A critical role for AKT activation in protecting cells from ionizing radiation-induced apoptosis and the regulation of acinus gene expression

Park, Hyung Sun; Yun, Yunha; Kim, Cha Soon; Yang, Kwang Hee; Jeong, Mi‐Ae; Ahn, Sung Kwan; Jin, Young-Woo; Nam, Sang Yong

doi:10.1016/j.ejcb.2009.05.004

Cited by 14 publications

(15 citation statements)

References 35 publications

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“…We previously reported that AKT is potently activated in response to ionizing radiation and regulates ionizing radiationinduced apoptosis (20). To identify whether ionizing radiationinduced AKT activation is related to CLK2 phosphorylation, we measured CLK2 phosphorylation after irradiation.…”

Section: Discussionmentioning

confidence: 99%

“…Associated with AKT Activation-We previously reported that ionizing radiation induces AKT activation and peaks 4 h postirradiation (20). We first sought to determine whether ionizing radiation induces CLK2 phosphorylation in normal human lung fibroblast CCD-18Lu cells.…”

Section: Clk2 Phosphorylation In Response To Ionizing Radiation Ismentioning

confidence: 99%

“…Ionizing radiation regulates cell survival by activating a variety of signaling cascades, including the phosphatidylinositol 3-kinase (PI3K)/AKT pathway. Our previous study showed that the activation of AKT is associated with cell protection against ionizing radiation-induced apoptosis (20). AKT directly phosphorylates acinus and regulates its expression via the nuclear factor B pathway, thereby controlling cell survival to ionizing radiation (20,21).…”

mentioning

confidence: 99%

“…Our previous study showed that the activation of AKT is associated with cell protection against ionizing radiation-induced apoptosis (20). AKT directly phosphorylates acinus and regulates its expression via the nuclear factor B pathway, thereby controlling cell survival to ionizing radiation (20,21). AKT control of diverse cellular responses may be dependent on the regulation of downstream substrates.…”

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confidence: 99%

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Phosphorylation of CLK2 at Serine 34 and Threonine 127 by AKT Controls Cell Survival after Ionizing Radiation

Nam

Seo

Park

et al. 2010

Journal of Biological Chemistry

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AKT phosphorylates components of the intrinsic cell survival machinery and promotes survival to various stimuli. In the present study, we identified CDC-like kinase 2 (CLK2) as a new substrate of AKT activation and elucidated its role in cell survival to ionizing radiation. AKT directly binds to and phosphorylates CLK2 on serine 34 and threonine 127, in vitro and in vivo. CLK2 phosphorylation was detected in HeLa cells overexpressing active AKT. In addition, we demonstrated that ionizing radiation induces CLK2 phosphorylation via AKT activation. In contrast, the suppression of endogenous AKT expression by siRNA inhibited CLK2 phosphorylation in response to 2 gray of ␥-ray or insulin. Furthermore, we examined the effect of CLK2 on the survival of irradiated CCD-18Lu cells overexpressing Myc-CLK2. CLK2 overexpression significantly increased cell growth and inhibited cell death induced by 2 gray. The role of CLK2 in cell survival to ionizing radiation was dependent on the phosphorylation of serine 34 and threonine 127. Our results suggest that AKT activation controls cell survival to ionizing radiation by phosphorylating CLK2, revealing an important regulatory mechanism required for promoting cell survival.

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Section: Discussionmentioning

confidence: 99%

Section: Clk2 Phosphorylation In Response To Ionizing Radiation Ismentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Phosphorylation of CLK2 at Serine 34 and Threonine 127 by AKT Controls Cell Survival after Ionizing Radiation

Nam

Seo

Park

et al. 2010

Journal of Biological Chemistry

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“…It was previously shown that ionizing radiation enhances cell protection through the activation of the AKT (protein kinase B, PKB) pathway (Park et al 2009). Th e serine/ threonine kinase AKT is a critical regulator of major cellular responses, including cell growth, glycogen metabolism, and cells proliferation (Bellacosa et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Chronic low-dose radiation inhibits the cells death by cytotoxic high-dose radiation increasing the level of AKT and acinus proteins via NF-κB activation

Park¹,

Seong²,

Kim³

et al. 2013

International Journal of Radiation Biology

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RETRACTED ARTICLE: TCRP1 promotes radioresistance of oral squamous cell carcinoma cells via Akt signal pathway

Fan

Liu

et al. 2011

Mol Cell Biochem

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Tongue cancer resistance-associated protein 1 (TCRP1) is a novel gene located on human chromosome 11q13.4 which has been reported as a candidate related to chemotherapeutic resistance to cisplatin. Results suggest that TCRP also contribute to radioresistance in oral squamous cell carcinoma (OSCC) cells. We previously established exogenous overexpression of TCRP1 cell line Tca8113/TCRP1 and TCRP1 knockdown cell line Tca8113/PYM-siRNA and paired control cell lines, which provides a cell model system to investigate the roles and mechanisms of TCRP1-mediated radioresponse in OSCC. In this study, we first compared the radiosensitivity of up/down-regulating expression of TCRP1 cell lines and paired control cell lines by a clonogenic survival assay, Hoechst 33258 staining, cell growth assay, and comet assay. The results indicated that TCRP1 played a significant role in mediating OSCC radioresistance through decreased cells apoptosis and increased cellular proliferation and long-term survival. The further study found that TCRP1 function by up-regulating Akt activity and levels and then elevating the level of NF-κB. In summary, these results provided strong evidence for the linkage between TCRP1 and radiation sensitivity and may provide theoretical base of TCRP1 as a potential molecular mark of estimating the response for irradiation in OSCC.

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A critical role for AKT activation in protecting cells from ionizing radiation-induced apoptosis and the regulation of acinus gene expression

Cited by 14 publications

References 35 publications

Phosphorylation of CLK2 at Serine 34 and Threonine 127 by AKT Controls Cell Survival after Ionizing Radiation

Phosphorylation of CLK2 at Serine 34 and Threonine 127 by AKT Controls Cell Survival after Ionizing Radiation

Chronic low-dose radiation inhibits the cells death by cytotoxic high-dose radiation increasing the level of AKT and acinus proteins via NF-κB activation

RETRACTED ARTICLE: TCRP1 promotes radioresistance of oral squamous cell carcinoma cells via Akt signal pathway

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