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miRNA-302b Suppresses Human Hepatocellular Carcinoma by Targeting AKT2 SCIE PubMed Scopus
期刊论文 | 2014 , 12 (2) , 190-202 | MOLECULAR CANCER RESEARCH | IF: 4.38
WoS CC Cited Count: 27
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Abstract :

miRNAs (miR) play a critical role in human cancers, including hepatocellular carcinoma. Although miR-302b has been suggested to function as a tumor repressor in other cancers, its role in hepatocellular carcinoma is unknown. This study investigated the expression and functional role of miR-302b in human hepatocellular carcinoma. The expression level of miR-302b is dramatically decreased in clinical hepatocellular carcinoma specimens, as compared with their respective nonneoplastic counterparts, and in hepatocellular carcinoma cell lines. Overexpression of miR-302b suppressed hepatocellular carcinoma cell proliferation and G(1)-S transition in vitro, whereas inhibition of miR-302b promoted hepatocellular carcinoma cell proliferation and G(1)-S transition. Using a luciferase reporter assay, AKT2 was determined to be a direct target of miR-302b. Subsequent investigation revealed that miR-302b expression was inversely correlated with AKT2 expression in hepatocellular carcinoma tissue samples. Importantly, silencing AKT2 recapitulated the cellular and molecular effects seen upon miR-302b overexpression, which included inhibiting hepatocellular carcinoma cell proliferation, suppressing G(1) regulators (Cyclin A, Cyclin D1, CDK2) and increasing p27Kip1 phosphorylation at Ser10. Restoration of AKT2 counteracted the effects of miR-302b expression. Moreover, miR-302b was able to repress tumor growth of hepatocellular carcinoma cells in vivo. (C) 2013 AACR.

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GB/T 7714 Wang, Lumin , Yao, Jiayi , Zhang, Xiaogang et al. miRNA-302b Suppresses Human Hepatocellular Carcinoma by Targeting AKT2 [J]. | MOLECULAR CANCER RESEARCH , 2014 , 12 (2) : 190-202 .
MLA Wang, Lumin et al. "miRNA-302b Suppresses Human Hepatocellular Carcinoma by Targeting AKT2" . | MOLECULAR CANCER RESEARCH 12 . 2 (2014) : 190-202 .
APA Wang, Lumin , Yao, Jiayi , Zhang, Xiaogang , Guo, Bo , Le, Xiaofeng , Cubberly, Mark et al. miRNA-302b Suppresses Human Hepatocellular Carcinoma by Targeting AKT2 . | MOLECULAR CANCER RESEARCH , 2014 , 12 (2) , 190-202 .
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miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a SCIE PubMed Scopus
期刊论文 | 2014 , 12 (3) , 313-321 | MOLECULAR CANCER RESEARCH | IF: 4.38
WoS CC Cited Count: 51
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Abstract :

Results from recent studies suggest that aberrant microRNA expression is common in numerous cancers. Although miR-338-3p has been implicated in hepatocellular carcinoma, its role in gastric cancer is unknown. To this end, we report that miR-338-3p is downregulated in both gastric cancer tissue and cell lines. Forced expression of miR-338-3p inhibited cell proliferation and clonogenicity and induced a G(1)-S arrest as well as apoptosis in gastric cancer cells. Furthermore, P-Rex2a (PREX2) was identified as a direct target of miR-338-3p, and silencing P-Rex2a resulted in the same biologic effects of miR-338-3p expression in gastric cancer cells. Furthermore, both enforced expression of miR-338-3p or silencing of P-Rex2a resulted in activation of PTEN, leading to a decline in AKT phosphorylation. Also, miR-338-3p markedly inhibited the in vivo tumorigenicity in a nude mouse xenograft model system. These results demonstrate that miR-338-3p affects gastric cancer progression through PTEN-AKT signaling by targeting P-Rex2a in gastric cancer cells, which posits miR-338-3p as a novel strategy for gastric cancer treatment. (C)2013 AACR.

