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Mitochondria AND mTOR

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https://www.readbyqxmd.com/read/29454865/inhibitory-effects-of-selenium-on-cadmium-induced-cytotoxicity-in-pc12-cells-via-regulating-oxidative-stress-and-apoptosis
#1
Kaniz Fatima Binte Hossain, Md Mostafizur Rahman, Md Tajuddin Sikder, Takeshi Saito, Toshiyuki Hosokawa, Masaaki Kurasaki
Purpose of this study is to investigate mechanism/s of cyto-protection by selenium (Na2 SeO3 ; Se4+ ) against cadmium (CdCl2 ; Cd2+ )-induced cytotoxicity using PC12 cells. In addition, Se (5, 10, 20 and 40 μM) and Cd (2.5, 5 and 10 μM)-induced cytotoxicity is determined. Cytotoxicity assays and western blot analyses confirmed that Se (≥10 μM) promotes autophagic cell death via inhibition of mTOR activation and p62 accumulation due to increase of cellular oxidative stress. On the other hand, co-presence of non-toxic Se (5 μM) and toxic Cd (5 μM) showed to increase cell viability, glutathione and glutathione peroxidase 1 (GPx1) levels, and to decrease DNA fragmentation and lactate dehydrogenase (LDH) activity compared to Cd-treated (5 μM) cells alone...
February 15, 2018: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/29420962/activation-of-serine-one-carbon-metabolism-by-calcineurin-a%C3%AE-1-reduces-myocardial-hypertrophy-and-improves-ventricular-function
#2
Laura Padrón-Barthe, María Villalba-Orero, Jesús M Gómez-Salinero, Rebeca Acín-Pérez, Sara Cogliati, Marina López-Olañeta, Paula Ortiz-Sánchez, Elena Bonzón-Kulichenko, Jesús Vázquez, Pablo García-Pavía, Nadia Rosenthal, José Antonio Enríquez, Enrique Lara-Pezzi
BACKGROUND: In response to pressure overload, the heart develops ventricular hypertrophy that progressively decompensates and leads to heart failure. This pathological hypertrophy is mediated, among others, by the phosphatase calcineurin and is characterized by metabolic changes that impair energy production by mitochondria. OBJECTIVES: The authors aimed to determine the role of the calcineurin splicing variant CnAβ1 in the context of cardiac hypertrophy and its mechanism of action...
February 13, 2018: Journal of the American College of Cardiology
https://www.readbyqxmd.com/read/29415881/tak1-regulates-skeletal-muscle-mass-and-mitochondrial-function
#3
Sajedah M Hindi, Shuichi Sato, Guangyan Xiong, Kyle R Bohnert, Andrew A Gibb, Yann S Gallot, Joseph D McMillan, Bradford G Hill, Shizuka Uchida, Ashok Kumar
Skeletal muscle mass is regulated by a complex array of signaling pathways. TGF-β-activated kinase 1 (TAK1) is an important signaling protein, which regulates context-dependent activation of multiple intracellular pathways. However, the role of TAK1 in the regulation of skeletal muscle mass remains unknown. Here, we report that inducible inactivation of TAK1 causes severe muscle wasting, leading to kyphosis, in both young and adult mice.. Inactivation of TAK1 inhibits protein synthesis and induces proteolysis, potentially through upregulating the activity of the ubiquitin-proteasome system and autophagy...
February 8, 2018: JCI Insight
https://www.readbyqxmd.com/read/29386287/rsv-replication-is-promoted-by-autophagy-mediated-inhibition-of-apoptosis
#4
Miao Li, Jian Li, Jianling Yang, Jianguo Liu, Zhengzheng Zhang, Xiaotian Song, Zhiyan Yao, Cuiqing Ma, Wenjian Li, Ruihong Zeng, Kai Wang, Lin Wei
Respiratory syncytial virus (RSV) is the main cause of acute lower respiratory tract infection (ALRI) in children worldwide. Virus-host interaction affects progression and prognosis of the infection. Autophagy plays important roles in virus-host interaction. Respiratory epithelial cells serve as the front line of host defense during RSV infection, However, it is still unclear how they interact with RSV. In this study, We found that RSV induced autophagy which favored RSV replication and exacerbated lung pathology in vivo Mechanistically, RSV induced complete autophagy flux through Reactive oxygen species (ROS) generation and activation of AMPK-MTOR (AMP-activated protein kinase/mammalian target of rapamycin) signaling pathway in Hep2 cells...
