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Jingping Yun - One of the best experts on this subject based on the ideXlab platform.
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abstract 3547 foxd3 regulated microrna 137 suppresses tumour growth and metastasis in human hepatocellular carcinoma by targeting akt2
Cancer Research, 2014Co-Authors: Lili Liu, Chris Zhiyi Zhang, Jingping YunAbstract:Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA Background and Aims: microRNAs, which are frequently deregulated in human cancer, have been implicated in the progression of hepatocarcinogenesis. Our study aims to investigate the role of Mir-137 in cell proliferation and metastasis of hepatocellular carcinoma and the underlying molecular mechanisms. Methods: Real-time PCR and western blot were used to examine the expressions of Mir-137, Akt2 and FoxD3 in HCC tissues and cells. The in vitro and in vivo effects of Mir-137 were determined. Luciferase reporter assay was conducted to confirm the association of Mir-137 and AKT2. CHIP assay was performed to test the regulation of Mir-137 by FoxD3. Results: We show that microRNA (miR)-137 is significantly down-regulated in hepatocellular carcinoma (HCC), and its decreased expression is associated with vein invasion, incomplete Involucrum, and tumour metastasis. Multivariate analysis suggests that Mir-137 is an independent indicator for poor survival. To determine its role in HCC development, we showed that overexpression of Mir-137 suppresses cell proliferation, invasion and metastasis in vitro. Conversely, Mir-137 inhibition promoted HCC cell growth. We also identified AKT2 as a key target of Mir-137 in this context. Statistical data revealed a reverse correlation of AKT2 and Mir-137 expression in HCC patients. Silencing of AKT2 phenotypically copied Mir-137-induced phenotypes, whereas re-expression of AKT2 reversed the suppressive effects of Mir-137. Further investigation showed that Mir-137 exerted its anti-tumour activity via inhibiting the AKT2/mTOR pathway. Moreover, we demonstrated that FoxD3 binds to the promoter of Mir-137 and activates its transcription. In vivo studies confirmed that FoxD3-regulated Mir-137 inhibition of HCC growth and metastasis via directly targeting AKT2. Conclusions: Our findings indicated that Mir-137 is a valuable biomarker for HCC prognosis and demonstrated that the FoxD3/Mir-137/AKT2 regulatory network plays an important role in HCC progression. Citation Format: Li-Li Liu, Shi-Xun Lu, Min Li, Jia Fu, Chris Zhiyi Zhang, Jing-Ping Yun. FoxD3-regulated microRNA-137 suppresses tumour growth and metastasis in human hepatocellular carcinoma by targeting AKT2. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3547. doi:10.1158/1538-7445.AM2014-3547
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foxd3 regulated microrna 137 suppresses tumour growth and metastasis in human hepatocellular carcinoma by targeting akt2
Oncotarget, 2014Co-Authors: Lili Liu, Chris Zhiyi Zhang, Yuan Zhong Yang, Rong Zhen Luo, Jingping YunAbstract:// Li-Li Liu 1,2,* , Shi-Xun Lu 1,2,* , Min Li 1,2 , Lin-Zi Li 1,2 , Jia Fu 1,2 , Wen Hu 1,2 , Yuan-Zhong Yang 1,2 , Rong-Zhen Luo 1,2 , Chris Zhiyi Zhang 1,2 , Jing-Ping Yun 1,2 1 Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine 2 Department of Pathology, Sun Yat-sen University Cancer Center * These authors contributed equally to this work Correspondence: Chris Zhiyi Zhang, email: // Jing-Ping Yun, email: // Keywords : Mir-137; AKT2; FoxD3; metastasis; HCC Received : May 3, 2014 Accepted : June 9, 2014 Published : June 10, 2014 Abstract microRNAs, frequently deregulated in human cancer, have been implicated in the progression of hepatocarcinogenesis. Here, we show that microRNA (miR)-137 is significantly down-regulated in hepatocellular carcinoma (HCC). Its decreased expression is associated with vein invasion, incomplete involucrum, and distant metastasis. Multivariate analysis suggests that Mir-137 is an independent indicator for poor survival. We next show that over-expression of Mir-137 suppresses cell proliferation, migration and invasion in vitro . Conversely, Mir-137 inhibition promotes HCC cell growth. We also identify AKT2 as a key target of Mir-137 in this context. Statistical data reveal a reverse correlation of AKT2 and Mir-137 expression in HCC patients. Silencing of AKT2 phenotypically copied Mir-137-induced phenotypes, whereas re-expression of AKT2 reversed the suppressive effects of Mir-137. Further investigations showed that Mir-137 exerted its anti-tumour activity via inhibiting the AKT2/mTOR pathway. Moreover, we demonstrate that FoxD3 directly binds to the promoter of Mir-137 and activates its transcription. In vivo studies confirm that FoxD3-regulated Mir-137 inhibited HCC growth and metastasis via targeting AKT2. Together, our findings indicate that Mir-137 is a valuable biomarker for HCC prognosis and the FoxD3/Mir-137/AKT2 regulatory network plays an important role in HCC progression.
