TitleOverexpression of CHMP6 Induces Cellular Oncosis and Apoptosis in HeLa Cells
AuthorsFu, Dongxu
Tian, Linjie
Peng, Zhi
Deng, Weiwei
Yuan, Jinsong
Ma, Dalong
Shi, Taiping
Li, Dianjun
Wang, Ying
AffiliationChinese Natl Human Genome Ctr, Beijing 100176, Peoples R China.
Harbin Med Univ, Sch Basic Med Sci, Lab Med Immunol, Harbin 150081, Peoples R China.
Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Lab Med Immunol, Beijing 100083, Peoples R China.
Peking Univ, Ctr Human Dis Genom, Beijing 100083, Peoples R China.
Chinese Natl Human Genome Ctr, 3-707 N YongChang Rd BDA, Beijing 100176, Peoples R China.
Keywordschromatin modifying protein 6 (CHMP6)
oncosis
apoptosis
transmission electron microscopy
ATP determination
MITOCHONDRIAL DYSFUNCTION
TRANSFERRIN RECEPTOR
DEATH
NECROSIS
PROTEIN
PHOSPHATIDYLSERINE
FORM
ACTIVATION
EXPOSURE
TRIGGERS
Issue Date2009
Publisherbioscience biotechnology and biochemistry
CitationBIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY.2009,73,(3),494-501.
AbstractCell death can proceed via at least two distinct pathways, apoptosis and oncosis. Apoptosis is an energy-dependent process characterized morphologically by cell shrinkage, whereas oncosis is defined as a prelethal pathway leading to cell death associated with cellular swelling, organelle swelling, and increased membrane permeability. In this study, we found that overexpression of chromatin modifying protein 6 (CHMP6) induced cell death by a series of experiments, including morphological observation, intracellular ATP determination, caspase-3 activity, and flow cytometry. Typical morphological characteristics consistent with oncosis were observed by transmission electron microscopy. Simultaneously, we obtained some results that indicated apoptosis, but the anti-apoptotic gene Bcl-xL and caspase family inhibitor Z-VAD-FMK had little effect on CHMP6-induced cell death. These results suggest that CHMP6 overexpression can cause cell death, predominantly via oncosis and to a certain extent via apoptosis, and that CHMP6 might be a novel regulator involved in both oncosis and apoptosis.
URIhttp://hdl.handle.net/20.500.11897/246453
ISSN0916-8451
DOI10.1271/bbb.80458
IndexedSCI(E)
EI
Appears in Collections:基础医学院

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