Disruption of de novo fatty acid biosynthesis rewires cellular lipid metabolism toward mTOR signaling
核心洞察
Researchers report that disrupting de novo fatty acid biosynthesis rewires cellular lipid metabolism toward mTOR (搜索) signaling, revealing a mechanistic link between lipid synthesis and growth control.
The study was supported by Kazusa DNA Research Institute (搜索) and multiple Japanese funding agencies, including AMED-CREST and JST FOREST, underscoring its institutional and scientific significance.
Findings suggest that targeting fatty acid biosynthesis may offer a strategy to modulate mTOR (搜索)-dependent pathways with potential therapeutic relevance.
Disruption of de novo fatty acid biosynthesis rewires cellular lipid metabolism toward mTOR (搜索) signaling, according to research published in Scientific Reports. The study, supported by Kazusa DNA Research Institute (搜索) and grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan, identifies a mechanistic connection between the inhibition of endogenous lipid synthesis and the activation of mTOR-dependent growth pathways.
The research was funded through multiple competitive grant mechanisms, including Grant-in-Aid for Scientific Research (B) (#20H03455, #24K02246), Challenging Research (Exploratory) (#20K21618, #24K22064), Grant-in-Aid for Transformative Research Areas (A) (#23H04794), and Early-Career Scientists (#21K15476 and #23K14552). Additional support came from AMED-CREST (JP22gm1810002) through the Japan Agency for Medical Research and Development, as well as FOREST (JPMJFR225X) from JST.
Mechanistic Focus on Lipid Metabolism and mTOR
The central finding of the study is that disruption of de novo fatty acid biosynthesis leads to a rewiring of cellular lipid metabolism that converges on mTOR (搜索) signaling. This suggests that cells compensate for the loss of endogenous fatty acid production by altering their lipid landscape in a manner that engages the mTOR pathway, a master regulator of cell growth and proliferation.
The work was further enabled by a broad consortium of foundations, including the Kato Memorial Bioscience Foundation, Takeda Science Foundation, Mochida Memorial Foundation for Medical and Pharmaceutical Research, Uehara Memorial Foundation, Astellas Foundation for Research on Metabolic Disorders, MSD Life Science Foundation, NAGASE Science Technology Foundation, Canon Foundation, ONO Medical Research Foundation, Princess Takamatsu Cancer Research Fund, Yasuda Medical Foundation, Mitsubishi Foundation, KOSE Cosmetology Research Foundation, Chemo-Sero-Therapeutic Research Institute, Toray Science Foundation, Shionogi Infectious Disease Research Promotion Foundation, and Ono Pharmaceutical Foundation for Oncology, Immunology, and Neurology.
Open Access and Scientific Dissemination
The article is published under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution, and reproduction in any medium or format, provided appropriate credit is given to the original authors and source, a link to the Creative Commons licence is included, and any changes are indicated. This open-access framework supports broad dissemination of the findings to the research community.
The study's emphasis on the intersection of lipid biosynthesis and mTOR (搜索) signaling highlights a potentially significant area for therapeutic exploration, as the mTOR pathway is implicated in numerous physiological and pathological processes related to cellular growth and metabolism.