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Updated: Feb 18, 2026

Author Spotlight: Transmitochondrial Cybrid Generation Using Cancer Cell Lines
Published on: March 17, 2023
Crosstalks between translation and metabolism in cancer
Stefano Biffo1, Nicola Manfrini2, Sara Ricciardi2
1National Institute of Molecular Genetics "Romeo ed Enrica Invernizzi", INGM, 20122 Milano, Italy; Department of Biosciences, University of Milano, 20133 Milano, Italy.
Abstract:
Albeit cancer patients' heterogeneity, all tumor cells have alterations of both metabolism and translation. The simplest explanation for this common feature is that several oncogenes coordinate a translational and metabolic reprogramming that is necessary for tumor cells to thrive. Overall, at least three oncogenic pathways, namely c-Myc, RAS and PI3K-mTOR, are known to affect both translation and metabolism by stimulating glycolysis and protein synthesis. The crosstalk between metabolite production and the translational machinery is, instead, less understood. What is known is that, on one side, translation initiation factors, such as eIF4E and eIF6, drive tumor growth and regulate metabolism through selective translation of nucleotide biosynthesis, glycolysis and fatty acid synthesis rate-limiting mRNAs, and on the other, that nutrient levels regulate the translational machinery by inducing full activity of translation factors. Therefore, translation and metabolism offer several therapeutic targets to be fully exploited in future studies.
Insights
Cancer cells share metabolic and translational reprogramming driven by oncogenes like c-Myc. Understanding the interplay between these processes offers new therapeutic targets for cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Metabolism
Background:
- Despite patient heterogeneity, all cancer cells exhibit altered metabolism and translation.
- Oncogenic pathways (c-Myc, RAS, PI3K-mTOR) reprogram translation and metabolism, stimulating glycolysis and protein synthesis.
- The intricate crosstalk between metabolite production and the translational machinery remains incompletely understood.
Purpose of the Study:
- To explore the coordinated reprogramming of translation and metabolism in cancer cells.
- To elucidate the role of oncogenic pathways in driving these cellular alterations.
- To identify potential therapeutic targets at the intersection of translation and metabolism.
Main Methods:
- Review of oncogenic pathways affecting translation and metabolism.
- Analysis of the role of translation initiation factors (e.g., eIF4E, eIF6) in cancer growth and metabolic regulation.
- Investigation of nutrient-sensing mechanisms that modulate the translational machinery.
Main Results:
- Key oncogenic pathways (c-Myc, RAS, PI3K-mTOR) significantly impact both translation and metabolism.
- Translation initiation factors selectively promote the translation of mRNAs involved in nucleotide biosynthesis, glycolysis, and fatty acid synthesis.
- Nutrient availability directly influences the activity of translation factors, highlighting a feedback loop.
Conclusions:
- The coordinated reprogramming of translation and metabolism is a hallmark of cancer, essential for tumor cell survival.
- Targeting translation and metabolism presents a promising therapeutic strategy for cancer treatment.
- Further research into the crosstalk between these pathways can uncover novel therapeutic interventions.
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