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Cancer mitochondria

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https://www.readbyqxmd.com/read/28337983/self-inflicted-dna-double-strand-breaks-sustain-tumorigenicity-and-stemness-of-cancer-cells
#1
Xinjian Liu, Fang Li, Qian Huang, Zhengxiang Zhang, Ling Zhou, Yu Deng, Min Zhou, Donald E Fleenor, He Wang, Michael B Kastan, Chuan-Yuan Li
DNA double-strand breaks (DSBs) are traditionally associated with cancer through their abilities to cause chromosomal instabilities or gene mutations. Here we report a new class of self-inflicted DNA DSBs that can drive tumor growth irrespective of their effects on genomic stability. We discover a mechanism through which cancer cells cause DSBs in their own genome spontaneously independent of reactive oxygen species or replication stress. In this mechanism, low-level cytochrome c leakage from the mitochondria leads to sublethal activation of apoptotic caspases and nucleases, which causes DNA DSBs...
March 24, 2017: Cell Research
https://www.readbyqxmd.com/read/28334197/ppar%C3%AE-regulates-tumor-cell-proliferation-and-senescence-via-a-novel-target-gene-carnitine-palmitoyltransferase-1c
#2
Yixin Chen, Yongtao Wang, Yaoyao Huang, Hang Zeng, Bingfang Hu, Lihuan Guan, Huizhen Zhang, Ai-Ming Yu, Caroline H Johnson, Frank J Gonzalez, Min Huang, Huichang Bi
Carnitine palmitoyltransferase 1C (CPT1C), an enzyme located in the outer mitochondria membrane, has a crucial role in fatty acid transport and oxidation. It is also involved in cell proliferation and is a potential driver for cancer cell senescence. However, its upstream regulatory mechanism is unknown. Peroxisome proliferator activated receptor α (PPARα) is a ligand-activated transcription factor that regulates lipid metabolism and tumor progression. The current study aimed to elucidate whether and how PPARα regulates CPT1C and then affects cancer cell proliferation and senescence...
March 3, 2017: Carcinogenesis
https://www.readbyqxmd.com/read/28333383/calcium-transport-and-signaling-in-mitochondria
#3
Roberto Bravo-Sagua, Valentina Parra, Camila López-Crisosto, Paula Díaz, Andrew F G Quest, Sergio Lavandero
Calcium (Ca2+) is a key player in the regulation of many cell functions. Just like Ca2+, mitochondria are ubiquitous, versatile, and dynamic players in determining both cell survival and death decisions. Given their ubiquitous nature, the regulation of both is deeply intertwined, whereby Ca2+ regulates mitochondrial functions, while mitochondria shape Ca2+ dynamics. Deregulation of either Ca2+ or mitochondrial signaling leads to abnormal function, cell damage or even cell death, thereby contributing to muscle dysfunction or cardiac pathologies...
March 16, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28333141/npas2-promotes-cell-survival-of-hepatocellular-carcinoma-by-transactivating-cdc25a
#4
Peng Yuan, Jibin Li, Feng Zhou, Qichao Huang, Jiansheng Zhang, Xu Guo, Zhuomin Lyu, Hongxin Zhang, Jinliang Xing
Emerging evidences show that disruption of the circadian rhythm is associated with tumor initiation and progression. Neuronal PAS domain protein 2 (NPAS2), one of the core circadian molecules, has been proved to be a potential prognostic biomarker in colorectal and breast cancers. However, to date, the potential functional roles and molecular mechanisms by which NPAS2 affects cancer cell survival are greatly unclear, especially in hepatocellular carcinoma (HCC). We first investigated the expression of NPAS2 and its clinical significance in HCC...
March 23, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28332314/the-mitochondrial-hinge-protein-uqcrh-is-a-novel-prognostic-factor-for-hepatocellular-carcinoma
#5
Eun-Ran Park, Sang-Bum Kim, Jee-San Lee, Yang-Hyun Kim, Dong-Hyoung Lee, Eung-Ho Cho, Sun-Hoo Park, Chul Ju Han, Bu-Yeo Kim, Dong Wook Choi, Young Do Yoo, Ami Yu, Jae Won Lee, Ja June Jang, Young Nyun Park, Kyung-Suk Suh, Kee-Ho Lee
Alterations in mitochondrial respiration contribute to the development and progression of cancer via abnormal biogenesis, including generation of reactive oxygen species. Ubiquinol-cytochrome c reductase hinge protein (UQCRH) consists of the cytochrome bc1 complex serving respiration in mitochondria. In the present study, we analyzed UQCRH abnormalities in hepatocellular carcinoma (HCC) and its association with clinical outcomes of patients. UQCRH expression in HCC was determined via semiquantitative and quantitative real-time reverse transcriptase polymerase chain reaction of 96 surgically resected HCC tissues positive for hepatitis B virus surface antigen...
