Volume 8 (2024)
MiR-200c reprograms fibroblasts to recapitulate the phenotype of CAFs in breast cancer progression
Zhao Lin1, Megan E. Roche1, Víctor Díaz-Barros1, Marina Domingo-Vidal2, Diana Whitaker-Menezes1, Madalina Tuluc3, Guldeep Uppal3, Jaime Caro4, Joseph M. Curry5 and Ubaldo Martinez-Outschoorn1
Mesenchymal-epithelial plasticity driving cancer progression in cancer-associated fibroblasts (CAFs) is undetermined. This work identifies a subgroup of CAFs in human breast cancer exhibiting mesenchymal-to-epithelial transition (MET) or epithelial-like profile with high miR-200c expression. MiR-200c overexpression in fibroblasts is sufficient to drive breast cancer aggressiveness. Oxidative stress in the tumor microenvironment induces miR-200c by DNA demethylation. Proteomics, RNA-seq and functional analyses reveal that miR-200c is a novel positive regulator of NFκB-HIF signaling via COMMD1 downregulation and stimulates pro-tumorigenic inflammation and glycolysis. Reprogramming fibroblasts toward MET via miR-200c reduces stemness and induces (...)
CircRNA regulates the liquid-liquid phase separation of ATG4B, a novel strategy to inhibit cancer metastasis?
Ziyuan Guo1,#, Yang Chen1,#, Yaran Wu1 and Jiqin Lian1
Metastasis is the leading cause of death in cancer patients. Currently, there are no effective treatments to prevent cancer metastases. Therefore, it is imperative to provide more effective biomarkers and
Pathogenic hyperactivation of mTORC1 by cytoplasmic EP300 in Hutchinson-Gilford progeria syndrome
Lucille Ferret1,2,3, Guido Kroemer1,2,4 and Mojgan Djavaheri-Mergny1,2
Mechanistic target of rapamycin complex 1 (mTORC1) is a multiprotein complex that serves as a pivotal regulator of cell growth, protein synthesis, metabolism and autophagy [1][2]. This complex compromises mTOR
The missing hallmark of health: psychosocial adaptation
Carlos López-Otín1,2,3 and Guido Kroemer1,4,5
INTRODUCTION The comprehension of health –defined in a positive fashion rather than as the absence of disease–requires a theory. We recently launched the bases of such a health theory by
MiR-200c reprograms fibroblasts to recapitulate the phenotype of CAFs in breast cancer progression
Zhao Lin1, Megan E. Roche1, Víctor Díaz-Barros1, Marina Domingo-Vidal2, Diana Whitaker-Menezes1, Madalina Tuluc3, Guldeep Uppal3, Jaime Caro4, Joseph M. Curry5 and Ubaldo Martinez-Outschoorn1
Mesenchymal-epithelial plasticity driving cancer progression in cancer-associated fibroblasts (CAFs) is undetermined. This work identifies a subgroup of CAFs in human breast cancer exhibiting mesenchymal-to-epithelial transition (MET) or epithelial-like profile with high miR-200c expression. MiR-200c overexpression in fibroblasts is sufficient to drive breast cancer aggressiveness. Oxidative stress in the tumor microenvironment induces miR-200c by DNA demethylation. Proteomics, RNA-seq and functional analyses reveal that miR-200c is a novel positive regulator of NFκB-HIF signaling via COMMD1 downregulation and stimulates pro-tumorigenic inflammation and glycolysis. Reprogramming fibroblasts toward MET via miR-200c reduces stemness and induces (...)
Saliva, a molecular reflection of the human body? Implications for diagnosis and treatment
Vincent Géli and Norbert Nabet
INTRODUCTION The possibility of using biological fluids such as blood, urine, saliva and other biofluids to diagnose pathologies is a relatively old idea that has taken on a new lease
CircRNA regulates the liquid-liquid phase separation of ATG4B, a novel strategy to inhibit cancer metastasis?
Ziyuan Guo1,#, Yang Chen1,#, Yaran Wu1 and Jiqin Lian1
Metastasis is the leading cause of death in cancer patients. Currently, there are no effective treatments to prevent cancer metastases. Therefore, it is imperative to provide more effective biomarkers and
Pathogenic hyperactivation of mTORC1 by cytoplasmic EP300 in Hutchinson-Gilford progeria syndrome
Lucille Ferret1,2,3, Guido Kroemer1,2,4 and Mojgan Djavaheri-Mergny1,2
Mechanistic target of rapamycin complex 1 (mTORC1) is a multiprotein complex that serves as a pivotal regulator of cell growth, protein synthesis, metabolism and autophagy [1][2]. This complex compromises mTOR
The missing hallmark of health: psychosocial adaptation
Carlos López-Otín1,2,3 and Guido Kroemer1,4,5
INTRODUCTION The comprehension of health –defined in a positive fashion rather than as the absence of disease–requires a theory. We recently launched the bases of such a health theory by