Lili Liu - One of the best experts on this subject based on the ideXlab platform.
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abstract 3547 foxd3 regulated microrna 137 suppresses tumour growth and metastasis in human hepatocellular carcinoma by targeting akt2
Cancer Research, 2014Co-Authors: Lili Liu, Chris Zhiyi Zhang, Jingping YunAbstract:Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA Background and Aims: microRNAs, which are frequently deregulated in human cancer, have been implicated in the progression of hepatocarcinogenesis. Our study aims to investigate the role of Mir-137 in cell proliferation and metastasis of hepatocellular carcinoma and the underlying molecular mechanisms. Methods: Real-time PCR and western blot were used to examine the expressions of Mir-137, Akt2 and FoxD3 in HCC tissues and cells. The in vitro and in vivo effects of Mir-137 were determined. Luciferase reporter assay was conducted to confirm the association of Mir-137 and AKT2. CHIP assay was performed to test the regulation of Mir-137 by FoxD3. Results: We show that microRNA (miR)-137 is significantly down-regulated in hepatocellular carcinoma (HCC), and its decreased expression is associated with vein invasion, incomplete Involucrum, and tumour metastasis. Multivariate analysis suggests that Mir-137 is an independent indicator for poor survival. To determine its role in HCC development, we showed that overexpression of Mir-137 suppresses cell proliferation, invasion and metastasis in vitro. Conversely, Mir-137 inhibition promoted HCC cell growth. We also identified AKT2 as a key target of Mir-137 in this context. Statistical data revealed a reverse correlation of AKT2 and Mir-137 expression in HCC patients. Silencing of AKT2 phenotypically copied Mir-137-induced phenotypes, whereas re-expression of AKT2 reversed the suppressive effects of Mir-137. Further investigation showed that Mir-137 exerted its anti-tumour activity via inhibiting the AKT2/mTOR pathway. Moreover, we demonstrated that FoxD3 binds to the promoter of Mir-137 and activates its transcription. In vivo studies confirmed that FoxD3-regulated Mir-137 inhibition of HCC growth and metastasis via directly targeting AKT2. Conclusions: Our findings indicated that Mir-137 is a valuable biomarker for HCC prognosis and demonstrated that the FoxD3/Mir-137/AKT2 regulatory network plays an important role in HCC progression. Citation Format: Li-Li Liu, Shi-Xun Lu, Min Li, Jia Fu, Chris Zhiyi Zhang, Jing-Ping Yun. FoxD3-regulated microRNA-137 suppresses tumour growth and metastasis in human hepatocellular carcinoma by targeting AKT2. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3547. doi:10.1158/1538-7445.AM2014-3547
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foxd3 regulated microrna 137 suppresses tumour growth and metastasis in human hepatocellular carcinoma by targeting akt2
Oncotarget, 2014Co-Authors: Lili Liu, Chris Zhiyi Zhang, Yuan Zhong Yang, Rong Zhen Luo, Jingping YunAbstract:// Li-Li Liu 1,2,* , Shi-Xun Lu 1,2,* , Min Li 1,2 , Lin-Zi Li 1,2 , Jia Fu 1,2 , Wen Hu 1,2 , Yuan-Zhong Yang 1,2 , Rong-Zhen Luo 1,2 , Chris Zhiyi Zhang 1,2 , Jing-Ping Yun 1,2 1 Sun Yat-sen University Cancer Center; State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine 2 Department of Pathology, Sun Yat-sen University Cancer Center * These authors contributed equally to this work Correspondence: Chris Zhiyi Zhang, email: // Jing-Ping Yun, email: // Keywords : Mir-137; AKT2; FoxD3; metastasis; HCC Received : May 3, 2014 Accepted : June 9, 2014 Published : June 10, 2014 Abstract microRNAs, frequently deregulated in human cancer, have been implicated in the progression of hepatocarcinogenesis. Here, we show that microRNA (miR)-137 is significantly down-regulated in hepatocellular carcinoma (HCC). Its decreased expression is associated with vein invasion, incomplete involucrum, and distant metastasis. Multivariate analysis suggests that Mir-137 is an independent indicator for poor survival. We next show that over-expression of Mir-137 suppresses cell proliferation, migration and invasion in vitro . Conversely, Mir-137 inhibition promotes HCC cell growth. We also identify AKT2 as a key target of Mir-137 in this context. Statistical data reveal a reverse correlation of AKT2 and Mir-137 expression in HCC patients. Silencing of AKT2 phenotypically copied Mir-137-induced phenotypes, whereas re-expression of AKT2 reversed the suppressive effects of Mir-137. Further investigations showed that Mir-137 exerted its anti-tumour activity via inhibiting the AKT2/mTOR pathway. Moreover, we demonstrate that FoxD3 directly binds to the promoter of Mir-137 and activates its transcription. In vivo studies confirm that FoxD3-regulated Mir-137 inhibited HCC growth and metastasis via targeting AKT2. Together, our findings indicate that Mir-137 is a valuable biomarker for HCC prognosis and the FoxD3/Mir-137/AKT2 regulatory network plays an important role in HCC progression.
