Cancer: when biotin becomes a therapeutic lever

By Elodie Vaz  | Published on February 27, 2026 | 3 min read

Cancer is characterized by uncontrolled cell proliferation, supported by profound metabolic reprogramming. Among the identified vulnerabilities, “glutamine dependence” plays a central role: many tumor cells require this amino acid to sustain protein and DNA synthesis and to maintain their energy cycle. In its absence, proliferation halts. Yet some tumors manage to circumvent this metabolic constraint.  

A study published on February 25 in Molecular Cell by a team from the University of Lausanne highlights an unexpected mechanism involving vitamin B7 (biotin), revealing a new vulnerability in tumor cells deprived of this essential cofactor.

Understanding escape from glutamine dependence  

The team led by Alexis Jourdain, Associate Professor in the Department of Immunobiology (DIB) at the Faculty of Biology and Medicine (FBM) of the University of Lausanne, set out to elucidate the mechanisms that allow cancer cells to continue proliferating despite glutamine restriction.  

Although glutamine dependence is a well-documented vulnerability, the ability of certain tumors to bypass it has so far limited the effectiveness of therapeutic strategies targeting this metabolic pathway. The study therefore aimed to identify the alternative pathways mobilized by tumor cells and the underlying molecular determinants.  

An integrated metabolic approach  

The work was conducted by Dr. Miriam Lisci, a postdoctoral researcher in Prof. Jourdain’s laboratory. The researchers combined functional and analytical approaches, in collaboration with the metabolomics and proteomics platforms of the FBM, as well as with the team of Professor Owen Skinner at Northeastern University (United States).  

The analysis highlighted the role of carbon-rich molecules, notably pyruvate, capable of sustaining cell division in the absence of glutamine. Experiments dissected the enzymatic conditions required for this metabolic compensation.  

Biotin as a “Metabolic License”  

The researchers demonstrate that the use of pyruvate in this context depends on a key mitochondrial enzyme: pyruvate carboxylase. This enzyme requires vitamin B7 to function. In the absence of biotin, pyruvate carboxylase is inactive, blocking pyruvate utilization and preventing cell proliferation.  


Biotin thus acts as a true “metabolic license,” allowing pyruvate to fuel the cellular energy cycle and compensate for glutamine deficiency. This mechanism reveals an unexpected dependence of tumor cells on a micronutrient, beyond classical energy substrates.   The study also highlights a previously unrecognized role of the gene FBXW7, frequently mutated in various cancers. “When FBXW7 is mutated, pyruvate carboxylase is partially lost, pyruvate is no longer used efficiently, and the cells become dependent on glutamine,” explains Miriam Lisci, first author of the study, in a press release. The researchers showed that certain FBXW7 mutations identified in patients directly induce this metabolic dependence.

These findings also shed light on the limitations of some glutamine-targeting therapies. Tumor cells can activate alternative metabolic pathways, notably via pyruvate, to maintain proliferation.  

Exploiting tumor metabolic flexibility  

By revealing the central role of biotin and pyruvate carboxylase in the metabolic adaptation of cancer cells, this study underscores the importance of integrating micronutritional factors into the analysis of tumor vulnerabilities.  

“In the longer term, this research opens new perspectives for better understanding the metabolic vulnerabilities of cancers and for designing innovative therapeutic strategies that take into account the high metabolic flexibility of tumor cells, particularly by simultaneously targeting multiple metabolic pathways,” concludes Alexis Jourdain, senior author of the study.  

These findings suggest that a combinatorial approach integrating vitamin status and mutational profiling—particularly of FBXW7—could refine patient stratification and improve the effectiveness of metabolic therapies. They pave the way for a more precise exploitation of tumor nutritional dependencies at the intersection of cell biology, oncogenetics, and precision medicine.




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About the Author – Elodie Vaz
Health journalist, CFPJ graduate (2023).
Élodie explores the marks diseases leave on bodies and, more broadly, on human life. A registered nurse since 2010, she spent twelve years at patients’ bedsides before exchanging her stethoscope for a notebook. She now investigates the links between environment and health, convinced that the vitality of life cannot be reduced to that of humans alone.