January 31, 2018: Journal of Virology
https://www.readbyqxmd.com/read/29378182/activation-of-mitochondrial-fusion-provides-a-new-treatment-for-mitochondria-related-diseases
#5
Aliz Szabo, Katalin Sumegi, Katalin Fekete, Eniko Hocsak, Balazs Debreceni, Gyorgy Setalo, Krisztina Kovacs, Laszlo Deres, Andras Kengyel, Dominika Kovacs, Jozsef Mandl, Miklos Nyitrai, Mark A Febbraio, Ferenc Gallyas, Balazs Sumegi
Mitochondria fragmentation destabilizes mitochondrial membranes, promotes oxidative stress and facilitates cell death, thereby contributing to the development and the progression of several mitochondria-related diseases. Accordingly, compounds that reverse mitochondrial fragmentation could have therapeutic potential in treating such diseases. BGP-15, a hydroxylamine derivative, prevents insulin resistance in humans and protects against several oxidative stress-related diseases in animal models. Here we show that BGP-15 promotes mitochondrial fusion by activating optic atrophy 1 (OPA1), a GTPase dynamin protein that assist fusion of the inner mitochondrial membranes...
January 26, 2018: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29353042/ginkgolic-acid-induces-interplay-between-apoptosis-and-autophagy-regulated-by-ros-generation-in-colon-cancer
#6
Yuxia Liu, Bin Yang, Lirong Zhang, Xianling Cong, Zhen Liu, Yu Hu, Jing Zhang, Haixia Hu
Presently, developing effective anti-colon cancer drugs still remains to be important. Ginkgolic acids (GA), as a botanical drug extracted from the seed coat of Ginkgo biloba L., possess various bioactive properties. Our findings, for the first time, indicated that GA suppressed colon cancer cell proliferation, migration and invasion. GA led to cell death through G0/G1 phase arrest. In addition, apoptosis was significantly induced by GA treatment. The intrinsic apoptosis pathway was included, proved by the release of cytochrome c (Cyto-c) from the mitochondria into the cytosol...
January 15, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29348263/phosphoinositide-3-kinase-gamma-inhibition-protects-from-anthracycline-cardiotoxicity-and-reduces-tumor-growth
#7
Mingchuan Li, Valentina Sala, Maria Chiara De Santis, James Cimino, Paola Cappello, Nicola Pianca, Anna Di Bona, Jean Piero Margaria, Miriam Martini, Edoardo Lazzarini, Flora Pirozzi, Luca Rossi, Irene Franco, Julia Bornbaum, Jacqueline Heger, Susanne Rohrbach, Alessia Perino, Carlo G Tocchetti, Braulio H F Lima, Mauro M Teixeira, Paolo E Porporato, Rainer Schulz, Annalisa Angelini, Marco Sandri, Pietro Ameri, Sebastiano Sciarretta, Roberto César P Lima-Júnior, Marco Mongillo, Tania Zaglia, Fulvio Morello, Francesco Novelli, Emilio Hirsch, Alessandra Ghigo
Background -Anthracyclines, such as doxorubicin (DOX), are potent anti-cancer agents for the treatment of solid tumors and hematological malignancies. However, their clinical use is hampered by cardiotoxicity. This study sought to investigate the role of PI3Kγ in DOX-induced cardiotoxicity and the potential cardio-protective and anti-cancer effects of PI3Kγ inhibition. Methods -Mice expressing a kinase-inactive PI3Kγ or receiving PI3Kγ selective inhibitors were subjected to chronic DOX treatment. Cardiac function was analyzed by echocardiography and DOX-mediated signaling was assessed in whole hearts or in isolated cardiomyocytes...
