Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells

Mantena, Sudheer K.; Sharma, Som D.; Katiyar, Säntosh K.

doi:10.1158/1535-7163.mct-05-0448

Cited by 325 publications

(245 citation statements)

References 44 publications

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“…Meanwhile, HepG2 cells that had a functional p53 were more sensitively damaged by IWE than Hep3B cells who did not have a functional p53, i.e., delete p53. G1-phase arrest of cell cycle progression provides an opportunity for cells to either undergo repair mechanisms or proceed by the apoptotic pathway (Mantena et al, 2006). p53 is a tumor suppressor gene encoding a transcription factor, the tumor-suppressive activity of which involves inhibition of cell proliferation through cell cycle arrest and/or apoptosis or subject to NDA repairing.…”

Section: Involving In the Arrest Of Cell Cycle In Cancer Cellsmentioning

confidence: 99%

Progress on Understanding the Anticancer Mechanisms of Medicinal Mushroom: Inonotus Obliquus

Song¹,

Liu²,

Kong³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Section: Involving In the Arrest Of Cell Cycle In Cancer Cellsmentioning

confidence: 99%

Progress on Understanding the Anticancer Mechanisms of Medicinal Mushroom: Inonotus Obliquus

Song¹,

Liu²,

Kong³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…GSP-induced apoptosis of the human NSCLC cells was determined by flow cytometry using the Annexin V-conjugated Alexa Fluor488 (Alexa488) Apoptosis Detection kit following the instructions of the manufacturer, and as described by us (28,29). Briefly, after overnight serum starvation, cells were treated with varying concentrations of GSPs for 48 h. The cells were then harvested, washed in PBS, and incubated with Alexa488 and propidium iodide in the dark at room temperature.…”

Section: Analysis Of Apoptotic Cell Death By Flow Cytometrymentioning

confidence: 99%

“…Following treatment of the NSCLC cells with or without GSPs, the cells were harvested, washed with cold PBS, and lysed with ice-cold lysis buffer supplemented with protease inhibitors, as detailed previously (28,29). Lysates of tumor xenografts were prepared similarly.…”

Section: Preparation Of Cell or Tumor Xenograft Lysates And Western Bmentioning

confidence: 99%

“…To determine whether the GSP-induced inhibition of cell proliferation or cell viability of the human lung cancer cells was associated with the induction of apoptosis, two representative cell lines, A549 and H1299, were treated with various concentrations of GSPs, and apoptosis was assessed using the Annexin V-conjugated Alexa Fluor 488 (Alexa488) Apoptotic Detection kit, as previously described (29). As shown in Fig.…”

Section: Gsps Induce Apoptotic Cell Death Of Human Nsclc Cellsmentioning

confidence: 99%

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Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

Sharma

Meeran

Katiyar

2010

Molecular Cancer Therapeutics

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Overexpression of cyclooxygenase-2 (COX-2) and prostaglandins (PG) is linked to a wide variety of human cancers. Here, we assessed whether the chemotherapeutic effect of grape seed proanthocyanidins (GSP) on non-small cell lung cancer (NSCLC) cells is mediated through the inhibition of COX-2 and PGE 2 /PGE 2 receptor expression. The effects of GSPs on human NSCLC cell lines in terms of proliferation, apoptosis, and expression of COX-2, PGE 2 , and PGE 2 receptors were determined using Western blotting, fluorescence-activated cell sorting analysis, and reverse transcription-PCR. In vitro treatment of NSCLC cells (A549, H1299, H460, H226, and H157) with GSPs resulted in significant growth inhibition and induction of apoptosis, which were associated with the inhibitory effects of GSPs on the overexpression of COX-2, PGE 2 , and PGE 2 receptors (EP1 and EP4) in these cells. Treatment of cells with indomethacin, a pan-COX inhibitor, or transient transfection of cells with COX-2 small interfering RNA, also inhibited cell growth and induced cell death. The effects of a GSP-supplemented AIN76A control diet fed to nude mice bearing tumor xenografts on the expression of COX-2, PGE 2 , and PGE 2 receptors in the xenografts were also evaluated. The growth-inhibitory effect of dietary GSPs (0.5%, w/w) on the NSCLC xenograft tumors was associated with the inhibition of COX-2, PGE 2 , and PGE 2 receptors (EP1, EP3, and EP4) in tumors. This preclinical study provides evidence that the chemotherapeutic effect of GSPs on lung cancer cells in vitro and in vivo is mediated, at least in part, through the inhibition of COX-2 expression and subsequently the inhibition of PGE 2 and PGE 2 receptors.Mol Cancer Ther; 9(3); 569-80. ©2010 AACR.

