Cancer, Lipids, and Metabolism

The paper shows that gap junctions between breast cancer cells and adipocytes transfer cAMP, activating lipolysis in the tumor microenvironment to support tumor growth.

This study identifies fatty acid desaturases SCD1 and FADS2 as critical for EBV-induced B cell proliferation and reveals their role in promoting metabolic pathways that support lymphoma growth.

The paper develops a high-throughput platform using catalytically active CPT1a to screen for modulators, validated with known inhibitors and a library of small molecules.

This study identifies PIKfyve as a targetable vulnerability in pancreatic cancer by showing its role in lipid metabolism and synthetic lethality with KRAS-MAPK inhibitors.

The paper uses proteomics and lipidomics to show OCIAD1 balances mitochondrial and peroxisomal lipid metabolism by affecting lipid composition and key enzymes.

This study identifies a mechanism by which tumor endothelium regulates fatty acid delivery to metastases, showing that mTORC1 inhibition in endothelial cells reduces metastatic disease by impairing T cell fatty acid uptake.

This study shows that inhibiting SCD in breast cancer brain metastases induces lipotoxicity and enhances anti-tumor immunity, improving survival in mouse models.

This study shows that Jerusalem artichoke extracts reduce FASN and ACACA expression, which are key enzymes in fatty acid biosynthesis, and links this effect to topoisomerase II activity.

This study shows that inhibiting FADS1 reduces renal cancer growth by inducing ER stress and ATF3-mediated responses, highlighting FADS1 as a therapeutic target.

This study examines FABP4 and FABP5 expression in breast cancer tissues, finding distinct roles in tumor progression and suggesting their potential as prognostic markers and therapeutic targets.

The paper shows that arginine restriction in the tumor microenvironment limits lipid synthesis in pancreatic cancers, making them susceptible to polyunsaturated fatty acids via ferroptosis.

This study identifies lipid metabolic reprogramming in endocrine-resistant breast cancer cells, showing TVB-2640 reduces lipid storage but not cell growth.

This study identifies ELOVL6 as a therapeutic target in pancreatic cancer by showing its role in c-MYC-driven lipid metabolism and its impact on chemotherapy efficacy.

This study evaluates how hypoxia affects the efficacy of the ChoK inhibitor JAS239 in GBM cells, showing variable responses across cell lines and metabolic pathway changes.

This study shows that inhibiting ACSLs in multiple myeloma cells reduces proliferation and causes mitochondrial dysfunction, suggesting ACSLs as potential therapeutic targets.

This study investigates how aging affects ovarian cancer progression by analyzing gene expression, lipid metabolism, and immune cell changes in rat models, finding that aged adipose microenvironment promotes tumor growth.

This study shows that P-cadherin-mediated mechanical forces on mesothelial cells enhance lipid production in ovarian cancer cells, promoting metastasis through lactate-driven lipogenesis.

This study shows that erythroblasts adapt to shear stress by accelerating maturation and upregulating cholesterol biosynthesis, enhancing osmotic resistance and enucleation.

This study shows that fatty acid lithium salts from Thamnidium elegans and Mortierella alpina inhibit prostate cancer cell proliferation and migration.

The paper investigates the kinetics of carbon-carbon bond formation in fatty acid synthase, revealing how the enzyme's activity and fidelity are influenced by substrate length and dimeric cooperativity.

The paper determines cryo-EM structures of human ACC1 in inactive and activated states, revealing structural dynamics and regulatory mechanisms.

This study shows that FABP4 in tumor-associated macrophages promotes breast cancer metastasis by mediating lipid accumulation and lipolysis in response to unsaturated fatty acids.

This study shows that ACSS2-mediated acetate conversion to acetyl-CoA promotes quiescence in ovarian cancer cells, linking metabolic reprogramming to therapeutic resistance.

This study shows that SREBP pathway inhibition slows PDAC tumor growth by disrupting lipid homeostasis, suggesting SCAP as a therapeutic target.

This paper identifies statins as having anticancer effects through synthetic lethality, validated in vitro on breast, ovarian, and cervical cancer cell lines.

This study identifies a synergistic effect between AKT inhibitors and pitavastatin in killing triple-negative breast cancer cells by targeting cholesterol trafficking.

The paper shows that de novo lipid synthesis and polarized prenylation are essential for cell invasion through basement membrane in C. elegans anchor cells.

This study shows that activation of the mevalonate pathway and Rac-1 in glioblastoma cells after anti-cancer treatments promotes recurrence, and statins combined with radiation improve survival in mouse models.