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Mitochondria-associated endoplasmic reticulum membranes allow adaptation of mitochondrial metabolism to glucose availability in the liver

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Journal of Molecular Cell Biology 2016年第2期8卷 129-143页

作者： Pierre Theurey Emily Tubbs Guillaume Vial Julien Jacquemetton Nadia Bendridi Marie-Agnes Chauvin Muhammad Rizwan Alam muriel le romancer Hubert Vidal Jennifer Rieusset INSERM UMR-1060 CarMeN LaboratoryLyon 1 UniversityINRA U1235INSA of LyonRockefeller and Charles Merieux Lyon-Sud medical UniversitiesF-69003 LyonFrance Cancer Research Center of Lyon Centre Leon BerardUMR INSERM 1052CNRS 5286F-69373 LyonFrance Hospices Civils de Lyon Lyon-Sud HospitalEndocrinologyDiabetology and Nutrition ServiceF-69310 Pierre BeniteFrance

Mitochondria-associated endoplasmic reticulum membranes(MAM)play a key role in mitochondrial dynamics and function and in hepatic insulin *** mitochondria are important regulators of energy metabolism,the nutritional regulation of MAM in the liver and its role in the adaptation of mitochondria physiology to nutrient availability are *** this study,we found that the fasted to postprandial transition reduced the number of endoplasmic reticulum-mitochondria contact points in mouse *** of potential hormonal/metabolic signals revealed glucose as the main nutritional regulator of hepatic MAM integrity both in vitro and in *** reduced organelle interactions through the pentose phosphate-protein phosphatase 2A(PP-PP2A)pathway,induced mitochondria fission,and impaired *** MAM reduction counteracted glucose-induced mitochondrial ***,disruption of MAM integrity mimicked effects of glucose on mitochondria dynamics and *** glucose-sensing system is deficient in the liver of insulin-resistant ob/ob and cyclophilin D-KO mice,both characterized by chronic disruption of MAM integrity,mitochondrial fission,and altered mitochondrial *** data indicate that MAM contribute to the hepatic glucose-sensing system,allowing regulation of mitochondria dynamics and function during nutritional *** disruption of MAM may participate in hepatic mitochondrial dysfunction associated with insulin resistance.

关键词： MAM mitochondria dynamics hepatocytes glucose sensing pentose phosphate pathway PP2A

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The scaffold protein menin is essential for activating the MYC locus and MYC-mediated androgen receptor transcription in androgen receptor-dependent prostate cancer cells

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Cancer Communications 2021年第12期41卷 1427-1430页

作者： Yakun Luo Virginie Vlaeminck-Guillem Romain Teinturier Razan Abou Ziki Philippe Bertolino muriel le romancer Chang Xian Zhang Department of Tumor Escape Resistance and ImmunityUniversitéLyonUniversitéClaude Bernard Lyon 1INSERM 1052CNRS 5286Centre Léon BérardCentre de Recherche en Cancérologie de LyonLyon 69008France Centre de Biologie Sud Hôpital Lyon SudHospices Civils de LyonPierre-Bénite 69310France

Dear Editor,The proto-oncogene MYC has a well-documented role in driving androgen receptor(AR)oncogenic functions in prostate cancer(PCa cells)[1]and was recently reported as a key activator in the regulation of AR transcription[2].Dissecting the mechanisms underlying MYC-mediated AR regulation may be crucial for better understanding PCa development and improving its *** recently demonstrated that menin,encoded by the MEN1 gene,plays an oncosuppressive role in the generation of ARlow/CD44+microinvasive prostate adenocarcinoma in mice but exerts oncogenic effects specifically in ARdependent human PCa cells,both likely by modulating AR transcription and AR targets[3].We herein wondered whether this oncogenic function of menin would occur through its interaction with other factors known to play a crucial role forAR transcription in PCa,in particular,MYC.

关键词： cancer likely MYC

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LKB1, A New Biomarker in Breast Cancer

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Journal of Cancer Therapy 2016年第10期7卷 690-699页

作者： Hanine Lattouf Coralie Poulard Isabelle Treilleux Nader Hussein Mona Diab-Assaf muriel le romancer Inserm U1052 Centre de Recherche en Cancérologie de Lyon Lyon France CNRS UMR5286 Centre de Recherche en Cancérologie de Lyon Lyon France Université Lyon 1 Lyon France Laboratory of Molecular and Cellular Biology Doctoral School of Sciences and Technologies Lebanese University Beirut Lebanon Department of Biochemistry and Molecular Biology Comprehensive Cancer Center University of Southern California Los Angeles CA USA Centre Léon Bérard Pathology Department Lyon France

Breast cancer is the most common cancer in women worldwide. Estrogen signaling pathways have been identified as efficient targets of breast cancer therapy, given their key role in promoting breast tumor growth. Agents blocking estrogen-mediated pathways are routinely used in clinical applications in patients displaying estrogen-sensitive breast cancer subtypes;however intrinsic or acquired resistance to treatment often occurs or develops, thus limiting their efficacy. This limitation has highlighted an imperative need to identify new predictive biomarkers. Recent findings have highlighted a role for the Liver Kinase B1 (LKB1) in breast cancer tumorigenesis. LKB1 is a serine/threonine kinase mutated in Peutz-Jeghers syndrome (PJS), implicated in many cellular processes including energy metabolism, cell polarization and cell cycle arrest and has also been shown to play an essential role as a tumor suppressor gene by negatively regulating the mTOR pathway. This review provides an overview of previous findings and ongoing research on LKB1, and substantiates the use of this kinase as a potential prognostic and predictive biomarker of breast cancer.

关键词： LKB1 Biomarker Breast Cancer Estrogen Signaling

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