March 23, 2017: Cancer Medicine
https://www.readbyqxmd.com/read/28328323/an-adaptable-high-throughput-technology-enabling-the-identification-of-specific-transcription-modulators
#6
Tim Bergbrede, Emily Hoberg, Nils-Göran Larsson, Maria Falkenberg, Claes M Gustafsson
Mitochondria harbor the oxidative phosphorylation (OXPHOS) system, which under aerobic conditions produces the bulk of cellular adenosine triphosphate (ATP). The mitochondrial genome encodes key components of the OXPHOS system, and it is transcribed by the mitochondrial RNA polymerase, POLRMT. The levels of mitochondrial transcription correlate with the respiratory activity of the cell. Therefore, compounds that can increase or decrease mitochondrial gene transcription may be useful for fine-tuning metabolism and could be used to treat metabolic diseases or certain forms of cancer...
April 2017: SLAS Discov
https://www.readbyqxmd.com/read/28327594/aspirin-induces-cell-death-by-directly-modulating-mitochondrial-voltage-dependent-anion-channel-vdac
#7
Debanjan Tewari, Dhriti Majumdar, Sirisha Vallabhaneni, Amal Kanti Bera
Aspirin induces apoptotic cell death in various cancer cell lines. Here we showed that silencing of VDAC1 protected HeLa cells from aspirin-induced cell death. Compared to the wild type cells, VDAC1 knocked down cells showed lesser change of mitochondrial membrane potential (Δψm), upon aspirin treatment. Aspirin augmented ATP and ionomycin-induced mitochondrial Ca(2+) uptake which was abolished in VDAC1 knocked down cells. Aspirin dissociated bound hexokinase II (HK-II) from mitochondria. Further, aspirin promoted the closure of recombinant human VDAC1, reconstituted in planar lipid bilayer...
March 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28324486/mitopho8%C3%AE-60-assay-as-a-tool-to-quantitatively-measure-mitophagy-activity
#8
Zhiyuan Yao, Xu Liu, Daniel J Klionsky
Mitophagy, a selective type of macroautophagy (hereafter referred to as autophagy), specifically mediates the vacuole/lysosome-dependent degradation of damaged or surplus mitochondria. Because this process regulates the number and quality of mitochondria, it is vital for proper cellular homeostasis. Mitophagy also plays critical roles in the clearance of paternal mitochondria in C. elegans embryos, in erythroid cell maturation, and in the prevention of neurodegenerative disease and cancer. In order to study the molecular mechanism and regulation of mitophagy, sensitive assays are necessary to quantitatively measure mitophagy activity...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28323499/antiproliferative-activity-of-egg-yolk-peptides-in-human-colon-cancer-cells
#9
Marwa N Yousr, Akram A Aloqbi, Ulfat M Omar, Nazlin K Howell
Egg yolk peptides were successfully prepared from egg yolk protein by-products after lecithin extraction. Defatted egg yolk protein was hydrolyzed with pepsin and pancreatin and purified by gel filtration to produce egg yolk gel filtration fraction (EYGF-33) with antiproliferative activity. The highlight of this study was that the peptide EYGF-33 (1.0 mg/ml) significantly inhibits cell viability of colon cancer cells (Caco-2) with no inhibitory effects on the viability of human colon epithelial normal cells (HCEC) after 48 h...
March 21, 2017: Nutrition and Cancer
https://www.readbyqxmd.com/read/28321271/parkin-in-cancer-mitophagy-related-unrelated-tasks
#10
EDITORIAL
Nabil Eid, Yoichi Kondo
Dysfunctional mitochondria may produce excessive reactive oxygen species, thus inducing DNA damage, which may be oncogenic if not repaired. As a major role of the PINK1-Parkin pathway involves selective autophagic clearance of damaged mitochondria via a process termed mitophagy, Parkin-mediated mitophagy may be a tumor-suppressive mechanism. As an alternative mechanism for tumor inhibition beyond mitophagy, Parkin has been reported to have other oncosuppressive functions such as DNA repair, negative regulation of cell proliferation and stimulation of p53 tumor suppressor function...
