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Exogenous expression of CC3/TIP30 in U373 cells with or without UV treatment

ABSTRACT: The pro-apoptotic protein CC3/TIP30 has an unusual cellular function as an inhibitor of nucleocytoplasmic transport. This function is likely to be activated under conditions of stress. Here we examined the potential role of CC3 in regulation of cellular responses to genotoxic stress. We found that forced expression of CC3 in CC3-negative cells delays repair of both UV-induced and oxidative DNA damage. Exogenously introduced CC3 negatively affects expression levels of DDB2 and p21CIP11 and inhibits induction of c-FOS after UV exposure, which is likely to contribute to the observed delay in DNA damage repair. The increase in nuclear localization of p21CIP11 observed after UV exposure is diminished in cells expressing exogenous CC3. Expression of CC3 also delays repair of oxidative DNA damage and leads to a decrease in levels of nucleoredoxin. Silencing of CC3 in CC3-positive cells has a modest delaying effect on repair of the UV induced damage, but has a much more significant negative affect on the translesion DNA synthesis after UV exposure. This could be related to the higher expression levels and increased nuclear localization of p21CIP11 in cells where expression of CC3 is silenced. Apparently, manipulation of the cellular levels of CC3 adversely affects DNA damage responses by affecting the levels and subcellular localization of relevant proteins.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20633 | GEO | 2010/03/05

SECONDARY ACCESSION(S): PRJNA124849

REPOSITORIES: GEO

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Project description:In the Central Andean region in South America, high-altitude ecosystems (3500-6000 masl) are distributed across Argentina, Chile, Bolivia and Peru, in which poly-extremophilic microbes thrive under extreme environmental conditions. In particular, in the Puna region, total solar irradiation and UV incidence are the highest on Earth, thus, restraining the physiology of individual microorganisms and the composition of microbial communities. UV-resistance of microbial strains thriving in High-Altitude Andean Lakes was demonstrated and their mechanisms were partially characterized by genomic analysis, biochemical and physiological assays. Then, the existence of a network of physiological and molecular mechanisms triggered by ultraviolet light exposure was hypothesized and called "UV-resistome". It includes some or all of the following subsystems: (i) UV sensing and effective response regulators, (ii) UV-avoidance and shielding strategies, (iii) damage tolerance and oxidative stress response, (iv) energy management and metabolic resetting, and (v) DNA damage repair. Genes involved in the described UV-resistome were recently described in the genome of Nesterenkonia sp. Act20, an actinobacterium which showed survival to high UV-B doses as well as efficient photorepairing capability. The aim of this work was to use a proteomic approach together with photoproduct measurements to help dissecting the molecular events involved in the adaptive response of a model High-Altitude Andean Lakes (HAAL) extremophilic actinobacterium, Nesterenkonia sp. Act20, under artificial UV-B radiation. Our results demonstrate that UV-B exposure induced over-abundance of a well-defined set of proteins while recovery treatments restored the proteomic profiles present before the UV-challenge. The proteins involved in this complex molecular network were categorized within the UV-resistome subsystems: damage tolerance and oxidative stress response, energy management and metabolic resetting, and DNA damage repair.

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Exogenous expression of CC3/TIP30 in U373 cells with or without UV treatment

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