound Targeting Cancer Survival Pathways
What Is Artemisinin and Why It Matters in Cancer?
Artemisinin is a compound extracted from the herb Artemisia annua, also known as sweet wormwood. It gained global attention for its role in curing malaria, and its discoverer, Youyou Tu, received the Nobel Prize in 2015. But its reach goes far beyond malaria. Scientists have been exploring how this ancient remedy can fight cancer, particularly aggressive forms like head and neck squamous cell carcinoma (HNSCC) and tongue cancer. What makes it so interesting is its ability to specifically target cancer cells while leaving healthy ones largely unharmed. Its action is based on the presence of an endoperoxide bridge, a molecular feature that reacts with iron—a metal found in high amounts inside cancer cells. This reaction unleashes reactive oxygen species (ROS) that damage the cancer cell’s internal machinery.
How It Creates Oxidative Stress to Kill Cancer
Cancer cells consume more iron than normal cells, which makes them vulnerable to artemisinin. When artemisinin encounters iron, it triggers the production of ROS—unstable molecules that damage proteins, DNA, and other essential parts of a cell. This burst of oxidative stress overwhelms the cancer cell’s ability to repair itself, leading to cell death. The result can be apoptosis (planned cell death) or ferroptosis, a special kind of cell death linked to iron overload. These forms of cell death are especially helpful in attacking cancers like tongue cancer, which are often resistant to chemotherapy. This makes artemisinin a strong candidate for use alongside traditional therapies or in natural treatment protocols.
Shutting Down Cancer’s Defense System
One of cancer’s strengths is its antioxidant shield—tools like glutathione and enzymes like GPX4 that help it survive stress. Artemisinin helps break this shield. In lab studies, dihydroartemisinin (DHA), a derivative of artemisinin, reduces glutathione levels and blocks GPX4, forcing the cancer cell to experience unfiltered oxidative damage. This makes artemisinin especially promising in cancers that rely on high antioxidant activity to thrive. In aggressive cancers like those of the tongue, where cells rapidly divide and generate internal stress, weakening this defense system can halt growth and spread. Researchers have also found that artemisinin increases the ratio of pro-apoptotic proteins (like Bax) to anti-apoptotic proteins (like Bcl-2), tilting the balance toward cell death.
Blocking the Fuel Lines and Growth Signals
Artemisinin also interferes with the cell cycle and the systems that tell cancer to grow. It suppresses cyclin D1 and CDK4—two proteins that help push the cancer cell through growth phases. In doing so, artemisinin forces the cells into arrest at G0/G1 or G2/M phases, pausing their uncontrolled replication. For tongue cancer patients, this could mean smaller tumors that grow more slowly or not at all. It also blocks the PI3K/Akt/mTOR pathway, a major growth signaling pathway in many cancers. By shutting down this internal fuel line, artemisinin doesn’t just kill—it starves the tumor of growth cues. These effects together limit cancer’s ability to multiply, invade tissue, and resist treatment.
Stopping Blood Vessel Formation and Metastasis
Tumors don’t just sit still—they grow blood vessels to feed themselves (angiogenesis) and spread (metastasize). Artemisinin can stop both. It lowers VEGF (vascular endothelial growth factor), which tumors use to build new blood vessels. It also blocks MMPs (matrix metalloproteinases), enzymes that help cancer cells cut through tissue and spread to other areas. In tongue cancer, where the cancer often spreads to nearby lymph nodes, this anti-metastatic action is crucial. Studies have shown that artemisinin boosts the expression of E-cadherin, a protein that keeps cells glued in place, and lowers N-cadherin and vimentin, which cancer cells use to move. These effects collectively reduce the chances of recurrence or distant metastasis.
Immune Boosting and Tumor Microenvironment Support
Artemisinin doesn’t only work by direct attack. It also adjusts the environment around the tumor, called the tumor microenvironment (TME). It reduces immunosuppressive molecules like PD-L1, allowing immune cells like T-cells to find and kill cancer cells more easily. Artemisinin has been shown to increase infiltration of CD8+ killer T cells into tumors, making the immune system part of the battle. This immune support is especially useful in combination with immunotherapy or when the patient has a weakened immune response. In addition, artemisinin may trigger immunogenic cell death (ICD), which makes cancer cells “visible” to the immune system after dying, enhancing long-term protection.
Resistance, Safety, and Future Outlook
Cancers often become resistant to standard chemotherapy, but artemisinin may help prevent this. It lowers expression of P-glycoprotein (P-gp), a pump cancer uses to eject chemo drugs. It also enhances the effects of drugs like cisplatin and vinorelbine. Artemisinin’s low toxicity is a major advantage. It shows selective cytotoxicity, harming cancer more than normal tissue. However, high-dose use (especially intravenous) can carry neurotoxicity risks, so oral or nano-formulated versions are often safer. Scientists are now studying improved delivery systems like nanoparticles to make artemisinin last longer and hit harder. It’s affordable (around $1 per dose), easy to access, and works on many levels. Clinical trials are needed to confirm its effectiveness in humans, especially in hard-to-treat cancers like tongue cancer. But early signs are promising, and for many, artemisinin represents hope—a natural compound with serious power.
