Realgar-induced apoptosis of cervical cancer cell line Siha via cytochrome c release and caspase-3 and caspase-9 activation

Cheng, Yanxiang; Liu, Rong; Wang, Qin; Li, Bing-shu; Xu, Xuexian; Hu, Min; Chen, Lu; Fu, Qiong; Pu, Demin; Li, Hong

doi:10.1007/s11655-011-0697-z

Cited by 18 publications

(8 citation statements)

References 21 publications

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“…Given that caspase-3 and caspase-9 are activated during the early stage of apoptosis, they are treated as markers of apoptotic cells (22). The present results indicated that caspase-3 and caspase-9 were activated in the BMAP-28-treated TT cells as the dose increased (Fig.…”

Section: Bmap-28 Activates Caspase-3 and Caspase-9 In Tt Cellsmentioning

confidence: 52%

“…Caspase-3, caspase-9, MMP3 and MMP9 expression was assessed using colorimetric assay kits according to the manufacturer's instructions (22). The TT cells were treated with various concentrations of BMAP-28 (ranging from 0 to 4 µM) for 24 h. Next, cell pellets were washed twice with PBS and scrapped with ice-cold lysis buffer.…”

Section: Cell Apoptosis Assay Cell Apoptosis Assaysmentioning

confidence: 99%

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Effect of BMAP-28 on human thyroid cancer TT cells is mediated by inducing apoptosis

et al. 2015

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Abstract. Thyroid cancer is the most common malignant endocrine tumor, with significant morbidity and mortality. Bovine myeloid antimicrobial peptide 28 (BMAP-28) is a cathelicidin that is found in bovine neutrophils. In the present study, the effect and relative mechanism of BMAP-28 on the human thyroid cancer TT cell line in vitro and in vivo were investigated. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry and a TT-xenograft mouse model were used in this study. The data obtained indicated that BMAP-28 significantly inhibited the proliferation of the TT cells in vitro. In addition, the Annexin V-fluorescein isothiocyanate/propidium iodide assay detected that BMAP-28 induced apoptotic effects in the TT cells. Moreover, the expression of activated caspase-3 and -9 was upregulated at the transcriptional and translational levels. Simultaneously, the expression of matrix metalloproteinase (MMP)3 and MMP9 was downregulated following BMAP-28 treatment. Finally, BMAP-28 significantly prevented the tumor growth in the TT-xenograft mouse model. These results indicated that BMAP-28 could be a potential agent for the treatment of thyroid cancer.

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Section: Bmap-28 Activates Caspase-3 and Caspase-9 In Tt Cellsmentioning

confidence: 52%

Section: Cell Apoptosis Assay Cell Apoptosis Assaysmentioning

confidence: 99%

Effect of BMAP-28 on human thyroid cancer TT cells is mediated by inducing apoptosis

et al. 2015

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“…Our results showed that VEGFR3 knockdown resulted in a greatly down-regulation of Bcl-2, indicating that the loss of VEGFC/VEGFR3 signaling may be associated with mitochondrial membrane damage. During apoptosis, mitochondrial cytochrome C release correlated with mitochondrial membrane damage led to the cleavage at Asp315 and Asp330 in Caspase-9 protein and produced p35 and p37 subunit and further processed Caspase-3 [60,61]. So we examined Caspase-3 and Caspase-9 in GC-1 cells with VEGFC treatment or VEGFR3 knockdown.…”

Section: Discussionmentioning

confidence: 99%

VEGFC/VEGFR3 Signaling Regulates Mouse Spermatogonial Cell Proliferation via the Activation of AKT/MAPK and Cyclin D1 Pathway and Mediates the Apoptosis by affecting Caspase 3/9 and Bcl-2

