Modulation of Orphan Nuclear Receptor Nur77-Mediated Apoptotic Pathway by Acetylshikonin and Analogues

Liu, Jie; Zhou, Wen; Li, Shaoshun; Sun, Zhe; Lin, Bingzhen; Lang, Yuanyuan; He, Jia‐You; Cao, Xihua; Yan, Tingdong; Wang, Li; Lu, Jiongming; Han, Young‐Hoon; Cao, Yu; Zhang, Xiaokun; Zeng, Jin-Zhang

doi:10.1158/0008-5472.can-08-1972

Cited by 69 publications

(56 citation statements)

References 31 publications

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“…Generally, tumorigenesis and tumor progression are strongly associated with abnormal apoptosis. It has been shown that shikonin and its derivatives induce apoptosis of tumor cells [16,19,20] . Our data demonstrate that acetylshikonin could also induce apoptosis of SGC-7901 cells with typical apoptotic alterations, including morphological changes and positive TUNEL assay, DNA fragmentation and apoptotic Apoptosis is a complex process regulated by a variety of factors [21,22] .…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 in vitro and in vivo

Zeng¹,

Liu²,

Zhou³

2009

WJG

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AIM:To investigate the inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS:MTT assay was used to assess the inhibitory effect of acetylshikonin on proliferation o f S G C-7 9 0 1 c e l l s . A p o p t o s i s -i n d u c i n g e f f e c t was determined by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling with Hoechst staining. Expression of mRNA and protein in Bcl-2 and Bax was analyzed by reverse transcription-polymerase chain reaction and Western blot. Antitumor effect of acetylshikonin on a mouse SGC-7901 model was also determined. RESULTS:

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Section: Discussionmentioning

confidence: 99%

Inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 in vitro and in vivo

Zeng¹,

Liu²,

Zhou³

2009

WJG

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“…Total proteins were prepared with a modified radioimmunoprecipitation assay buffer (33). Cytoplasmic proteins were purified with Buffer A [10 mmol/L HEPES-KOH (pH 7.9), 1.5 mmol/L MgCl 2 , 10 mmol/L KCl, and 0.5 mmol/L DTT], whereas nuclear proteins were prepared by resuspending the pellets in high-salt Buffer C [20 mmol/L HEPES-KOH (pH 7.9), 25% glycerol, 420 mmol/L NaCl, 1.…”

Section: Methodsmentioning

confidence: 99%

Oncogenic Potential of Retinoic Acid Receptor-γ in Hepatocellular Carcinoma

Yan

Zhang

et al. 2010

Cancer Research

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Retinoic acid receptors (RAR; α, β, and γ), members of the nuclear receptor superfamily, mediate the pleiotropic effects of the vitamin A metabolite retinoic acid (RA) and derivatives (retinoids) in normal and cancer cells. Abnormal expression and function of RARs are often involved in the growth and development of cancer. However, the underlying molecular mechanisms remain largely elusive. Here, we report that levels of RARγ were significantly elevated in tumor tissues from a majority of human hepatocellular carcinoma (HCC) and in HCC cell lines. Overexpression of RARγ promoted colony formation by HCC cells in vitro and the growth of HCC xenografts in animals. In HepG2 cells, transfection of RARγ enhanced, whereas downregulation of RARγ expression by siRNA approach impaired, the effect of RA on inducing the expression of α-fetoprotein, a protein marker of hepatocarcinogenesis. In studying the possible mechanism by which overexpression of RARγ contributed to liver cancer cell growth and transformation, we observed that RARγ resided mainly in the cytoplasm of HCC cells, interacting with the p85α regulatory subunit of phosphatidylinositol 3-kinase (PI3K). The interaction between RARγ and p85α resulted in activation of Akt and NF-κB, critical regulators of the growth and survival of cancer cells. Together, our results show that overexpression of RARγ plays a role in the growth of HCC cells through nongenomic activation of the PI3K/Akt and NF-κB signaling pathways. Cancer Res; 70(6); 2285-95. ©2010 AACR.

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“…NGFI-B, an orphan member of the steroid/thyroid/ retinoid receptor superfamily of transcription factors in the nucleus (Liu et al 2008;Hamid et al 2008;Liang et al 2007;Eells et al 2000), plays an important role in cell proliferation and apoptosis (Kolluri et al 2008;Tao and Hancock 2008;Winoto 1997;Wilson et al 1991a, b). Recent investigation indicates that in cells treated with apoptosis inducers, NGFI-B translocates from nucleus to cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

NGFI-B targets mitochondria and induces cardiomyocyte apoptosis in restraint-stressed rats by mediating energy metabolism disorder

Wang¹,

Liu²,

Kong³

et al. 2009

Cell Stress and Chaperones

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NGFI-B/Nur77/TR3, originally identified as an immediate-early gene rapidly induced by serum and growth factors, is a member of the steroid hormone nuclear receptor superfamily with no identified endogenous ligand. NGFI-B induces apoptosis in a number of cell lineages exposed to proapoptotic stimuli by directly targeting the mitochondria, inducing cytochrome c release. The present study was designed to determine the role of NGFI-B in cardiomyocytes of restraintstressed rats. The NGFI-B content was increased in mitochondria and reduced in plasma as apoptosis increased. Analysis showed that NGFI-B induces cardiomyocyte apoptosis in restraint-stressed rats by mediating mitochondrial energy metabolism disorder. Several novel mitochondrial proteins, which correlate with NGFI-B, were reported in cardiomyocyte apoptosis of restraint-stressed rats. Five proteins associated with NGFI-B participate directly in mitochondrial energy metabolism. Studies of mitochondrial respiratory efficiency and ATP synthase activity strongly support the findings. These results provide significant information for comprehensively understanding the cellular mechanism of cardiovascular diseases.

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Modulation of Orphan Nuclear Receptor Nur77-Mediated Apoptotic Pathway by Acetylshikonin and Analogues

Cited by 69 publications

References 31 publications

Inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 in vitro and in vivo

Inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 in vitro and in vivo

Oncogenic Potential of Retinoic Acid Receptor-γ in Hepatocellular Carcinoma

NGFI-B targets mitochondria and induces cardiomyocyte apoptosis in restraint-stressed rats by mediating energy metabolism disorder

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