Britannin induces apoptosis through AKT-FOXO1 pathway in human pancreatic cancer cells

Moeinifard, Marzieh; Hassan, Zuhair Mohammad; Fallahian, Faranak; Hamzeloo-Moghadam, Maryam; Taghikhani, Mohammad

doi:10.1016/j.biopha.2017.08.025

Cited by 40 publications

(32 citation statements)

References 34 publications

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“…Many anticancer agents exert their inhibitory effects through the generation of ROS and promotion of oxidative stress-induced cancer cell death. 26 In our study, we found that the levels of intracellular ROS to be significantly elevated by D. maritima treatment in MCF-7 and MDA-MB-468 cells. Increased ROS levels also can induce ER stress response, which in the case of prolonged ER stress could initiate apoptotic death signals.…”

Section: Discussionsupporting

confidence: 48%

Cytotoxic effect of <em>Drimia maritima</em> bulb extract and induction of mitochondrial apoptotic signaling in human breast cancer cells, MCF-7 and MDA-MB-468

Hamzeloo-Moghadam

Aghaei

Abdolmohammadi

et al. 2018

OTT

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BackgroundDrimia maritima (D. maritima) is a plant belonging to the family Asparagaceae, which has been used for the treatment of several ailments including cancer around the world. To our knowledge, there is no comprehensive study about the molecular mechanisms of anticancer activity of this plant, yet.Materials and methodsIn the current study, cell viability, apoptosis induction, ROS production, mitochondrial apoptotic pathway, and ER stress mediators have been evaluated in breast cancer cells, MCF7, and MDA-MB-468 treated with D. maritima.ResultsSignificant cytotoxic effects were observed in MCF-7 and MDA-MB-468 cells after exposure to D. maritima. Apoptosis induction was determined using Annexin-V-FITC and propidium iodide staining. Furthermore, an increase of ROS, loss of mitochondrial membrane potential, the release of cytochrome c, activation of caspases, and elevation in the Bax/Bcl-2 ratio was determined. D. maritima dose-dependently increased the mRNA expression of ER stress markers such as CHOP, ATF-4, GADD34, and TRIB3 in MCF-7, and MDA-MB-468 cells.ConclusionThese data suggest that D. maritima induces apoptosis in human breast cancer cells via the mitochondrial-mediated pathway. In addition, endoplasmic reticulum stress seems to be involved in D. maritima-induced cell death.

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Section: Discussionsupporting

confidence: 48%

Cytotoxic effect of <em>Drimia maritima</em> bulb extract and induction of mitochondrial apoptotic signaling in human breast cancer cells, MCF-7 and MDA-MB-468

Hamzeloo-Moghadam

Aghaei

Abdolmohammadi

et al. 2018

OTT

Self Cite

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“…AKT kinase, which is a serine/threonine kinase, plays an important role in a number of biological processes, including cell proliferation, differentiation and apoptosis (39,40). A number of studies have demonstrated that natural compounds can induce cancer cell apoptosis through the suppression of the AKT signaling pathway (41)(42)(43). Additionally, Wang et al (11) revealed that TS I induced breast cancer cell apoptosis by regulating the PI3K/AKT/mammalian target of rapamycin signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Tanshinone I induces apoptosis and protective autophagy in human glioblastoma cells via a reactive oxygen species‑dependent pathway