March 8, 2017: World Journal of Hepatology
https://www.readbyqxmd.com/read/28320429/chrysin-inhibited-tumor-glycolysis-and-induced-apoptosis-in-hepatocellular-carcinoma-by-targeting-hexokinase-2
#11
Dong Xu, Junzhe Jin, Hao Yu, Zheming Zhao, Dongyan Ma, Chundong Zhang, Honglei Jiang
BACKGROUND: Hexokinase-2(HK-2) plays dual roles in glucose metabolism and mediation of cell apoptosis, making it an attractive target for cancer therapy. Chrysin is a natural flavone found in plant extracts which are widely used as herb medicine in China. In the present study, we investigated the antitumor activity of chrysin against hepatocellular carcinoma (HCC) and the role of HK-2 played for chrysin to exert its function. METHODS: The expression of HK-2 in HCC cell line and tumor tissue was examined by western blotting and immunohistochemistry staining...
March 20, 2017: Journal of Experimental & Clinical Cancer Research: CR
https://www.readbyqxmd.com/read/28319809/abt-737-synergizes-with-cisplatin-bypassing-aberration-of-apoptotic-pathway-in-non-small-cell-lung-cancer
#12
Eun Young Kim, Ji Ye Jung, Arum Kim, Yoon Soo Chang, Se Kyu Kim
A subset of non-small cell lung cancer (NSCLC), which does not have a druggable driver mutation, is treated with platinum-based cytotoxic chemotherapy, but it develops resistance triggered by DNA damage responses. Here, we investigated the effect of activation of STAT3 by cisplatin on anti-apoptotic proteins and the effectiveness of a co-treatment with cisplatin and a BH3 mimetic, ABT-737. We analyzed the relationship between cisplatin and STAT3 pathway and effect of ABT-737, when combined with cisplatin in NSCLC cells and K-ras mutant mouse models...
March 17, 2017: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/28314935/a-disease-with-a-sweet-tooth-exploring-the-warburg-effect-in-alzheimer-s-disease
#13
REVIEW
Anna Atlante, Lidia de Bari, Antonella Bobba, Giuseppina Amadoro
After more than 80 years from the revolutionary discoveries of Otto Warburg, who observed high glucose dependency, with increased glycolysis and lactate production regardless of oxygen availability in most cancer cells, the 'Warburg effect' returns to the fore in neuronal cells affected by Alzheimer's disease (AD). Indeed, it seems that, in the mild phase of AD, neuronal cells "prefer" to use the energetically inefficient method of burning glucose by glycolysis, as in cancer, proving to become resistant to β-amyloid (Aβ)-dependent apoptosis...
March 17, 2017: Biogerontology
https://www.readbyqxmd.com/read/28314780/non-coding-rnas-the-dark-side-of-nuclear-mitochondrial-communication
#14
REVIEW
Roberto Vendramin, Jean-Christophe Marine, Eleonora Leucci
Mitochondria are critical hubs for the integration of several key metabolic processes implicated in cell growth and survival. They originated from bacterial ancestors through endosymbiosis, following the transfer of more than 90% of their endosymbiont genome to the host cell nucleus. Over time, a mutually beneficial symbiotic relationship has been established, which relies on continuous and elaborate signaling mechanisms between this life-essential organelle and its host. The ability of mitochondria to signal their functional state and trigger compensatory and adaptive cellular responses has long been recognized, but the underlying molecular mechanisms involved have remained poorly understood...
March 17, 2017: EMBO Journal
https://www.readbyqxmd.com/read/28301251/chrysin-as-an-anti-cancer-agent-exerts-selective-toxicity-by-directly-inhibiting-mitochondrial-complex-ii-and-v-in-cll-b-lymphocytes
#15
Ahmad Salimi, Mehryar Habibi Roudkenar, Enayatollah Seydi, Leila Sadeghi, Alireza Mohseni, Nahal Pirahmadi, Jalal Pourahmad
We investigated the effect of chrysin on isolated normal and chronic lymphocytic leukemia (CLL) B-lymphocytes and their isolated mitochondria. We report that a selective and significant increase in cytotoxicity, intracellular reactive oxygen species, mitochondrial membrane potential collapse, ADP/ATP ratio, caspase 3 activation and finally apoptosis in chrysin-treated CLL B- lymphocytes. Also we determined that chrysin selectively inhibits complex II and ATPases in cancerous mitochondria. In this study we proved that the ability of chrysin to promote apoptosis in CLL B-lymphocytes performed by selectively targeting of mitochondria...
