Emodin induces apoptosis in human prostate cancer cell LNCaP

Yu, Chunxiao; Zhang, Xiaoqian; Kang, Lan; Zhang, Pengju; Chen, Weiwen; Liu, Wen; Liu, Qingwei; Zhang, Jianye

doi:10.1111/j.1745-7262.2008.00397.x

Cited by 48 publications

(39 citation statements)

References 32 publications

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“…These results are in line with previous studies. Emodin induced apoptosis of LNCaP cells through the alterations in expression of Bax and Bcl2 genes which had the same result as ours (21). In another study, the increased Bax concurrent with the decrease of Bcl-2 indicated that emodin induces apoptosis in human chronic myeloid leukemia K562 cell lines (22).…”

Section: Discussionsupporting

confidence: 69%

Cytotoxic Effect of Emodin on Growth of SKBR3 Breast Cancer Cells

et al. 2017

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Section: Discussionsupporting

confidence: 69%

Cytotoxic Effect of Emodin on Growth of SKBR3 Breast Cancer Cells

et al. 2017

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“…Emodin, 1,2,8-trihydroxy-6-methylanthraquinone, is an active component contained in the root and rhizome of Rheum palmatum L. (Polygonaceae). Wogonin is one of the primary active compounds of Scutellaria baicalensis, and decreases prostate cancer cells in a p53-dependent mechanism [2,3]. The MDM2 antagonist Nutlin-3 specifically inhibits proliferation of LNCaP cells through cell cycle arrest and apoptosis by increasing levels of p53-responsive p21 and MDM2 expressions, demonstrating that MDM2 antagonists retain functional p53 and androgen receptor signaling in human prostate cancers [4].…”

Section: Introductionmentioning

confidence: 99%

“…The MDM2 antagonist Nutlin-3 specifically inhibits proliferation of LNCaP cells through cell cycle arrest and apoptosis by increasing levels of p53-responsive p21 and MDM2 expressions, demonstrating that MDM2 antagonists retain functional p53 and androgen receptor signaling in human prostate cancers [4]. Melatonin, a circadian indoleamine hormone secreted by the human pineal gland, is able to directly induced cell death of several types of human tumor cells [1][2][3][4][5][6][7][8][9]. Many recent reports have shown that melatonin inhibits the growth of androgen-sensitive human LNCaP prostate cancer cells [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Melatonin Induces Apoptotic Cell Death via p53 in LNCaP Cells

Kim

Yoo

2010

Korean J Physiol Pharmacol

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In this study, we examined whether melatonin promotes apoptotic cell death via p53 in prostate LNCaP cells. Melatonin treatment significantly curtailed the growth of LNCaP cells in a dose-and time-dependent manner. Melatonin treatment (0 to 3 mM) induced the fragmentation of poly(ADPribose) polymerase (PARP) and activation of caspase-3, caspase-8, and caspase-9. Moreover, melatonin markedly activated Bax expression and decreased Bcl-2 expression in dose increments. To investigate p53 and p21 expression, LNCaP cells were treated with 0 to 3 mM melatonin. Melatonin increased the expressions of p53, p21, and p27. Treatment with mitogen-activated protein kinase (MAPK) inhibitors, PD98059 (ERK inhibitor), SP600125 (JNK inhibitor) and SB202190 (p38 inhibitor), confirmed that the melatonin-induced apoptosis was p21-dependent, but ERK-independent. W ith the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease. These effects were opposite to the expression of p-p53, p21, and MDM2 observed with SP600125 and SB202190 treatments. Together, these results suggest that p53-dependent induction of JNK/p38 MAPK directly participates in apoptosis induced by melatonin.

