Volatile Oil of Acori Graminei Rhizoma-Induced Apoptosis and Autophagy are dependent on p53 Status in Human Glioma Cells

Chen, Lu; Jiang, Zhuyun; Ma, Hui; Ning, Ling; Chen, Hongdan; Li, Li; Hu, Qi

doi:10.1038/srep21148

Cited by 23 publications

(18 citation statements)

References 55 publications

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“…15, 16, 28, 29, 30 We exposed mesangial cells to a combination of AGEs and autophagy inhibitors (Beclin-1 siRNA and Bafilomycin A1) and examined apoptotic cell death to determine the role of autophagy in AGE-mediated apoptotic cell death. The results showed that Beclin-1 siRNA and Bafilomycin A1 increased the percentage of apoptosis cells induced with AGEs ( P <0.01) (Figures 7a and b).…”

Section: Resultsmentioning

confidence: 99%

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Inhibition of autophagy increased AGE/ROS-mediated apoptosis in mesangial cells

Fan

Wang

et al. 2016

Cell Death Dis

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The aim of our study was to investigate the role of autophagy, a homeostatic process involved in the lysosomal degradation of damaged cell organelles and proteins, in regulating the survival of mesangial cells treated with advanced glycation end products (AGEs). In the present study, AGEs induced mitochondrial depolarization and led to mitochondrial-dependent apoptosis in mesangial cells, as shown by the loss of the mitochondrial membrane potential; increased Bax processing; increased Caspase-9, Caspase-3 and PARP cleavage; and decreased Bcl-2 expression. Meanwhile, AGEs also triggered autophagy flux in mesangial cells, as confirmed by the presence of autophagic vesicles, the conversion of LC3II/LC3I and the increase/decrease in Beclin-1/p62 expression. Interestingly, this study reported apparent apoptosis and autophagy that were dependent on reactive oxygen species (ROS) production. Scavenging ROS with N-acetyl-l-cysteine could prevent the appearance of the autophagic features and reverse AGE-induced apoptosis. Moreover, AGE-triggered mitophagy, which was confirmed by the colocalization of autophagosomes and mitochondria and Parkin translocation to mitochondria, played a potential role in reducing ROS production in mesangial cells. Additionally, inhibition of autophagy significantly enhanced AGE-induced cell apoptosis. Taken together, our data suggest that ROS were the mediators of AGE-induced mesangial cell apoptosis and that autophagy was likely to be the mechanism that was triggered to repair the ROS-induced damage in the AGE-treated cells and thereby promote cell survival. This study provides new insights into the molecular mechanism of autophagy involved in AGE-induced apoptosis in mesangial cells.

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Section: Resultsmentioning

confidence: 99%

“…28, 29, 41 However, little is known about the function of autophagy in mesangial cells under stress conditions. Although increased ROS production triggered autophagy in AGE-treated cells, we observed increased intracellular ROS and mitochondrial ROS generation in mesanigal cells, accompanied by increased autophagic clearance.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of autophagy increased AGE/ROS-mediated apoptosis in mesangial cells

Fan

Wang

et al. 2016

Cell Death Dis

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“…The mTOR pathway is one autophagy-associated pathway but numerous other signaling pathways and translations may regulate the autophagy of cells (30). Depending on its subcellular location, p53 may activate or inhibit autophagy (31). Autophagy may also be regulated by certain proteins, including AMP-activated proteases, Akt, p38, mitogen-activated protein kinase/extracellular signal-regulating enzymes and protease C (32).…”

Section: Discussionmentioning

confidence: 99%

Triptolide induces protective autophagy and apoptosis in human cervical cancer cells by downregulating Akt/mTOR activation

Qin

Xue

2018

Oncol Lett

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Triptolide exhibits immunosuppressive, anti-inflammatory, antifertility and antineoplastic functions. However, the anticancer effect of triptolide on cervical cancer and the underlying mechanism remains to be fully understood. The present study assessed the mechanisms underlying the effect of triptolide on the viability and apoptosis of human cervical cancer cells. SiHa cells were treated with 12.5-100.0 nM triptolide for 12, 24 or 48 h. The present study demonstrated that triptolide inhibited viability and induced apoptosis in SiHa cells time- and dose-dependently. Furthermore, treatment with triptolide promoted autophagy and activated microtubule associated protein 1 light chain 3 α expression in SiHa cells. Triptolide treatment suppressed the expression of phosphorylated (p)-protein kinase B (Akt), p-mechanistic target of rapamycin (mTOR), and p-p70S6K, activated the expression of p-p38, mitogen-activated protein kinase (MAPK) and p53 and inhibited the expression of p-forkhead box O3 (Foxo3a) in SiHa cells. These results suggested that triptolide induces protective autophagy, suppresses cell viability and promotes apoptosis in human cervical cancer cells by inducing the autophagy-targeting phosphoinositide 3-kinase/Akt/mTOR, p38, MAPK, p53 and Foxo3a pathways.

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“…It has been proved that U251 and Ln229 cells were p53 mutation cell lines [ 36 ] rather than p53 wild type cell lines U87 and A172 cells [ 37 ]. The functions of p53 in U251 and Ln229 cells were lost or changed into other way [ 38 , 39 ]. So even though miR-141-3p decreased expression of p53 protein, it could not promote U251 and Ln229 cells growth significantly.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-141-3p promotes glioma cell growth and temozolomide resistance by directly targeting p53

Zhou

Zeng

et al. 2017

Oncotarget

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Glioblastoma multiforme is the most common primary malignancy in the brain and confers a uniformly poor prognosis. MicroRNAs have been shown to activate or inhibit tumorigenesis. Abnormalities in the p53 signaling pathway are found in various cancers and correlate with tumor formation. We examined the expression of microRNA-141-3p (miR-141-3p) in glioma of different grades by analysis of expression profiling databases and clinical specimens. Cell proliferation and flow cytometry assays were performed to evaluate the promotion of miR-141-3p in proliferation, cell cycle, apoptosis, and temozolomide resistance of glioblastoma cells in vitro. Bioinformatics analyses, luciferase reporter assays, and immunoblotting showed that p53 is a target gene of miR-141-3p. A significant inverse correlation was observed between expression of miR-141-3p and p53 in glioma and normal brain tissues (R2=0.506, P<0.0001). Rescue experiments indicated that overexpression of p53 significantly reversed the alterations in proliferation, cell cycle distribution, and temozolomide resistance measured by cell apoptosis induced by miR-141-3p overexpression. In an orthotopic mouse model of human glioma, inhibition of miRNA-141-3p reduced the proliferation and growth of glioma cells in the brain and significantly prolonged the survival of glioma-bearing mice. We suggest that miR-141-3p promotes glioblastoma progression and temozolomide resistance by altering p53 expression and therefore may serve as a new diagnostic marker and therapeutic target for glioma in the future.

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Volatile Oil of Acori Graminei Rhizoma-Induced Apoptosis and Autophagy are dependent on p53 Status in Human Glioma Cells

Cited by 23 publications

References 55 publications

Inhibition of autophagy increased AGE/ROS-mediated apoptosis in mesangial cells

Inhibition of autophagy increased AGE/ROS-mediated apoptosis in mesangial cells

Triptolide induces protective autophagy and apoptosis in human cervical cancer cells by downregulating Akt/mTOR activation

MicroRNA-141-3p promotes glioma cell growth and temozolomide resistance by directly targeting p53

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