March 16, 2017: Cancer Investigation
https://www.readbyqxmd.com/read/28300784/the-molecular-basis-of-toxins-interactions-with-intracellular-signaling-via-discrete-portals
#16
REVIEW
Adi Lahiani, Ephraim Yavin, Philip Lazarovici
An understanding of the molecular mechanisms by which microbial, plant or animal-secreted toxins exert their action provides the most important element for assessment of human health risks and opens new insights into therapies addressing a plethora of pathologies, ranging from neurological disorders to cancer, using toxinomimetic agents. Recently, molecular and cellular biology dissecting tools have provided a wealth of information on the action of these diverse toxins, yet, an integrated framework to explain their selective toxicity is still lacking...
March 16, 2017: Toxins
https://www.readbyqxmd.com/read/28300190/a-mechanistic-study-of-gold-nanoparticle-radiosensitisation-using-targeted-microbeam-irradiation
#17
Mihaela Ghita, Stephen J McMahon, Laura E Taggart, Karl T Butterworth, Giuseppe Schettino, Kevin M Prise
Gold nanoparticles (GNPs) have been demonstrated as effective radiosensitizing agents in a range of preclinical models using broad field sources of various energies. This study aimed to distinguish between these mechanisms by applying subcellular targeting using a soft X-ray microbeam in combination with GNPs. DNA damage and repair kinetics were determined following nuclear and cytoplasmic irradiation using a soft X-ray (carbon K-shell, 278 eV) microbeam in MDA-MB-231 breast cancer and AG01522 fibroblast cells with and without GNPs...
March 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28291330/cancer-cell-specific-mitochondria-targeted-drug-delivery-by-dual-ligand-functionalized-nanodiamonds-circumvent-drug-resistance
#18
Miu Shan Chan, Ling Sum Liu, Hoi Man Leung, Pik Kwan Lo
We demonstrate a nanotechnology approach for the development of cancer-cell-specific subcellular organelle-targeted drug nanocarriers based on photostable nanodiamonds (ND) functionalized with folic acid and mitochondrial localizing sequence (MLS) peptides. We showed that these multifunctional NDs not only distinguish between cancer cells and normal cells, and transport the loaded drugs across the plasma membrane of cancer cells, but also selectively deliver them to mitochondria and induce significant cytotoxicity and cell death compared with free Dox localized in lysosomes...
March 21, 2017: ACS Applied Materials & Interfaces
https://www.readbyqxmd.com/read/28287607/mitoception-transferring-isolated-human-msc-mitochondria-to-glioblastoma-stem-cells
#19
Brice Nzigou Mombo, Sabine Gerbal-Chaloin, Aleksandra Bokus, Martine Daujat-Chavanieu, Christian Jorgensen, Jean-Philippe Hugnot, Marie-Luce Vignais
Mitochondria play a central role for cell metabolism, energy production and control of apoptosis. Inadequate mitochondrial function has been found responsible for very diverse diseases, ranging from neurological pathologies to cancer. Interestingly, mitochondria have recently been shown to display the capacity to be transferred between cell types, notably from human mesenchymal stem cells (MSC) to cancer cells in coculture conditions, with metabolic and functional consequences for the mitochondria recipient cells, further enhancing the current interest for the biological properties of these organelles...
February 22, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28287444/bufalin-induces-apoptosis-of-human-osteosarcoma-u-2-os-cells-through-endoplasmic-reticulum-stress-caspase-and-mitochondria-dependent-signaling-pathways
#20
Ching-Hsiao Lee, Yung-Luen Shih, Mei-Hui Lee, Man-Kuan Au, Yung-Liang Chen, Hsu-Feng Lu, Jing-Gung Chung
Bone cancer is one of the cancer-related diseases, and there are increased numbers of patients with bone cancer worldwide. Therefore the efficacy of treatment of bone cancer is considered extremely vital. Bufalin has been showed to have biological activities including anticancer activities in vitro and in vivo. However, the exact associated mechanisms for bufalin induced apoptosis in human bone cancer cells are still unclear. In the present study, we investigated the effect of bufalin on the cytotoxic effects in U-2 OS human osteosarcoma cells...
March 10, 2017: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
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