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“…Prostate cancer is induced by various factors such as age, genetics, diet, race, lifestyle and medication, and the rate of mortality caused by prostate cancer is increasing. 27,28) Interestingly, HIF-1a overexpression is associated with the growth and metastasis of rat and human prostate cancer cell lines. 29) During the growth of prostate cancer, hypoxia causes low tissue oxygen and activates the expression of HIF-1a.…”

Section: Discussionmentioning

confidence: 99%

1,2,3,4,6-Penta-O-galloly-beta-D-glucose Suppresses Hypoxia-Induced Accumulation of Hypoxia-Inducible Factor-1.ALPHA. and Signaling in LNCaP Prostate Cancer Cells

Park

Lee

Jeong

et al. 2010

Biological & Pharmaceutical Bulletin

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Hypoxia-inducible factor-1 (HIF-1) is a heterodimeric transcription factor that plays a role in cell survival in response to hypoxia and is overexpressed in many human solid cancers. HIF-1 consists of two subunits, HIF-1a and HIF1b.1) HIF-1a is steadily degraded by the ubiquitin-proteasome pathway under normoxic condition and stabilized under hypoxic condition, in contrast to HIF-1b, which is constitutively expressed. In the presence of iron and oxygen, HIF-1a is hydroxylated by prolyl hydroxylase domain (PHD) on residues 402 and 564, which are in the oxygendependent degradation (ODD) region. 2,3)HIF-1a plays important roles in the promotion of cancer angiogenesis, cell proliferation, and erythropoiesis. [4][5][6] HIF1a activates transcription of the promoter of vascular endothelial growth factor (VEGF), a key factor in tumor angiogenesis. 7) Angiogenesis is the process involving the growth of new blood vessels from pre-existing vessels 8) and is crucial for tumor growth and metastasis. 9) Thus, HIF-1a/VEGF system has been considered a promising target for antiangiogenic and anti-cancer therapy. 10)In addition, HIF-1a has been linked to the oncogenic phosphoinositide 3-kinase (PI3K)/AKT signaling pathway in many types of cancer.11,12) Accumulation of HIF-1a protein also depends on the AKT/mammalian target of rapamycin (mTOR) pathway. 13)Recently, many anti-tumor herbal drugs and natural compounds have become very attractive due to little side effects at nontoxic concentrations. We and others have reported that 1,2,3,4,6-penta-O-galloyl-b-D-glucose (PGG), a naturally occurring gallotannin polyphenolic compound highly enriched in a number of medicinal herbals such as Rhus chinensis MILL and Paeonia suffruticos, possesses potent anti-angiogenic activity in a battery of in vitro angiogenesis tests using human umbilical vein endothelial cell (HUVEC) and in vivo angiogenesis and Lewis lung carcinoma (LLC) allograft models.14,15) Our collaborative team and others have recently demonstrated the in vivo efficacy of PGG against prostate xenograft models. 16,17) PGG also has been shown to exert various biological activities such as anti-cancer, anti-angiogenic, anti-diabetic, and anti-oxidation effects. 14,18,19) While the anti-angiogenic activity of PGG has been implicated as a contributor to tumor growth suppression, no studies have examined the direct impact of PGG on HIF-1a accumulation and angiogenic signaling pathway in prostate cancer cells.In the present study, we demonstrate the effects of PGG on hypoxia-induced protein accumulation, transcriptional activation of HIF-1a, and PI3K/AKT/mTOR pathway in LNCaP prostate cancer cells. MATERIALS AND METHODSIsolation of PGG Isolation of PGG (molecular weight (MW)ϭ940) from the gallnut of R. chinensis has been described previously. 15)Cell Culture and Hypoxia Induction LNCaP human prostate cancer cells were obtained from the Korea Cell Line Bank (KCLB) (Seoul, South Korea) and maintained in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS), 0.45% D-glucose, 10...

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Emodin induces apoptosis in human prostate cancer cell LNCaP

Abstract: In prostate cancer cell line, LNCaP, emodin inhibites the proliferation by AR and p53-p21 pathways, and induces apoptosis via the mitochondrial pathway.

Cited by 48 publications

References 32 publications

Cytotoxic Effect of Emodin on Growth of SKBR3 Breast Cancer Cells

Cytotoxic Effect of Emodin on Growth of SKBR3 Breast Cancer Cells

Melatonin Induces Apoptotic Cell Death via p53 in LNCaP Cells

1,2,3,4,6-Penta-O-galloly-beta-D-glucose Suppresses Hypoxia-Induced Accumulation of Hypoxia-Inducible Factor-1.ALPHA. and Signaling in LNCaP Prostate Cancer Cells

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