Summary Highlights:
Safe, Affordable, and Evolving
The compound is low-cost (~$1 per dose), has minimal side effects when dosed properly, and is being developed into advanced forms like nano-delivery systems. Clinical trials are still needed, but early data supports its promise in cancer therapy.
The compound’s unique endoperoxide bridge reacts with iron—which is abundant in cancer cells—to release reactive oxygen species (ROS). This oxidative burst damages cancer cell DNA and proteins, leading to apoptosis (cell death) and ferroptosis (iron-based cell death).
It Shuts Down Cancer’s Antioxidant Shield
Derivatives like DHA reduce glutathione and inhibit GPX4, stripping cancer cells of their antioxidant defenses. This makes them more vulnerable to oxidative stress, especially useful in fast-growing tumors like those in the tongue.
Stops Cancer Cell Growth and Division
It halts the cell cycle by suppressing proteins like cyclin D1 and CDK4, and blocks the PI3K/Akt/mTOR pathway, slowing or halting tumor growth.
Disrupts Angiogenesis and Metastasis
Artemisinin lowers VEGF levels and blocks matrix metalloproteinases (MMPs), preventing tumors from building blood vessels or spreading. It reverses EMT markers to keep cancer cells from detaching and traveling.
Strengthens the Immune Response
Artemisinin reduces PD-L1 (a molecule that helps cancer hide from immune cells), enhances killer T-cell infiltration, and may trigger immunogenic cell death—training the immune system to attack future cancer cells
Combats Chemotherapy Resistance
It downregulates drug-efflux proteins like P-glycoprotein and improves the effectiveness of traditional chemo drugs like cisplatin. Its selective toxicity favors cancer cell death with fewer side effects
🛒 Please consider showing your support by purchasing through our Amazon links, (it’s usually 1% to the site)— help keep this platform alive for someone who needs it tomorrow.
Purchase Sweet Wormwood (Artemisia annua)
Research Links
- Artemisinin derivatives differently affect cell death of lung cancer subtypes (2025)
- Link: Nature – Artemisinin derivatives in NSCLC
- Description: Demonstrates DHA and artesunate reduce tumor proliferation and enhance cisplatin efficacy in NSCLC, relevant for HNSCC’s similar pathways.
- Artemisinin and its derivatives: therapeutic mechanisms (2025)
- Link: Springer – Artemisinin therapeutic potential
- Description: Reviews ROS, autophagy, and ferroptosis mechanisms, applicable to HNSCC’s iron-rich TME.
- New clinical application prospects of artemisinin (2023)
- Link: PubMed – Artemisinin scoping review
- Description: Scoping review of 16 anti-tumor studies, highlighting artemisinin’s efficacy and safety in cancers.
- A comprehensive overview of artemisinin as anticancer agents (2023)
- Link: ScienceDirect – Artemisinin anticancer overview
- Description: Details artemisinin’s mechanisms (ROS, apoptosis, anti-angiogenesis) across cancers, relevant for HNSCC.
- Artemisinins as a novel anti-cancer therapy (2024)
- Link: PubMed – Artemisinins in cancer
- Description: Discusses drug repurposing, emphasizing artemisinin’s affordability and efficacy in LMICs.
- Antitumor research on artemisinin and its derivatives (2018)
- Link: Springer – Artemisinin antitumor research
- Description: Highlights artemisinin’s pleiotropic effects (apoptosis, cell cycle arrest, anti-metastasis) in cancers.
- Artemisinin and its derivatives as potential anticancer agents (2020)
- Link: PMC – Artemisinin anticancer agents
- Description: Reviews pharmacological effects and clinical trials, supporting artemisinin’s role in cancer therapy.
- DHA induces ferroptosis in head and neck carcinoma cells (2018)
- Link: PubMed – DHA in HNSCC
- Description: Shows DHA’s ferroptosis induction in HNSCC, relevant for tongue cancer’s iron-rich cells.
- Artemisinin for cancer treatment (2024)
- Link: PMC – Artemisinin in cancer therapy
- Description: Discusses artemisinin’s anti-angiogenic and apoptotic effects, with implications for HNSCC.
- Artesunate in combination therapy for NSCLC (2008)
- Link: PubMed – Artesunate in NSCLC
- Description: Demonstrates artesunate’s synergy with chemotherapy, applicable to tongue cancer.
Table of Contents
