Synergistic effect of a combination of nanoparticulate Fe3O4 and gambogic acid on phosphatidylinositol 3-kinase/Akt/Bad pathway of LOVO cells

Fang, Liang-hua; Chen, Baoan; Liu, Shenlin; Wang, Ruiping; Hu, Sindy; Xia, Guohua; Tian, Yingjie; Cai, Xueting

doi:10.2147/ijn.s32475

Cited by 9 publications

(4 citation statements)

References 37 publications

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“…Over the past half-century, pharmacological studies have revealed that GA has strong antitumor activities against various tumors including human leukemia, hepatoma, oral, breast, gastric, pancreatic, prostate, epithelial cervical and lung cancer [9] , [12] , [13] . Recently, GA has also been reported to have a marked anti-tumor effect for CRC cells in vivo and in vitro [14] , [15] . Due to the wide spectrum of anti-tumor activity with minimal toxicity to normal cells, GA has been approved by the Chinese Food and Drug Administration for the treatment of various cancers and has finished phase II clinical trials [7] , [16] .…”

Section: Introductionmentioning

confidence: 99%

ROS-Mediated Autophagy Induced by Dysregulation of Lipid Metabolism Plays a Protective Role in Colorectal Cancer Cells Treated with Gambogic Acid

Zhang

Yuan

et al. 2014

PLoS ONE

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Gambogic acid (GA), the main active component of gamboge resin, has potent antitumor activity both in vivo and in vitro. However, the underlying molecular mechanisms remain unclear. In this study, we found that GA could initiate autophagy in colorectal cancer cells, and inhibition of the autophagy process accelerated the effect of proliferative inhibition and apoptotic cell death induced by GA, implying a protective role of autophagy. Two-dimensional electrophoresis-based proteomics showed that GA treatment altered the expression of multiple proteins involved in redox signaling and lipid metabolism. Functional studies revealed that GA-induced dysregulation of lipid metabolism could activate 5-lipoxygenase (5-LOX), resulting in intracellular ROS accumulation, followed by inhibition of Akt-mTOR signaling and autophagy initiation. Finally, results using a xenograft model suggested ROS-induced autophagy protect against the antitumor effect of GA. Taken together, these data showed new biological activities of GA against colorectal cancer underlying the protective role of ROS-induced autophagy. This study will provide valuable insights for future studies regarding the anticancer mechanisms of GA.

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Section: Introductionmentioning

confidence: 99%

ROS-Mediated Autophagy Induced by Dysregulation of Lipid Metabolism Plays a Protective Role in Colorectal Cancer Cells Treated with Gambogic Acid

Zhang

Yuan

et al. 2014

PLoS ONE

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“…Chitchumroonchokchai et al confirmed that MAG inhibits the proliferation of HT-29 cells and reduces the expression of BCL-2 and β-catenin [32]. Similarly, the cytotoxic effect of natural mangosteen xanthones and GA in colorectal cancer cells (LoVo) was confirmed by Fang and Yu [34,35]. Aisha et al observed that MAG not only increased apoptosis but also impaired migration, insert invasion, and xenograft tumor growth in HCT-116 colon cancer cells [36].…”

Section: Discussionmentioning

confidence: 92%

Novel Xanthone Derivatives Impair Growth and Invasiveness of Colon Cancer Cells In Vitro

et al. 2021

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Natural xanthones are a large group of compounds from which promising anticancer properties could be further developed by chemical modifications. This study aimed to investigate the influence of four novel xanthone derivatives based on a naturally occurring xanthone skeleton on the invasiveness of colon cancer cells in vitro. First, the concentrations required to inhibit growth of three colorectal cancer cell lines to 50% (GI50) of all the studied compounds, as well as the natural xanthones used as a reference (gambogic acid and α-mangostin), have been established (MTS reduction test). Next, the assays determining several aspects of the GI25 xanthones influence on colorectal cancer cells, including cytotoxicity, migration and invasion potential, interaction with extracellular matrix and endothelial cells, as well as expression of selected invasiveness related genes have been performed. Our results demonstrate that these novel xanthone derivatives impair colorectal cancer proliferation, motility, adhesion to extracellular matrix and to endothelial cells, and also induce apoptosis and cell death. Moreover, their activity is comparable to cisplatin and 5-fluorouracil, used as reference compounds. Conducted research indicates our compounds for further research and development as novel drugs in colorectal cancer treatment.