N T Phan - One of the best experts on this subject based on the ideXlab platform.
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atmospheric radionuclides from the fukushima dai ichi nuclear reactor accident observed in vietnam
Journal of Environmental Radioactivity, 2012Co-Authors: N Q Long, Y Truong, P D Hien, N T Binh, L N Sieu, T V Giap, N T PhanAbstract:Abstract Radionuclides from the reactor accident at the Fukushima Dai-ichi Nuclear Power Plant were observed in the surface air at stations in Hanoi, Dalat, and Ho Chi Minh City (HCMC) in Vietnam, about 4500 km southwest of Japan, during the period from March 27 to April 22, 2011. The maximum activity concentrations in the air measured at those three sites were 193, 33, and 37 μBq m −3 for 131 I, 13 4 Cs, and 13 7 Cs, respectively. Peaks of radionuclide concentrations in the air corresponded to arrival of the air mass from Fukushima to Vietnam after traveling for 8 d over the Pacific Ocean. Cesium-134 was detected with the 134 Cs/ 137 Cs activity ratio of about 0.85 in line with observations made elsewhere. The 131 I/ 137 Cs activity ratio was observed to decrease exponentially with time as expected from radioactive decay. The ratio at Dalat, where is 1500 m high, was higher than those at Hanoi and HCMC in low lands, indicating the relative enrichment of the iodine in comparison to cesium at high altitudes. The time-integrated surface air concentrations of the Fukushima-derived radionuclides in the Southeast Asia showed exponential decrease with distance from Fukushima.
H Yokoyama - One of the best experts on this subject based on the ideXlab platform.
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atmospheric radionuclides transported to fukuoka japan remote from the fukushima dai ichi nuclear power complex following the nuclear accident
Journal of Environmental Radioactivity, 2012Co-Authors: Noriyuki Momoshima, Shinji Sugihara, R Ichikawa, H YokoyamaAbstract:Abstract Radionuclides were detected from the Fukushima nuclear accident at Fukuoka, Japan, 1000 km west of the Fukushima Dai-ichi nuclear power complex. Iodine-131 was first detected 3 d after the accident, indicating that it was probably transported dispersively because of local meteorological conditions, and not global air circulation. The maximum concentrations, 5.07 mBq m −3 for 131 I, 4.04 mBq m −3 for 134 Cs, and 4.12 mBq m −3 for 137 Cs, were recorded in particles collected on April 6, 2011. However, these concentration levels decreased below the detection limit by April 26, 2011. Gaseous 131 I accounted for 30%–67% of the total 131 I content. The increase in dose by inhalation was negligible at Fukuoka.
Mark R D Seaward - One of the best experts on this subject based on the ideXlab platform.
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137cs concentrations in foliose lichens within tsukuba city as a reflection of radioactive fallout from the fukushima dai ichi nuclear power plant accident
Journal of Environmental Radioactivity, 2015Co-Authors: Yoshihito Ohmura, Kimiyo Matsukura, Kentaro Hosaka, Masanori Tamaoki, Terumi Dohi, Makoto Kakishima, Mark R D SeawardAbstract:Abstract 137 Cs concentrations in ten species of foliose lichens collected within Tsukuba-city in August 2013 ranged from 1.7 to 35 kBq/kg. The relationships between 137 Cs in two dominant species, Dirinaria applanata and Physcia orientalis , and the air dose rate (μSv/h) at the sampling sites were investigated. 137 Cs in P. orientalis measured about 1 year after the Fukushima nuclear accident was correlated ( r 2 = 0.80) more closely with the air dose rate than those measured after about 2 years ( r 2 = 0.65), possibly demonstrating its continued value as a biomonitor to reflect ambient fall-out levels. In contrast, those of Dirinaria applanata were not correlated with the air dose rate in either year.