Synergistic Effects of 5-Fluorouracil and Gambogenic Acid on A549 Cells: Activation of Cell Death Caused by Apoptotic and Necroptotic Mechanisms &lt;i&gt;via&lt;/i&gt; the ROS-Mitochondria Pathway

Su, Jingjing; Cheng, Hui; Zhang, Dandan; Wang, Mei; Xie, Chenye; Hu, Yawen; Chang, Hebron C.; Li, Qinglin

doi:10.1248/bpb.b13-00972

Cited by 24 publications

(33 citation statements)

References 27 publications

(29 reference statements)

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“…This is a common phenomenon in today’s chemotherapy with widely spread drug resistance effects from tumors. Most treatments using single anticancer drugs over time have very limited therapeutic efficacy40 due to the drug resistance effect. It is well known that tumor cells exposed to chemotherapeutic agents over time may develop, both in vivo and in vitro , a multidrug resistant (MDR) phenotype, which is generally associated with over-expression of P-glycoprotein (P-gp), the family of multidrug resistance-associated proteins (MRPs) and lung resistance-related protein (LRP)41.…”

Section: Resultsmentioning

confidence: 99%

Extreme Activity of Drug Nanocrystals Coated with A Layer of Non-Covalent Polymers from Self-Assembled Boric Acid

Zhan

Liang

2016

Sci Rep

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Non-covalent polymers have remarkable advantages over synthetic polymers for wide biomedical applications. In this study, non-covalent polymers from self-assembled boric acid were used as the capping reagent to replace synthetic polymers in drug crystallization. Under acidic pH, boric acid self-assembled on the surface of drug nanocrystals to form polymers with network-like structures held together by hydrogen bonds. Coating driven by boric acid self-assembly had negligible effects on drug crystallinity and structure but resulted in drug nanocrystals with excellent dispersion properties that aided in the formation of a more stable suspension. Boric acid coating improved drug stability dramatically by preventing drug molecules from undergoing water hydrolysis in a neutral environment. More importantly, the specific reactivity of orthoboric groups to diols in cell glycocalyx facilitated a rapid cross-membrane translocation of drug nanocrystals, leading to efficient intracellular drug delivery, especially on cancer cells with highly expressed sialic acids. Boric acid coated nanocrystals of camptothecin, an anticancer drug with poor aqueous solubility and stability, demonstrated extreme cytotoxic activity (IC50 < 5.0 μg/mL) to cancer cells compared to synthetic polymer coated CPT nanocrystals and free CPT. Surface coating using non-covalent polymers from self-assembled boric acid will have wide biomedical applications especially in biomaterials and drug delivery field.

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Section: Resultsmentioning

confidence: 99%

Extreme Activity of Drug Nanocrystals Coated with A Layer of Non-Covalent Polymers from Self-Assembled Boric Acid

Zhan

Liang

2016

Sci Rep

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“…Previous studies reported about natural active compound can induce apoptosis and cell cycle arrest in human lung cancer (Peng et al, 2016;Su et al, 2014). Dysregulation of cell proliferation, together with inhibition of the apoptosis pathway, is associated with tumorigenesis (Evan and Vousden, 2001).…”

Section: Discussionmentioning

confidence: 99%

Promising Anticancer Effect of Aurisin A Against the Human Lung Cancer A549 Cell Line

