Mirror-image cysteine slows cancer growth without harming healthy cells

Scientists have identified a mirror-image version of the amino acid cysteine, known as D-cysteine, that can slow the growth of certain cancers while sparing healthy cells. The molecule targets a specific transporter on cancer cell surfaces, disrupting key metabolic processes inside. In mouse studies, it significantly reduced aggressive breast tumor progression without major side effects.

An international research team from the Universities of Geneva and Marburg has developed a potential cancer therapy using D-cysteine, a rare mirror-image form of the amino acid cysteine. Unlike conventional treatments that often damage healthy tissues, D-cysteine is selectively absorbed by certain cancer cells via a unique surface transporter. Once inside, it inhibits the mitochondrial enzyme NFS1, which is essential for producing iron-sulfur clusters needed for cellular respiration, DNA production, and genetic stability.

The discovery stems from experiments showing that D-cysteine strongly suppresses cancer cell proliferation in lab settings, while healthy cells remain unaffected. "This difference between cancer cells and healthy cells is easily explained: D-Cys is imported into cells via a specific transporter that is present only on the surface of certain cancer cells," said Joséphine Zangari, a PhD student in Jean-Claude Martinou's lab at the University of Geneva and the study's first author.

Further analysis revealed that blocking NFS1 leads to reduced cellular respiration, increased DNA damage, and halted cell division in cancer cells. Collaborating with Roland Lill's team at the University of Marburg, the researchers detailed how this disruption starves cancer cells of vital energy sources. "It blocks an essential enzyme called NFS1, located in the mitochondria -- the cell's 'powerhouses'. This enzyme plays a key role in producing iron-sulfur clusters, small structures that are indispensable for many processes such as cellular respiration, DNA and RNA production, and maintaining genetic integrity," Lill explained.

In vivo tests on mice with aggressive mammary tumors demonstrated promising results: tumor growth slowed substantially, and the animals exhibited no significant adverse effects. "This is a very positive signal -- we now know it's possible to exploit this specificity to target certain cancer cells," noted Jean-Claude Martinou, honorary professor at the University of Geneva. The findings, published in Nature Metabolism in 2025, suggest D-cysteine could offer a selective treatment for cancers expressing high levels of the transporter, potentially aiding in preventing metastasis. Additional human studies are needed to assess safety and dosing.

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Scientific illustration of researchers discovering SLC35F2 transporter enabling queuine and queuosine uptake in human cells.
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Researchers identify SLC35F2 as a transporter that brings the micronutrients queuine and queuosine into human cells

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An international research team has identified the human gene SLC35F2 as a transporter that enables cellular uptake of the micronutrients queuine and queuosine—compounds acquired from diet and gut bacteria. The work, published in the Proceedings of the National Academy of Sciences, addresses a long-standing question about how these tRNA-related nutrients enter human cells.

Researchers at Oregon Health & Science University have created a molecule called SU212 that blocks a key enzyme in triple-negative breast cancer cells. In mouse models, the compound reduced tumor growth and metastasis. The findings offer potential new treatment options for this hard-to-treat form of the disease.

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Scientists at Oregon State University say they have engineered an iron-based nanomaterial that exploits acidic, peroxide-rich conditions inside tumors to generate two types of reactive oxygen species and kill cancer cells while largely sparing healthy cells. In mouse tests using human breast-cancer tumors, the team reports complete tumor regression without observable adverse effects, though the work remains preclinical.

Scientists at McMaster University and the Hospital for Sick Children in Canada have discovered that oligodendrocytes, cells typically supporting nerve function, aid the growth of glioblastoma by sending signals to tumor cells. Blocking this communication slowed tumor progression in lab models. The findings suggest an existing HIV drug, Maraviroc, could be repurposed for treatment.

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Researchers at Shandong University have modified the probiotic bacterium Escherichia coli Nissle 1917 to produce the anticancer drug Romidepsin directly in tumors. In mouse models of breast cancer, the engineered bacteria accumulated in tumors and released the drug. The findings were published on March 17 in PLOS Biology.

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