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“…These findings suggest that G2/M phase arrest is one of the mechanisms through which evodiamine induces cytotoxicity in SGC-7901 cells. Numerous chemotherapeutic and chemopreventive agents have potential antiproliferative effects via arresting the cell division at certain checkpoints of the cell cycle (51,52).…”

Section: Resultsmentioning

confidence: 99%

Cytotoxic effect of evodiamine in SGC-7901 human gastric adenocarcinoma cells via simultaneous induction of apoptosis and autophagy

2012

Oncol Rep

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Abstract. Evodiamine, an alkaloid isolated from Evodia rutaecarpa, possesses potent anticancer activity. Although many reports have elucidated the cytotoxic effects of evodiamine in a variety of cancer cells, little is known about the mechanism of evodiamine-induced cytotoxic activity in gastric cancer cells. To date, no report has addressed the synchronized role of autophagy and apoptosis in evodiamineinduced cytotoxic activity. This study was conducted to investigate the synchronized role of autophagy and apoptosis in evodiamine-induced cytotoxic activity on SGC-7901 human gastric adenocarcinoma cells and further to elucidate the underlying molecular mechanisms. The MTT assay was used to examine the cytotoxicity of evodiamine against SGC-7901 gastric adenocarcinoma cells. The effects of evodiamine on the cell cycle and apoptosis were measured by flow cytometry and cellular morphology was observed under a phase contrast microscope. Acridine orange (AO) staining was used to detect autophagy. The expression levels of Bcl-2 and Bax were detected by Western blotting. The expression level of Beclin-1 in SGC-7901 cells was monitored by reverse transcription-polymerase chain reaction (RT-PCR). Here, we found that evodiamine significantly inhibited the proliferation of SGC-7901 cells and induced G2/M phase cell cycle arrest. Furthermore, both autophagy and apoptosis were activated during the evodiamine-induced death of SGC-7901 cells. Evodiamine-induced autophagy is partially involved in the death of SGC-7901 cells which was confirmed by using the autophagy inhibitor 3-methyladenine (3-MA). Additionally, Beclin-1 is involved in evodiamine-induced autophagy and the pro-apoptotic mechanisms of evodiamine may be associated with down-regulation of Bcl-2 and up-regulation of Bax expression. The inhibitory effects on SGC-7901 cells were associated with apoptosis, autophagy and cell cycle arrest at the G2/M phase in a dose-dependent manner. These results suggest that evodiamine is an effective natural compound for the treatment of gastric cancer and may represent a candidate for in vivo studies of monotherapies or combined antitumor therapies.

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Berberine, a natural product, induces G1-phase cell cycle arrest and caspase-3-dependent apoptosis in human prostate carcinoma cells

Cited by 325 publications

References 44 publications

Progress on Understanding the Anticancer Mechanisms of Medicinal Mushroom: Inonotus Obliquus

Progress on Understanding the Anticancer Mechanisms of Medicinal Mushroom: Inonotus Obliquus

Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

Cytotoxic effect of evodiamine in SGC-7901 human gastric adenocarcinoma cells via simultaneous induction of apoptosis and autophagy

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