Boueroy

Boonmars

Kanokmedhakul

et al. 2020

Asian Pac J Cancer Prev

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Objective: To investigate the anticancer effect of aurisin A and the underlying mechanisms of its action on the human lung cancer A549 cell line. Methods: Cell viability was determined by sulforhodamine B (SRB) assay, while cell cycle distribution and apoptosis were measured by flow cytometry. The molecular underlying mechanisms of anti-cancer properties of aurisin A was determined by western blot analysis. Results: Aurisin A exerts its anticancer effects by inhibiting cell growth (p<0.001), increasing the proportion of cells at the G0/G1 phase (p<0.001), and decreasing the expression of cyclin D (p<0.05) and cyclin-dependent kinase 4 (Cdk-4) (p<0.001). Nuclear morphological changes were observed in aurisin A-treated cells, demonstrated by a dose-dependent increase in the number of apoptosis cells (p<0.001). After aurisin A treatment, B-cell lymphoma 2 (Bcl-2) was down-regulated (p<0.05), cleaved caspase-3 was up-regulated (p<0.05). In addition, aurisin A inhibits migration of cancer cells in a dose-dependent manner (p<0.001) and decreases the expression of epidermal growth factor receptor (EGFR) (p<0.05) and phosphorylated p38 (pp38) (p<0.05). Conclusion: These results indicated that in-vitro treatment of aurisin A against this human lung cancer cell line inhibits cell proliferation and migration, and induces apoptosis and cell-cycle arrest. Aurisin A is a promising anticancer agent for use against human lung cancer.

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“…The FLIP L protein can also block the recruitment of caspase-8 to DISC, suppressing death receptor-mediated apoptosis (38). Previous studies showed that GA could markedly sensitize chemotherapeutic drug-induced cell death in a range of cancer cells (6,(39)(40)(41). Therefore, based on these studies, this study examined whether GA-induced cFLIP L downregulation could increase the sensitivity to the death ligands, including TRAIL, TNF-α and FasL in human renal cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Gambogic acid induces apoptosis and sensitizes TRAIL-mediated apoptosis through downregulation of cFLIPL in renal carcinoma Caki cells

Jang

Kim

Sung

et al. 2015

International Journal of Oncology

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Gambogic acid (GA) is a natural compound derived from brownish gamboge resin that shows a range of bioactivity, such as antitumor and antimicrobial properties. Although, GA is already known to induce cell death in a variety of cancer cells, the molecular basis for GA-induced cell death in renal cancer cells is unclear. In this study, a treatment with GA induced cell death in human renal carcinoma Caki cells in a dose-dependent manner. Treatment of Caki cells with GA decreased the levels of antiapoptotic proteins, such as Bcl-2 and XIAP in a dose-dependent manner. In addition, GA decreased the expression of the cFLIPL protein, which was downregulated at the transcriptional level without any change in the levels of cFLIPs expression. z-VAD (pan-caspase inhibitor) partially blocked GA-mediated cell death. GA-induced apoptotic cell death in Caki cells is mediated partly by the AIF translocation from the mitochondria into the nucleus via a caspase-independent pathway. In contrast, N-acetylcysteine (NAC), a ROS scavenger, had no effect on GA-induced cell death. The restoration of cFLIPL attenuated GA-induced cell death in Caki cells. Furthermore, a sub-toxic dose of GA sensitized TRAIL-mediated apoptosis in Caki cells. Pretreatment with z-VAD completely blocked GA plus TRAIL-mediated apoptosis. On the contrary, pretreatment with NAC partially inhibited GA plus TRAIL-induced apoptosis. Our findings suggested that GA induces apoptosis via the downregulation of cFLIPL and sensitized TRAIL-mediated apoptosis in Caki cells.

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Synergistic Effects of 5-Fluorouracil and Gambogenic Acid on A549 Cells: Activation of Cell Death Caused by Apoptotic and Necroptotic Mechanisms <i>via</i> the ROS-Mitochondria Pathway

Cited by 24 publications

References 27 publications

Extreme Activity of Drug Nanocrystals Coated with A Layer of Non-Covalent Polymers from Self-Assembled Boric Acid

Extreme Activity of Drug Nanocrystals Coated with A Layer of Non-Covalent Polymers from Self-Assembled Boric Acid

Promising Anticancer Effect of Aurisin A Against the Human Lung Cancer A549 Cell Line

Gambogic acid induces apoptosis and sensitizes TRAIL-mediated apoptosis through downregulation of cFLIPL in renal carcinoma Caki cells

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