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“…With magnetic hyperthermia, nanoparticles leaked into the cytoplasm and produced reactive oxidative species, which led to DNA and mitochondrial damage and protein oxidation. Fang et al37 proposed that magnetic nanoparticles increase the activation of the phosphatidylinositol 3-kinase/Akt/Bad pathway in LOVO cells, leading to the expression of cytochrome c, caspase 9, and caspase 3 proteins. Using TEM, we observed magnetic nanoparticles that were internalized into Y79 retinoblastoma cells.…”

Section: Discussionmentioning

confidence: 99%

Magnetic Hyperthermia in Y79 Retinoblastoma and ARPE-19 Retinal Epithelial Cells: Tumor Selective Apoptotic Activity of Iron Oxide Nanoparticle

Demirci

Slimani

Pawar

et al. 2019

Trans. Vis. Sci. Tech.

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Purpose: To evaluate selective apoptosis of Y79 retinoblastoma versus ARPE-19 retinal pigment epithelial cells by using different doses of dextran-coated iron oxide nanoparticles (DCIONs) in a magnetic hyperthermia paradigm. Methods: Y79 and ARPE-19 cells were exposed to different concentrations of DCIONs, namely, 0.25, 0.5, 0.75, and 1 mg/ml. After 2 hours of incubation, cells were exposed to a magnetic field with a frequency of 250 kHz and an amplitude of 4 kA/m for 30 minutes to raise the cellular temperature between 42 and 468C. Y79 and ARPE-19 cells incubated with DCION without magnetic field exposure were used as controls. Cell viability and apoptosis were assessed at 4, 24, and 72 hours after hyperthermia treatment. Results: At 4 hours following magnetic hyperthermia, cell death for Y79 cells was 1%, 8%, 17%, and 17% for 0.25, 0.5, 0.75 and 1 mg/ml of DCION, respectively. Cell death increased to 47%, 59%, 70%, and 75% at 24 hours and 16%, 45%, 50%, and 56% at 72 hours for 0.25, 0.5, 0.75, and 1 mg/ml of DCIONs, respectively. Magnetic hyperthermia did not have any significant toxic effects on ARPE-19 cells at all DCION concentrations, and minimal baseline cytotoxicity of DCIONs on Y79 and ARPE-19 cells was observed without magnetic field activation. Gene expression profiling showed that genes involved in FAS and tumor necrosis factor alpha signaling pathways were activated in Y79 cells following hyperthermia. Caspase 3/7 activity in Y79 cells increased following treatment, consistent with the activation of caspase-mediated apoptosis and loss of cell viability by magnetic hyperthermia. Conclusion: Magnetic hyperthermia using DCIONs selectively kills Y79 cells at 0.5 mg/ ml or higher concentrations via the activation of apoptotic pathways. Translational Relevance: Magnetic hyperthermia using DCIONs might play a role in targeted management of retinoblastoma.

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Synergistic effect of a combination of nanoparticulate Fe3O4 and gambogic acid on phosphatidylinositol 3-kinase/Akt/Bad pathway of LOVO cells

Cited by 9 publications

References 37 publications

ROS-Mediated Autophagy Induced by Dysregulation of Lipid Metabolism Plays a Protective Role in Colorectal Cancer Cells Treated with Gambogic Acid

ROS-Mediated Autophagy Induced by Dysregulation of Lipid Metabolism Plays a Protective Role in Colorectal Cancer Cells Treated with Gambogic Acid

Novel Xanthone Derivatives Impair Growth and Invasiveness of Colon Cancer Cells In Vitro

Magnetic Hyperthermia in Y79 Retinoblastoma and ARPE-19 Retinal Epithelial Cells: Tumor Selective Apoptotic Activity of Iron Oxide Nanoparticle

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