January 18, 2018: Circulation
https://www.readbyqxmd.com/read/29343514/trpm2-channel-mediated-regulation-of-autophagy-maintains-mitochondrial-function-and-promotes-gastric-cancer-cell-survival-via-the-jnk-signaling-pathway
#8
Shekoufeh Almasi, Barry E Kennedy, Mariam El Aghil, Andra M Sterea, Shashi Gujar, Santiago Partida-Sánchez, Yassine El Hiani
A lack of effective treatment is one of the main factors contributing to gastric cancer-related death. Discovering effective targets and understanding their underlying anticancer mechanism is key to achieving the best response to treatment and to limiting side effects. Although recent studies have shown that the cation channel transient receptor potential melastatin-2 (TRPM2) is crucial for cancer cell survival, the exact mechanism remains unclear, limiting its therapeutic potential. Here, using molecular and functional assays, we investigated the role of TRPM2 in survival of gastric cancer cells...
January 17, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29331805/synthesis-characterization-and-anticancer-activity-in%C3%A2-vitro-and-in%C3%A2-vivo-evaluation-of-an-iridium-iii-polypyridyl-complex
#9
Qiao-Yan Yi, Dan Wan, Bing Tang, Yang-Jie Wang, Wen-Yao Zhang, Fan Du, Miao He, Yun-Jun Liu
An iridium (III) complex [Ir(ppy)2(BDPIP)]PF6 (Ir-1) was reported to show high anticancer activity and may be used as a potent anticancer drug. In the current study, we designed and synthesized a novel iridium (III) complex and evaluated its potential inhibitory effect on the cancer cell growth in vitro and in vivo. This complex was found to display high cytotoxic activity in vitro and in vivo against A549 cell with a low IC50 value of 3.6 ± 0.3 μM and inhibiting percentage of tumor growth is 63.84% compared with the control...
December 1, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/29331753/an-iridium-iii-complex-as-potent-anticancer-agent-induces-apoptosis-and-autophagy-in-b16%C3%A2-cells-through-inhibition-of-the-akt-mtor-pathway
#10
Bing Tang, Dan Wan, Yang-Jie Wang, Qiao-Yan Yi, Bo-Hong Guo, Yun-Jun Liu
A new ligand THPDP (THPDP = 11-(6,7,8,9-tetrahydrophenazin-2-yl)dipyrido[3,2-a:2',3'-c]phenazine) and its iridium(III) complex [Ir(ppy)2(THPDP)]PF6 (Ir-1) was synthesized and characterized by elemental analysis, IR, ESI-MS, 1H NMR and 13C NMR. The cytotoxicity in vitro of the complex against cancer cells B16, A549, Eca-109, SGC-7901, BEL-7402 and normal NIH 3T3 cell lines was evaluated using MTT method. The IC50 values of the complex toward B16, A549 and Eca-109 cells are 1.0 ± 0.02, 1.4 ± 0...
December 30, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/29314656/mammalian-target-of-rapamycin-inhibition-attenuates-myocardial-ischaemia-reperfusion-injury-in-hypertrophic-heart
#11
Lei-Lei Ma, Xin Ma, Fei-Juan Kong, Jun-Jie Guo, Hong-Tao Shi, Jian-Bing Zhu, Yun-Zeng Zou, Jun-Bo Ge
Pathological cardiac hypertrophy aggravated myocardial infarction and is causally related to autophagy dysfunction and increased oxidative stress. Rapamycin is an inhibitor of serine/threonine kinase mammalian target of rapamycin (mTOR) involved in the regulation of autophagy as well as oxidative/nitrative stress. Here, we demonstrated that rapamycin ameliorates myocardial ischaemia reperfusion injury by rescuing the defective cytoprotective mechanisms in hypertrophic heart. Our results showed that chronic rapamycin treatment markedly reduced the phosphorylated mTOR and ribosomal protein S6 expression, but not Akt in both normal and aortic-banded mice...
January 4, 2018: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/29286187/mitochondrial-atad3a-regulates-milk-biosynthesis-and-proliferation-of-mammary-epithelial-cells-from-dairy-cow-via-the-mtor-pathway
#12
Dongying Chen, Xiaohan Yuan, Lijie Liu, Minghui Zhang, Bo Qu, Zhen Zhen, Xuejun Gao
ATPase family AAA-domain containing protein 3A (ATAD3A) is a nuclear-encoded mitochondrial membrane protein, which is essential for cell growth and metabolism. The mechanism by which ATAD3A acts is still not fully understood. In this study, we explored the regulatory role of ATAD3A on milk biosynthesis and proliferation of bovine mammary epithelial cell. We showed that ATAD3A is localized in mitochondria and the expression of ATAD3A was up-regulated in response to extracellular stimuli such as amino acids and hormones...
