An important part of cancer treatment is reducing the tumor burden, or the total mass of cancerous tissue in the body.
Tumors actively produce byproducts like lactate, cortisol, and estrogen, which contribute to inflammation, stress, metabolic disruption, and create conditions for cancer growth. They can also invade nearby tissues and disrupt healthy structure and function.
So, a core goal of treatment is to shrink the tumor and relieve the systemic stress the tumor creates. Many common cancer treatments are designed with this goal: chemotherapy, radiation, surgery, etc. However, these treatments tend to be very harsh on the body, invasive, and expensive.
Researchers continue to search for safer, cheaper alternatives. And one promising area of exploration is the use of antivirals and antibiotics.
For example, doxycycline, a broad-spectrum antibiotic that has been used safely for over 60 years. It’s one of the most widely prescribed antibiotics in the world for its reliable oral absorption and relatively low risk of side effects.
While commonly prescribed for acne, rosacea, respiratory infections, and Lyme disease, doxycycline has also been studied as a repurposed drug in cancer treatment.
Doxycycline works by disrupting mitochondria, the cellular structure where energy (ATP) is produced.
Interestingly, our mitochondria evolved from bacteria. Around two billion years ago, a single-celled organism engulfed a free-living bacteria. Instead of breaking it down, the host cell formed a symbiotic relationship with the bacteria, which eventually became the mitochondria. Today, mitochondria and bacteria still share some structural features. Mitochondria:
- Have their own circular DNA, just like bacteria
- Reproduce independently of the cell through a process similar to bacterial division
- Have ribosomes (the protein-building machinery) that more closely resemble bacterial ribosomes than human ones
Doxycycline is designed to block protein production in bacteria by targeting their ribosomes. And because mitochondrial ribosomes are similar, doxycycline can also interfere with protein production in mitochondria in our cells.
This reduces the mitochondria’s ability to function properly and as a result disrupts energy production. Without enough energy, the cell dies. Cancer cells, particularly cancer stem cells, rely heavily on mitochondria to grow. So, by impairing mitochondrial function, doxycycline makes these cells more vulnerable and slows the cancer growth.
Doxycycline also works by:
- Targeting cancer stem cells (CSCs). Cancer stem cells are responsible for recurrence, metastasis, and resistance to conventional treatment. Doxycycline reduces CSC activity by impairing mitochondrial function. Studies have shown that exposure to doxycycline has been shown to suppress tumor formation and limit the self-renewal capacity of these cells.
- Inhibiting matrix metalloproteinases (MMPs). Doxycycline inhibits enzymes such as MMP-2 and MMP-9, which are used by cancer cells to degrade surrounding tissue and facilitate invasion & spread. By blocking these enzymes, doxycycline helps reduce tumor spread and metastasis.
- Reducing inflammation and angiogenesis. Doxycycline interferes with inflammatory signaling pathways (NF-κB), which are often overactive in tumors. It also has mild anti-angiogenic effects, limiting the tumor’s ability to form new blood vessels needed for growth.
Doxycycline has been studied in:
- breast cancer
- prostate cancer
- glioblastoma
- ovarian cancer
- melanoma
- lung cancer
- colorectal cancer
- leukemia
- multiple myeloma
Doses of 100–200 mg are typically used in the research. But instead of the usual short (~10-day) course used for infections, it usually needs to be taken over a longer stretch to have an anticancer effect.
Doxycycline may be especially useful in aggressive or fast-growing cancers because they heavily rely on mitochondrial function to replicate quickly. Because healthy cells are not metabolically stressed, they’re less affected. This makes it a low-toxicity therapy, because it doesn’t harm healthy cells.
However, while it can help shrink tumors and lower the risk of recurrence, it doesn’t address the deeper factors that allowed the cancer to form in the first place, such as chronic inflammation, hormonal imbalance, or metabolic stress. That’s why it’s best viewed as a supportive therapy and needs to be a part of a greater approach that targets both the tumor and the environment that sustains it.
It’s not a silver bullet. But drug repurposing like this opens up new possibilities—especially because doxycycline is inexpensive, widely available, and already well understood.