et al. 2018

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We have previously shown that the transcript levels of Vegfc and its receptor Vegfr3 were high in spermatogonia and extremely low in spermatocytes and spermatids. However, it remains unknown about the functions and the mechanisms of VEGFC/VEGFR3 signaling in regulating the fate determinations of spermatogonia. To this end, here we explored the role and signaling pathways of VEGFC/VEGFR3 by using a cell line derived from immortalized mouse spermatogonia retaining markers of mitotic germ cells, namely GC-1 cells. VEGFR3 was expressed in mouse primary spermatogonia and GC-1 cells. VEGFC stimulated the proliferation and DNA synthesis of GC-1 cells and enhanced the phosphorylation of PI3K-AKT and MAPK, whereas LY294002 (an inhibitor for AKT) and CI-1040 (an inhibitor for MAPK) blocked the effect of VEGFC on GC-1 cell proliferation. Furthermore, VEGFC increased the transcripts of c-fos and Egr1 and protein levels of cyclin D1, PCNA and Bcl-2. Conversely, the blocking of VEGFC/VEGFR3 signaling by VEGFR3 knockdown reduced the phosphorylation of AKT/MAPK and decreased the levels of cyclin D1 and PCNA. Additionally, VEGFR3 knockdown not only resulted in more apoptosis of GC-1 cells but also led to a decrease of Bcl-2 and promoted the cleavage of Caspase-3/9 and PARP. Collectively, these data suggested that VEGFC/VEGFR3 signaling promotes the proliferation of GC-1 cells via the AKT /MAPK and cyclin D1 pathway and it inhibits the cell apoptosis through Caspase-3/9, PARP and Bcl-2. Thus, this study sheds a novel insight to the molecular mechanisms underlying the fate decisions of mammalian spermatogonia.

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“…Among constituents of Chijongdan, Rhus verniciflua was known to have antitumor activity in A549 lung cancer [24], MCF-7 breast cancer [25], lymphoma [26], osteosarcoma [27] and renal cancer [28] and also processed Panax ginseng was reported to exert antitumor effect in AGS gastric cancer. Also, Persicaria tinctoria contained tyrosine kinase inhibitory compounds [29] and Realgar was reported to be too cytotoxic and apoptotic in chronic lymphocytic leukemia or cervical cell lines [30, 31]. Here, based on previous antitumor evidences of its constituents, antitumor activity of Chijongdan was hypothesized.…”

Section: Discussionmentioning

confidence: 99%

Activation of caspases and inhibition of ribosome biogenesis mediate antitumor activity of Chijongdan in A549 non-small lung cancer cells

Kim

Kwon

Sohn

et al. 2014

BMC Complement Altern Med

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BackgroundThough herbal medicines have been used for cancer prevention and treatment, their scientific evidences still remain unclear so far. Thus, complementary and alternative medicine (CAM) project has been actively executed to reveal the scientific evidences in the USA and other countries. In the present study, we elucidated antitumor mechanism of Chijongdan, an oriental prescription of Rhus verniciflua, processed Panax ginseng, Persicaria tinctoria and Realgar, that has been traditionally applied for cancer treatment in Korea.MethodsChijongdan was prepared with extracts of Rhus verniciflua, processed Panax ginseng, Persicaria tinctoria and processed Realgar. The cytotoxicity of Chijongdan was measured by MTT colorimetric assay. Cell cycle analysis was performed by FACS. Western blot was performed to see the apoptosis related proteins.ResultsChijongdan significantly exerted cytotoxicity in A549, H460 and H1299 non-small cell lung carcinoma (NSCLC) cells by MTT assay and also increased the number of ethidium homodimer positively stained cells in A549 NSCLC cells. Also, cell cycle analysis showed that Chijongdan increased sub-G1 population in a concentration dependent manner in A549 cells. In addition, Western blotting revealed that Chijongdan activated cleaved PARP, and caspase 9/3, while attenuated the expression of survival genes such as Bcl-2, Bcl-XL and survivin in A549 cells. Furthermore, Chijongdan suppressed the expression of ribosomal biogenesis related proteins such as upstream binding factor (UBF), Fibrillarin, NPM (B23) and Importin-7 (IPO7) and conversely pan-caspase inhibitor Z--VAD-FMK reversed the apoptotic ability of Chijongdan to cleave PARP and caspase 3 and attenuate the expression of UBF and Fibrillarin in A549 cells.ConclusionsThese findings suggest that Chijongdan induces apoptosis and inhibits ribosomal biogenesis proteins via caspase activation.

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Realgar-induced apoptosis of cervical cancer cell line Siha via cytochrome c release and caspase-3 and caspase-9 activation

Abstract: The induction of apoptosis by realgar is mediated through a cytochrome c-dependent pathway, which sequentially activates caspase-9 and caspase-3.

Cited by 18 publications

References 21 publications

Effect of BMAP-28 on human thyroid cancer TT cells is mediated by inducing apoptosis

Effect of BMAP-28 on human thyroid cancer TT cells is mediated by inducing apoptosis

VEGFC/VEGFR3 Signaling Regulates Mouse Spermatogonial Cell Proliferation via the Activation of AKT/MAPK and Cyclin D1 Pathway and Mediates the Apoptosis by affecting Caspase 3/9 and Bcl-2

Activation of caspases and inhibition of ribosome biogenesis mediate antitumor activity of Chijongdan in A549 non-small lung cancer cells

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