December 29, 2017: Cell Biology International
https://www.readbyqxmd.com/read/29232555/mtorc2-promotes-tumorigenesis-via-lipid-synthesis
#13
Yakir Guri, Marco Colombi, Eva Dazert, Sravanth K Hindupur, Jason Roszik, Suzette Moes, Paul Jenoe, Markus H Heim, Isabelle Riezman, Howard Riezman, Michael N Hall
Dysregulated mammalian target of rapamycin (mTOR) promotes cancer, but underlying mechanisms are poorly understood. We describe an mTOR-driven mouse model that displays hepatosteatosis progressing to hepatocellular carcinoma (HCC). Longitudinal proteomic, lipidomics, and metabolomic analyses revealed that hepatic mTORC2 promotes de novo fatty acid and lipid synthesis, leading to steatosis and tumor development. In particular, mTORC2 stimulated sphingolipid (glucosylceramide) and glycerophospholipid (cardiolipin) synthesis...
December 11, 2017: Cancer Cell
https://www.readbyqxmd.com/read/29208466/chetomin-induces-apoptosis-in-human-triple-negative-breast-cancer-cells-by-promoting-calcium-overload-and-mitochondrial-dysfunction
#14
Jayant Dewangan, Sonal Srivastava, Sakshi Mishra, Prabhash Kumar Pandey, Aman Divakar, Srikanta Kumar Rath
Human triple-negative breast cancer (TNBC) is poorly diagnosed and unresponsive to conventional hormone therapy. Chetomin (CHET), a fungal metabolite synthesized by Chaetomium cochliodes, has been reported as a promising anticancer and antiangiogenic agent but the complete molecular mechanism of its anticancer potential remains to be elucidated. In our study, we explored the anti-neoplastic action of CHET on TNBC cells. Cytotoxicity studies were performed in human TNBC cells viz. MDA-MB-231 and MDA-MB-468 cells by Sulforhodamine B assay...
December 2, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29184100/akt-mtor-signaling-modulates-the-dynamics-of-ire1-rnase-activity-by-regulating-er-mitochondria-contacts
#15
Miguel Sanchez-Alvarez, Miguel Angel Del Pozo, Chris Bakal
Inositol Requiring Enzyme-1 (IRE1) is the most conserved transducer of the Unfolded Protein Response (UPR), a surveillance mechanism that ensures homeostasis of the endoplasmic reticulum (ER) in eukaryotes. IRE1 activation orchestrates adaptive responses, including lipid anabolism, metabolic reprogramming, increases in protein folding competency, and ER expansion/remodeling. However, we still know surprisingly little regarding the principles by which this ER transducer is deactivated upon ER stress clearance...
November 28, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29157834/16-hydroxycleroda-3-13-dien-15-16-olide-inhibits-the-proliferation-and-induces-mitochondrial-dependent-apoptosis-through-akt-mtor-and-mek-erk-pathways-in-human-renal-carcinoma-cells
#16
Cheng Liu, Wei-Chang Lee, Bu-Miin Huang, Yi-Chen Chia, Yu-Chi Chen, Yung-Chia Chen
BACKGROUND: Renal cell carcinoma (RCC) is well known that it cannot be treated with traditional chemotherapy or radiotherapy. 16-Hydroxycleroda-3,13-dien-15,16-olide (CD), isolated from Polyalthia longifolia Benth. & Hook. f. var. pendula had been reported to display significant efficacy against cancer cell lines. PURPOSE: To determine the anti-tumour activities of CD in two clear cell type RCC (ccRCC) cell lines (A-498 and 786-O). In addition, the underlying mechanisms were also examined...
