Tanshinone I induces human colorectal cancer cell apoptosis: The potential roles of Aurora A-p53 and survivin-mediated signaling pathways

Lu, Ming; Wang, Chen; Wang, Jian

doi:10.3892/ijo.2016.3565

Cited by 34 publications

(17 citation statements)

References 37 publications

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“…These results suggested that SETDB1 were indeed up-regulated in CRC as well as in other solid tumors [22,24]. On the other hand, survivin is an oncogene that regulates the apoptosis, proliferation, and invasion of many cancers [25][26][27]. Knockdown of survivin by using siRNA could dramatically suppress the proliferation and invasion of bladder cancer cells [8].…”

Section: Discussionmentioning

confidence: 92%

LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells

Qin

Zhou

et al. 2019

Cell Cycle

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This study was to investigate the biological function and underlying mechanisms of FENDRR in cholangiocarcinoma (CCA) cell proliferation, migration and invasion. FENDRR and survivin expression in CCA tissues or cell lines were measured by qRT-PCR. In QBC939 and HuCCTl cells, cell proliferation was detected by CCK-8, cell migration and invasion were using transwell assay. RNA pull-down and RIP assay were performed to determine whether FENDRR can combine with SETDB1 in CCA cell. The effect of SETDB1 on survivin and H3K9me1 expression in CCA cells were determined by western blotting. ChIP analysis was performed to analyze the combination of SETDB1 with survivin promoter in CCA cell. The effect of SETDB1 knockdown on survivin and H3K9me1 expression in CCA cells after transfection with FENDRR were determined by western blotting. The results showed that lncRNA FENDRR was downregulated in CCA tissues and cells, and was negatively correlated with survivin expression. Further investigation demonstrated that FENDRR represses CCA cell proliferation, migration and invasion through regulating survivin expression. FENDRR associated with SETDB1 and H3K9 to epigenetically silence survivin and then regulated cell proliferation, migration and invasion. These findings indicate an important role for FENDRR-survivin axis in CCA cell proliferation, migration and invasion, and reveal a novel epigenetic mechanism for survivin silencing. Our data indicated that FENDRR silences survivin via SETDB1-mediated H3K9 methylation, thereby represses CCA cell proliferation, migration and invasion. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 92%

LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells

Qin

Zhou

et al. 2019

Cell Cycle

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“…Despite multibiological activities of Tan I such as anti‐inflammatory (Park et al, ), antitumor (Jing et al, ; Lu, Wang, & Wang, ; Zhou, Zhang, Wang, & Sun, ), and antibacterial effect (Lee, Lee, Noh, & Hong, ), its antitumor mechanism is not fully understood compared with another component Tan IIA from Dansen. Thus, in the current study, the underlying mechanisms of Tan I from S .…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species‐mediated phosphorylation of p38 signaling is critically involved in apoptotic effect of Tanshinone I in colon cancer cells

Kim

Shin

Kim

et al. 2018

Phytotherapy Research

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Though Tanshinone I (Tan I), a phenolic compound from Salvia miltiorrhiza, is known to have anticancer activity in several cancers, its anticancer mechanisms are not fully understood in colon cancer cells. Thus, in the present study, the underlying molecular mechanism of Tan I was explored in HCT116 and HT29 colorectal cancer cells (CRCs). Here, Tan I suppressed viability in HCT116 and HT29 cells in a time- and dose-dependent manner. Also, Tan I increased the number of terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL)-positive cells and sub-G1 population in HCT116 and HT29 cells. Consistently, Tan I cleaved poly (adenosine diphosphate-ribose) polymerase (PARP) and caspase-8, caspase-3, attenuated the expression of Bid and activated tBid as a caspase-8 substrate and activated phosphorylation of p38 MAPK in HCT116and HT29 cells. Of note, Tan I generated reactive oxygen species (ROS) and conversely an ROS scavenger, N-acetyl- -cysteine, reversed ROS production, PARP cleavage, caspase-3 activation, and p38 MAPK phosphorylation induced by Tan I in HCT116 cells. Furthermore, p38 MAPK inhibitor SB203580 reduced cytotoxicity, increase of TUNEL-positive cells, cleavages of PARP and caspase-3 induced by Tan I in HCT116 cells. Overall, our findings for the first time suggest that ROS-dependent activation of p38 MAPK and caspase-3 is critically involved in Tan I induced apoptosis in CRCs as a potent anticancer agent.

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“…In accordance with these studies, our research found that TSN inhibited the proliferation and migration ability of SGC-7901 cells in a dose-dependent manner. As a multi-target drug, the molecular targets of TSN include apoptotic-regulating proteins, transcription and growth factors, ion channels and inflammatory mediators (6,7,24,25). In the present study, we found that TSN decreases the expression of FOXM1 in SGC-7901 cells in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA suppresses gastric cancer cell proliferation and migration by downregulation of FOXM1

Wang

et al. 2017

Oncology Reports

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Tanshinone IIA (TSN) exhibits a variety of anticancer effects. However, whether it inhibits gastric cancer (GC) cell proliferation and migration and the mechanism remain unclear. In the present study, different concentrations of TSN were co-incubated with SGC-7901 cells. The pcDNA-FOXM1 or FOXM1-siRNA plasmid was transfected into cells before treatment with 5 µg/l TSN. The proliferation and migration abilities of the SGC-7901 cells were tested by MTT and wound healing assays. Western blotting was used to investigate the expression levels of P21, Ki-67, PCNA, MMP-2, MMP-9 and FOXM1. We found that compared with the control, the proliferation and migration abilities of the SGC-7901 cells were decreased after incubation with different concentrations of TSN in a dose-dependent manner (p<0.01). Moreover, the expression levels of Ki-67, PCAN, MMP-2, MMP-9 and FOXM1 were decreased, and P21 was increased in the TSN-treated SGC-7901 cells (p<0.01). In addition, downregulation of FOXM1 by FOXM1-siRNA had the same effect as TSN on SGC-7901 cells, and overexpression of FOXM1 partly abrogated TSN-mediated inhibition of SGC-7901 cell proliferation and migration. These results suggested that TSN inhibits SGC-7901 cell proliferation and migration by downregulation of FOXM1.

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Tanshinone I induces human colorectal cancer cell apoptosis: The potential roles of Aurora A-p53 and survivin-mediated signaling pathways

Cited by 34 publications

References 37 publications

LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells

LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells

Reactive oxygen species‐mediated phosphorylation of p38 signaling is critically involved in apoptotic effect of Tanshinone I in colon cancer cells

Tanshinone IIA suppresses gastric cancer cell proliferation and migration by downregulation of FOXM1

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