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GB/T 7714 Guo, Bo , Liu, Liying , Yao, Jiayi et al. miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a [J]. | MOLECULAR CANCER RESEARCH , 2014 , 12 (3) : 313-321 .
MLA Guo, Bo et al. "miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a" . | MOLECULAR CANCER RESEARCH 12 . 3 (2014) : 313-321 .
APA Guo, Bo , Liu, Liying , Yao, Jiayi , Ma, Ruili , Chang, Dongmin , Li, Zongfang et al. miR-338-3p Suppresses Gastric Cancer Progression through a PTEN-AKT Axis by Targeting P-REX2a . | MOLECULAR CANCER RESEARCH , 2014 , 12 (3) , 313-321 .
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Epigenetic Mechanism Involved in the HBV/HCV-Related Hepatocellular Carcinoma Tumorigenesis SCIE Scopus
期刊论文 | 2014 , 20 (11) , 1715-1725 | CURRENT PHARMACEUTICAL DESIGN | IF: 3.452
WoS CC Cited Count: 27
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Abstract :

Hepatitis B virus (HBV) and hepatitis C virus (HCV) infection were known to be risk factors for HCC, they were suspected to promote its development by eliciting epigenetic changes. However, the precise gene targets and underlying mechanisms have not been elucidated. Epigenetic regulation of gene expression has emerged as a fundamental aspect of cancer development and progression. The molecular mechanisms of carcinogenesis in hepatocellular carcinoma involve a complex interplay of both genetic and epigenetic factors. DNA methylation, post-translational modifications of histone proteins, chromatin remodeling, and noncoding RNAs are four major types of mechanistic layers in the field of epigenetics. HBV infection could affect methylation on p16(INK4A), GSTP1, CDH1(E-cadherin), RASSF1A, p21(WAF1/CIP1) genes, which may play important roles in the development of HCC. HCV infection was related to aberrant methylation on SOCS-1, Gadd45 beta, MGMT, STAT1 and APC. Other epigenetic alterations included histone proteins, chromatin remodeling, and noncoding RNAs were described in literature. Uncovering the epigenetic alterations of HBV/HCV-induced HCC carcinogenesis could highlight a new strategy for deciphering the mechanism of HCC tumorigenesis and development, as well as a potential diagnostic advantage.

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HBV HCV Epigenetic hepatocellular carcinoma DNA methylation and histone modification

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GB/T 7714 Liang Rongrui , Huang Na , Li Zongfang et al. Epigenetic Mechanism Involved in the HBV/HCV-Related Hepatocellular Carcinoma Tumorigenesis [J]. | CURRENT PHARMACEUTICAL DESIGN , 2014 , 20 (11) : 1715-1725 .
MLA Liang Rongrui et al. "Epigenetic Mechanism Involved in the HBV/HCV-Related Hepatocellular Carcinoma Tumorigenesis" . | CURRENT PHARMACEUTICAL DESIGN 20 . 11 (2014) : 1715-1725 .
APA Liang Rongrui , Huang Na , Li Zongfang , Ji Fanpu , Jiang Shiwen . Epigenetic Mechanism Involved in the HBV/HCV-Related Hepatocellular Carcinoma Tumorigenesis . | CURRENT PHARMACEUTICAL DESIGN , 2014 , 20 (11) , 1715-1725 .
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Baicalein induces apoptosis via a mitochondrial-dependent caspase activation pathway in T24 bladder cancer cells SCIE PubMed Scopus
期刊论文 | 2013 , 7 (1) , 266-270 | MOLECULAR MEDICINE REPORTS | IF: 1.484
WoS CC Cited Count: 24
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Abstract :

Recurrence of bladder cancer following transurethral resection of bladder tumor (TURBt) is an obstacle in clinical management. In the current study, we investigated the antitumor activity of baicalein, a Chinese herbal medicine, against T24 bladder cancer cells in vitro. Baicalein inhibited growth and caused G1/S arrest of the cell cycle in the T24 cells. Moreover, baicalein induced apoptosis via loss of mitochondrial transmembrane potential (Delta Psi m), release of cytochrome c and activation of caspase-9 and caspase-3. Baicalein inhibited Akt phosphorylation, downregulated Bcl-2 expression and upregulated Bax expression, which in turn increased the ratio of Bax/Bcl-2. Our results demonstrate that baicalein repressed growth inhibition and induced apoptosis via loss of Delta Psi m and activation of caspase-9 and caspase-3 in T24 bladder cancer cells, which indicates that baicalein may be an effective agent in the clinical management of bladder cancer.