December 1, 2017: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
https://www.readbyqxmd.com/read/29150352/dysregulation-of-mrna-translation-and-energy-metabolism-in-cancer
#17
REVIEW
Matthew Leibovitch, Ivan Topisirovic
Dysregulated mRNA translation and aberrant energy metabolism are frequent in cancer. Considering that mRNA translation is an energy demanding process, cancer cells must produce sufficient ATP to meet energy demand of hyperactive translational machinery. In recent years, the mammalian/mechanistic target of rapamycin (mTOR) emerged as a central regulatory node which coordinates energy consumption by the translation apparatus and ATP production in mitochondria. Aberrant mTOR signaling underpins the vast majority of cancers whereby increased mTOR activity is thought to be a major determinant of both malignant translatomes and metabolomes...
November 2, 2017: Advances in Biological Regulation
https://www.readbyqxmd.com/read/29138276/metabolic-reprogramming-ensures-cancer-cell-survival-despite-oncogenic-signaling-blockade
#18
Hui-Wen Lue, Jennifer Podolak, Kevin Kolahi, Larry Cheng, Soumya Rao, Devin Garg, Chang-Hui Xue, Juha K Rantala, Jeffrey W Tyner, Kent L Thornburg, Ann Martinez-Acevedo, Jen-Jane Liu, Christopher L Amling, Charles Truillet, Sharon M Louie, Kimberly E Anderson, Michael J Evans, Valerie B O'Donnell, Daniel K Nomura, Justin M Drake, Anna Ritz, George V Thomas
There is limited knowledge about the metabolic reprogramming induced by cancer therapies and how this contributes to therapeutic resistance. Here we show that although inhibition of PI3K-AKT-mTOR signaling markedly decreased glycolysis and restrained tumor growth, these signaling and metabolic restrictions triggered autophagy, which supplied the metabolites required for the maintenance of mitochondrial respiration and redox homeostasis. Specifically, we found that survival of cancer cells was critically dependent on phospholipase A2 (PLA2) to mobilize lysophospholipids and free fatty acids to sustain fatty acid oxidation and oxidative phosphorylation...
October 15, 2017: Genes & Development
https://www.readbyqxmd.com/read/29129468/inhibition-of-rac1-ameliorates-neuronal-oxidative-stress-damage-via-reducing-bcl-2-rac1-complex-formation-in-mitochondria-through-pi3k-akt-mtor-pathway
#19
Yundan Pan, Na Wang, Pingping Xia, E Wang, Qulian Guo, Zhi Ye
Although the neuroprotective effects of Rac1 inhibition have been reported in various cerebral ischemic models, the molecular mechanisms of action have not yet been fully elucidated. In this study, we investigated whether the inhibition of Rac1 provided neuroprotection in a diabetic rat model of focal cerebral ischemia and hyperglycemia-exposed PC-12 cells. Intracerebroventricular administration of lentivirus expressing the Rac1 small hairpin RNA (shRNA) and specific Rac1 inhibitor NSC23766 not only decreased the infarct volumes and improved neurologic deficits with a correlated significant activation of mitochondrial DNA specific proteins, such as OGG1 and POLG, but also elevated Bcl-2 S70 phosphorylation in mitochondria...
November 10, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/29118925/bardoxolone-methyl-cddo-me-or-rta402-induces-cell-cycle-arrest-apoptosis-and-autophagy-via-pi3k-akt-mtor-and-p38-mapk-erk1-2-signaling-pathways-in-k562-cells
#20
Xin-Yu Wang, Xue-Hong Zhang, Li Peng, Zheng Liu, Yin-Xue Yang, Zhi-Xu He, Hong-Wan Dang, Shu-Feng Zhou
Chronic myeloid leukemia (CML) treatment remains a challenge due to drug resistance and severe side effect, rendering the need on the development of novel therapeutics. CDDO-Me (Bardoxolone methyl), a potent Nrf2 activator and NF-κB inhibitor, is a promising candidate for cancer treatment including leukemia. However, the underlying mechanism for CDDO-Me in CML treatment is unclear. This study aimed to evaluate the molecular interactome of CDDO-Me in K562 cells using the quantitative proteomics approach stable-isotope labeling by amino acids in cell culture (SILAC) and explore the underlying mechanisms using cell-based functional assays...
2017: American Journal of Translational Research
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