ORCID Profile
0000-0002-7468-6194
Current Organisation
University of Amsterdam
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Publisher: Elsevier BV
Date: 04-2010
DOI: 10.1016/J.MAM.2010.02.008
Abstract: The role of oncoproteins and tumor suppressor proteins in promoting the malignant transformation of mammalian cells by affecting properties such as proliferative signalling, cell cycle regulation and altered adhesion is well established. Chemicals, viruses and radiation are also generally accepted as agents that commonly induce mutations in the genes encoding these cancer-causing proteins, thereby giving rise to cancer. However, more recent evidence indicates the importance of two additional key factors imposed on proliferating cells that are involved in transformation to malignancy and these are hypoxia and/or stressful conditions of nutrient deprivation (e.g. lack of glucose). These two additional triggers can initiate and promote the process of malignant transformation when a low percentage of cells overcome and escape cellular senescence. It is becoming apparent that hypoxia causes the progressive elevation in mitochondrial ROS production (chronic ROS) which over time leads to stabilization of cells via increased HIF-2alpha expression, enabling cells to survive with sustained levels of elevated ROS. In cells under hypoxia and/or low glucose, DNA mismatch repair processes are repressed by HIF-2alpha and they continually accumulate mitochondrial ROS-induced oxidative DNA damage and increasing numbers of mutations driving the malignant transformation process. Recent evidence also indicates that the resulting mutated cancer-causing proteins feedback to lify the process by directly affecting mitochondrial function in combinatorial ways that intersect to play a major role in promoting a vicious spiral of malignant cell transformation. Consequently, many malignant processes involve periods of increased mitochondrial ROS production when a few cells survive the more common process of oxidative damage induced cell senescence and death. The few cells escaping elimination emerge with oncogenic mutations and survive to become immortalized tumors. This review focuses on evidence highlighting the role of mitochondria as drivers of elevated ROS production during malignant transformation and hence, their potential as targets for cancer therapy. The review is organized into five main sections concerning different aspects of "mitochondrial malignancy". The first concerns the functions of mitochondrial ROS and its importance as a pacesetter for cell growth versus senescence and death. The second considers the available evidence that cellular stress in the form of hypoxic and/or hypoglycaemic conditions represent two of the major triggering events for cancer and how oncoproteins reinforce this process by altering gene expression to bring about a common set of changes in mitochondrial function and activity in cancer cells. The third section presents evidence that oncoproteins and tumor suppressor proteins physically localize to the mitochondria in cancer cells where they directly regulate malignant mitochondrial programs, including apoptosis. The fourth section covers common mutational changes in the mitochondrial genome as they relate to malignancy and the relationship to the other three areas. The last section concerns the relevance of these findings, their importance and significance for novel targeted approaches to anti-cancer therapy and selective triggering in cancer cells of the mitochondrial apoptotic pathway.
Publisher: Elsevier BV
Date: 06-2022
Publisher: Elsevier BV
Date: 09-2021
Publisher: Springer Science and Business Media LLC
Date: 27-04-2011
Publisher: Elsevier BV
Date: 07-2021
Publisher: American Chemical Society (ACS)
Date: 22-04-2021
Publisher: Elsevier BV
Date: 07-2020
Publisher: Mary Ann Liebert Inc
Date: 12-2011
Abstract: Recent research has shown that tumors contain a small subpopulation of stem-like cells that are more resistant to therapy and that are likely to produce second-line tumors. Cancer stem-like cells (CSCs) have been characterized by a variety of markers, including, for a number of types of cancer, high expression of the plasma membrane protein CD133, which is also indicative of the increase of stemness of cultured cancer cells growing as spheres. While the function of this protein has not yet been clearly defined, it may have a role in the stem-like phenotype of CSCs that cause (re-)initiation of tumors as well as their propagation. We hypothesize that CD133 selects for CSC survival against not only immunosurveillance mechanisms but also stress-induced apoptosis. High level of expression of CD133 may be a useful marker of more aggressive tumors that are recalcitrant toward established therapies. Compelling preliminary data indicate that drugs targeting mitochondria may be utilized as a novel, efficient cancer therapeutic modality.
Publisher: Elsevier BV
Date: 10-2019
Publisher: American Chemical Society (ACS)
Date: 29-11-2016
Publisher: American Chemical Society (ACS)
Date: 14-01-2016
Publisher: Elsevier BV
Date: 2021
Publisher: Elsevier BV
Date: 07-2017
Publisher: Trans Tech Publications, Ltd.
Date: 09-2013
DOI: 10.4028/WWW.SCIENTIFIC.NET/AMR.807-809.1347
Abstract: The influencing factors of reaction such as reaction temperature, reaction time and the ratio of liquid to solid are investigated by analyzing the iodine distribution in the semi-hydrate wet process of phosphoric acid. The result shows that with the increase of reaction temperature, reaction time and the ratio of liquid to solid, the iodine distribution in the phases of liquid and solid presents has the tendency of decrease, in the range between 20% and 30%, while the iodine distribution in the gas phase tends to increase, the maximum value is 67.54%.
Location: Australia
Location: China
No related grants have been discovered for Hongqi Wang.