Taurine: Substance Present in Energy Drinks May Feed Cancer

Researchers have discovered that a natural nutrient in the body called taurine, normally seen as beneficial, can help certain aggressive types of leukemia grow. In tests on human cells and mice, blocking the production or use of taurine caused cancer cells to stop growing. This finding shows that the environment around a tumor can fuel cancer and paves the way for new treatments that disrupt this “communication” between cells.

Cancers, especially those that affect the blood and bone marrow, such as certain types of leukemia, do not grow in isolation. They thrive within a very specific environment called the tumor microenvironment.

This microenvironment is made up of many neighboring cells and chemicals that constantly interact with cancer cells, either helping or hindering their growth. Understanding how these interactions occur is key to finding new treatments.

In this study, the researchers wanted to understand how the bone marrow microenvironment contributes to the growth and resilience of leukemia stem cells, known as LSCs. These cells are particularly difficult to eliminate with current treatments.

The scientists focused on two aggressive types of leukemia: acute myeloid leukemia (AML) and chronic myeloid leukemia in blast crisis (bCML), both of which are difficult to treat and have a high risk of relapse.

To investigate this, the researchers used a technique called scRNA-seq, which allows them to analyze which genes are active in each individual cell.

Using this tool, they mapped thousands of bone marrow cells, both healthy and affected by leukemia, and observed how they change over time as the disease progresses. This helped them understand how surrounding cells behave and influence cancer cells.

The main focus was to identify chemical signals present in the microenvironment that "talk" to receptors on leukemia cells. These receptors are located on the surface of the cells and act as antennas.

If a surrounding cell sends a substance and the cancer cell has the receptor to receive it, this interaction can favor tumor growth. By studying these signals, the researchers sought to discover which could be effective targets for treatment.

To confirm the importance of these signals, the scientists used the genetic tool CRISPR to turn off specific genes in mouse models. This helped them see whether blocking these interactions actually hindered leukemia growth.

One of the most surprising findings was the involvement of taurine, a substance found naturally in the body and even in energy drinks, in stimulating the growth of leukemia cells.

Taurine binds to a specific receptor called TAUT, which is highly present on leukemia cells. Taurine is normally thought of as beneficial because it can protect the brain and heart. However, in this context, it appeared to fuel cancer growth.

The study showed that bone marrow cells, especially those attached to the bone, produce taurine, and this production increases as leukemia progresses.

To confirm the role of taurine, the researchers blocked its production in bone marrow cells and also prevented cancer cells from using the TAUT receptor.

As a result, the growth of leukemia cells was significantly reduced. This suggests that taurine, in this environment, may have the opposite effect than expected and could be a new therapeutic target.

In addition, the scientists used a combination of techniques called “omics analysis,” which studies all the molecules involved in cellular functions, to better understand how taurine influences leukemia.

This image shows cells analyzed by immunofluorescence to investigate how taurine influences the localization of the mTOR protein under different genetic conditions. The images are divided into two rows: the top one shows cells without taurine (–Taurine), and the bottom one shows the same experimental conditions with taurine supplementation (+Taurine). The columns represent different combinations of genetic manipulations: WT + vector: wild-type cells (without genetic mutations) with a control vector. WT + RAGA: wild-type cells with overexpression of the RAGA protein. KO + vector: cells with RAGA deletion (knockout, KO) with control vector. KO + RAGA: knockout cells with replacement of the RAGA protein. The colors indicate the presence of specific proteins in the cells: Green (mTOR): shows the localization of the mTOR protein, an important metabolic sensor that regulates cell growth and response to nutrients. Purple (LAMP1): marker of lysosomes, organelles responsible for cellular digestion. The colocalization of mTOR and LAMP1 indicates that mTOR is associated with lysosomes, where it is activated. Blue (DAPI): marks the cell nucleus, allowing visualization of the position of the nucleus in relation to other structures. White arrows point to regions where mTOR (green) is colocalized with LAMP1 (purple), suggesting activation of mTOR in lysosomes. This is particularly evident in WT cells with RAGA, both with and without taurine, and less evident in KO cells, showing that the presence of RAGA and taurine influences the activation and localization of mTOR. This figure supports the idea that taurine can modulate cellular signaling through the RAGA–mTOR axis, which may be important for understanding how certain nutrients and their transporters affect cancer cell growth.

These approaches included studying the genes that are activated, the proteins that are produced, and the chemical reactions that occur in the cells. This comprehensive view revealed how taurine can alter the inner workings of cancer cells.

In summary, this study has identified a new pathway of communication between cells in the bone marrow microenvironment and leukemia cells, with taurine playing an important role.

This discovery opens the door to the development of new treatments that block this interaction and help stop the progression of aggressive leukemias, especially those that are resistant to current drugs.

READ MORE:

Taurine from tumour niche drives glycolysis to promote leukaemogenesis

Sonali Sharma, Benjamin J. Rodems, Cameron D. Baker, Christina M. Kaszuba, Edgardo I. Franco, Bradley R. Smith, Takashi Ito, Kyle Swovick, Kevin Welle, Yi Zhang, Philip Rock, Francisco A. Chaves, Sina Ghaemmaghami, Laura M. Calvi, Archan Ganguly, W. Richard Burack, Michael W. Becker, Jane L. Liesveld, Paul S. Brookes, Joshua C. Munger, Craig T. Jordan, John M. Ashton, and Jeevisha Bajaj

Nature. 14 May 2025

DOI: 10.1038/s41586-025-09018-7

Abstract:

Signals from the microenvironment are known to be critical for development, stem cell self-renewal and oncogenic progression. Although some niche-driven signals that promote cancer progression have been identified1,2,3,4,5, concerted efforts to map disease-relevant microenvironmental ligands of cancer stem cell receptors have been lacking. Here, we use temporal single-cell RNA-sequencing (scRNA-seq) to identify molecular cues from the bone marrow stromal niche that engage leukaemia stem-enriched cells (LSCs) during oncogenic progression. We integrate these data with our human LSC RNA-seq and in vivo CRISPR screen of LSC dependencies6 to identify LSC–niche interactions that are essential for leukaemogenesis. These analyses identify the taurine–taurine transporter (TAUT) axis as a critical dependency of aggressive myeloid leukaemias. We find that cysteine dioxygenase type 1 (CDO1)-driven taurine biosynthesis is restricted to osteolineage cells, and increases during myeloid disease progression. Blocking CDO1 expression in osteolineage cells impairs LSC growth and improves survival outcomes. Using TAUT genetic loss-of-function mouse models and patient-derived acute myeloid leukaemia (AML) cells, we show that TAUT inhibition significantly impairs in vivo myeloid leukaemia progression. Consistent with elevated TAUT expression in venetoclax-resistant AML, TAUT inhibition synergizes with venetoclax to block the growth of primary human AML cells. Mechanistically, our multiomic approaches indicate that the loss of taurine uptake inhibits RAG-GTP dependent mTOR activation and downstream glycolysis. Collectively, our work establishes the temporal landscape of stromal signals during leukaemia progression and identifies taurine as a key regulator of myeloid malignancies.