et al. 2020

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Glioma is the most common primary malignancy of the central nervous system and is associated with high mortality rates. despite the available treatment options including surgery, radiotherapy and chemotherapy, the median patient survival rate is low. Therefore, the development of novel anticancer agents for the treatment of glioma is urgently required. Tanshinone I (TS I) is a tanshinone compound that is isolated from danshen. Accumulating evidence indicates that TS I exhibits antiproliferative activity in a variety of cancer types. However, the role of TS I and its mechanism of action in human glioma remain to be elucidated. In the present study, the anticancer potential of TS I against human glioma U87 MG cells was investigated. The results indicated that TS I exerted a potential cytotoxic effect on human glioma U87 MG cells. TS I was found to induce cell proliferation, inhibition, cell cycle arrest, apoptosis and autophagy in U87 MG cells. Mechanistic experiments indicated that TS I activated endoplasmic reticulum (ER) stress and inhibited AKT signaling and apoptosis in human glioma U87 MG cells. Furthermore, the present study demonstrated that TS I induced protective autophagy in U87 MG cells. Additionally, ER stress and AKT signal-mediated apoptosis and protective autophagy were found to be induced by TS I via intracellular reactive oxygen species accumulation. The results of the present study demonstrated that TS I may be a potential anticancer drug candidate that may be of value in the treatment of human glioma.

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“…This result coincided well with the enhancement in nuclear localization and the potentiated cytoplasmic degradation of FOXO1 observed in immunofluorescence images. Activation of FOXO1 subsequently led to transcriptional activation of genes controlling cell cycle arrest or cell apoptosis, such as proapoptotic proteins [ 47 ]. We verified in this study that their ability of permeabilizing mitochondrial membrane could result in activation of executioner caspases such as caspase-9, caspase-3, and pinnacle of cell death [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Xihuang Pill Induces Apoptosis of Human Glioblastoma U‐87 MG Cells via Targeting ROS‐Mediated Akt/mTOR/FOXO1 Pathway

Shao

Yin

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Xihuang pill (XHP), a traditional Chinese herbal formula, has long been used as an effective agent against multiple tumors. The aim of this study is to evaluate the effects of XHP on the growth inhibition and apoptosis in glioblastoma U-87 MG cells. Gas chromatography-mass spectrometry (GC-MS) was performed for constituent analysis of XHP. Cell viability, cell cycle arrest, generation of reactive oxygen species (ROS), and apoptosis were measured by CCK-8 assay, PI/RNase staining, DCFH-DA assay, TUNEL assay, Annexin V-FITC/PI double staining, and JC-1 assay, respectively. The role of XHP in the regulation of Akt/mTOR/FOXO1 interaction was clarified by using Western Blotting (WB), immunofluorescence (IF), pharmacological inhibitor or antioxidant, and siRNA silencing. The results suggested that XHP could inhibit U-87 MG cells growth and arrest cells in S-phase cell cycle significantly and that the generation of ROS, collapse of mitochondrial membrane potential, enhancement of Bax/Bcl-xL ratio, and reduction of the precursor forms of caspase-9 and caspase-3 caused by XHP prompted that a ROS-mediated mitochondria-dependent apoptosis was possibly involved. Furthermore, XHP affected the Akt/mTOR/FOXO1 pathway via inhibiting the phosphorylation of Akt, mTOR, and FOXO1 and increasing both prototype and nuclear translocation of FOXO1. Inhibition of Akt, mTOR, and FOXO1 by specific inhibitors or siRNA could interpose the apoptotic induction. In conclusion, we demonstrate for the first time that XHP may regulate glioblastoma U-87 MG cell apoptosis via ROS-mediated Akt/mTOR/FOXO1 pathway.

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Britannin induces apoptosis through AKT-FOXO1 pathway in human pancreatic cancer cells

Cited by 40 publications

References 34 publications

Cytotoxic effect of <em>Drimia maritima</em> bulb extract and induction of mitochondrial apoptotic signaling in human breast cancer cells, MCF-7 and MDA-MB-468

Cytotoxic effect of <em>Drimia maritima</em> bulb extract and induction of mitochondrial apoptotic signaling in human breast cancer cells, MCF-7 and MDA-MB-468

Tanshinone I induces apoptosis and protective autophagy in human glioblastoma cells via a reactive oxygen species‑dependent pathway

Xihuang Pill Induces Apoptosis of Human Glioblastoma U‐87 MG Cells via Targeting ROS‐Mediated Akt/mTOR/FOXO1 Pathway

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