Javier A. Menendez

TL;DR: This work explored how metformin treatment impacted mitochondrial biogenesis in cultured breast cancer cells overexpressing the membrane tyrosine kinase receptor HER2, the best-characterized downregulator of MHC-I and found restored antigenicity and immunogenicity of tumor cells may represent a previously unrecognized primary mode of action underlying the cancer-preventive effects of met formin.

TL;DR: In metabolic tissues, the suppression of autophagy increases inflammation with the overexpression of cytokines, resulting in an activation of Autophagy, and the physiological role of these apparently contradictory findings remains uncertain but exemplifies future challenges in the therapeutic modulation of autophile in the management of disease.

TL;DR: This work suggests exploring how metabolism-dependent regulation of epigenetics can play a role in directing CSC states beyond conventional energetic demands of stage-specific cancer cell states, opening a new dimension of cancer in which the “physiological state” of CSC might be governed not only by cell-autonomous cues but also by local micro-environmental and systemic metabolo-epigenetic interactions.

TL;DR: Findings on the mechanism(s) of action of metformin with the potential for therapeutic interpretations are discussed, including the way in which organismal bioenergetics remodel one-carbon metabolism.

TL;DR: Nucleolar- and NOR-associated P-RaptorSer706 may physically link mTORC1 signaling to ever-growing nucleolus plurifunctionality including ribosome biogenesis, cell stress sensor and cell cycle/aging control.