Keyword :

bladder cancer apoptosis Bcl-2 baicalein Akt

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GB/T 7714 Li, Hong-Liang , Zhang, Shu , Wang, Yuan et al. Baicalein induces apoptosis via a mitochondrial-dependent caspase activation pathway in T24 bladder cancer cells [J]. | MOLECULAR MEDICINE REPORTS , 2013 , 7 (1) : 266-270 .
MLA Li, Hong-Liang et al. "Baicalein induces apoptosis via a mitochondrial-dependent caspase activation pathway in T24 bladder cancer cells" . | MOLECULAR MEDICINE REPORTS 7 . 1 (2013) : 266-270 .
APA Li, Hong-Liang , Zhang, Shu , Wang, Yuan , Liang, Rong-Rui , Li, Jun , An, Peng et al. Baicalein induces apoptosis via a mitochondrial-dependent caspase activation pathway in T24 bladder cancer cells . | MOLECULAR MEDICINE REPORTS , 2013 , 7 (1) , 266-270 .
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Preferential inhibition of hepatocellular carcinoma by the flavonoid Baicalein through blocking MEK-ERK signaling SCIE PubMed Scopus
期刊论文 | 2012 , 41 (3) , 969-978 | INTERNATIONAL JOURNAL OF ONCOLOGY | IF: 2.657
WoS CC Cited Count: 34
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Abstract :

Baicalein is a purified flavonoid extracted from the roots of Scutellaria baicalensis or Scutellaria radix. Although previous studies have suggested that Baicalein possesses an in vitro anti-hepatocellular carcinoma activity, its in vivo effects and mechanisms of action are still not completely understood. In this study, Baicalein at concentrations of 40-120 mu M exhibited significant cytotoxicity to three hepatocellular carcinoma (HCC) cell lines but marginal cytotoxicity to a normal liver cell line in vitro. Compared to a standard chemotherapy drug, 5-fluorouracil (5-FU), Baicalein had greater effect on HCC cells but less toxicity on normal liver cells. Treatment with Baicalein dramatically reduced mitochondrial transmembrane potential, and activated caspase-9 and caspase-3. Blockade of Baicalein-induced apoptosis with a pan-caspase inhibitor partially attenuated Baicalein-induced growth inhibition in HCC. Baicalein treatment significantly inhibited tumor growth of HCC xenografts in mice. Induction of apoptosis was demonstrated in Baicalein-treated xenograft tumors by the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Furthermore, Baicalein treatment dramatically decreased the levels of phosphorylation of MEK1, ERK1/2 and Bad in vitro and in vivo. Overexpression of human MEK1 partially blocked Baicalein-induced growth inhibition. Consequently, these findings suggest that Baicalein preferentially inhibits HCC tumor growth through inhibition of MEK-ERK signaling and by inducing intrinsic apoptosis.

Keyword :

apoptosis hepatocellular carcinoma Baicalein MEK ERK

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GB/T 7714 Liang, Rong-Rui , Zhang, Shu , Qi, Jun-An et al. Preferential inhibition of hepatocellular carcinoma by the flavonoid Baicalein through blocking MEK-ERK signaling [J]. | INTERNATIONAL JOURNAL OF ONCOLOGY , 2012 , 41 (3) : 969-978 .
MLA Liang, Rong-Rui et al. "Preferential inhibition of hepatocellular carcinoma by the flavonoid Baicalein through blocking MEK-ERK signaling" . | INTERNATIONAL JOURNAL OF ONCOLOGY 41 . 3 (2012) : 969-978 .
APA Liang, Rong-Rui , Zhang, Shu , Qi, Jun-An , Wang, Zhi-Dong , Li, Jun , Liu, Pei-Jun et al. Preferential inhibition of hepatocellular carcinoma by the flavonoid Baicalein through blocking MEK-ERK signaling . | INTERNATIONAL JOURNAL OF ONCOLOGY , 2012 , 41 (3) , 969-978 .
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