scholarly journals Role of oxidative stress in anti-cancer activity of Tripterygium wilfordii

2021 ◽  
Vol 6 (6) ◽  
pp. 50
Author(s):  
LiPing Yang ◽  
Jian Hao ◽  
Dan Chen
Keyword(s):  
Oxidative Stress ◽  
Tripterygium Wilfordii ◽  
Anti Cancer ◽  
Cancer Activity

Synthesis and Anticancer Activity of 9-O-Pyrazole Alkyl Substituted Berberine Derivatives

2019 ◽  
Vol 18 (11) ◽  
pp. 1639-1648 ◽  
Author(s):  
Daipeng Xiao ◽  
Fen He ◽  
Dongming Peng ◽  
Min Zou ◽  
Junying Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Docking ◽  
Anticancer Activity ◽  
Cell Lines ◽  
Human Lung Cancer ◽  
Drug Candidate ◽  
Molecular Docking Study ◽  
Protective Function ◽  
Anti Cancer ◽  
Cancer Activity

Background: Berberine (BBR), an isoquinoline plant alkaloid isolated from plants such as Coptis chinensis and Hydrastis canadensis, own multiple pharmacological activities. Objective: In this study, seven BBR derivatives were synthesized and their anticancer activity against HeLa cervical and A549 human lung cancer cell lines were evaluated in vitro. Methods: The anti-cancer activity was measured by MTT assay, and apoptosis was demonstrated by the annexin V-FITC/PI staining assay. The intracellular oxidative stress was investigated through DCFH-DA assay. The molecular docking study was carried out in molecular operating environment (MOE). Results: Compound B3 and B5 showed enhanced anti-cancer activity compared with BBR, the IC50 for compound B3 and B5 were significantly lower than BBR, and compound B3 at the concentration of 64 or 128 µM induced apoptosis in HeLa and A549 cell lines. The reactive oxygen species (ROS) was generated in both cell lines when treated with 100 µM of all the compounds, and compound B3 and B5 induced higher activity in the generation of ROS, while compound B3 exhibited the highest activity, these results are in accordance with the cytotoxicity results, indicating the cytotoxicity were mostly generated from the oxidative stress. In addition, molecular docking analysis showed that compound B3 had the greatest affinity with Hsp90. Upon binding, the protective function of Hsp90 was lost, which might explain its higher cytotoxicity from molecular interaction aspect. Conclusion: All the results demonstrated that compound B3 and B5 showed significantly higher anti-cancer ability than BBR, and compound B3 is a promising anticancer drug candidate.

scholarly journals The Multifaceted Role of Flavonoids in Cancer Therapy: Leveraging Autophagy with a Double-Edged Sword

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1138
Author(s):  
Zhe Zhang ◽  
Jiayan Shi ◽  
Edouard C. Nice ◽  
Canhua Huang ◽  
Zheng Shi
Keyword(s):  
Cancer Therapy ◽  
Dosage Forms ◽  
Pharmacological Effects ◽  
Autophagy Flux ◽  
Normal Tissues ◽  
Anti Cancer ◽  
New Perspective ◽  
New Research ◽  
Cancer Activity

Flavonoids are considered as pleiotropic, safe, and readily obtainable molecules. A large number of recent studies have proposed that flavonoids have potential in the treatment of tumors by the modulation of autophagy. In many cases, flavonoids suppress cancer by stimulating excessive autophagy or impairing autophagy flux especially in apoptosis-resistant cancer cells. However, the anti-cancer activity of flavonoids may be attenuated due to the simultaneous induction of protective autophagy. Notably, flavonoids-triggered protective autophagy is becoming a trend for preventing cancer in the clinical setting or for protecting patients from conventional therapeutic side effects in normal tissues. In this review, focusing on the underlying autophagic mechanisms of flavonoids, we hope to provide a new perspective for clinical application of flavonoids in cancer therapy. In addition, we highlight new research ideas for the development of new dosage forms of flavonoids to improve their various pharmacological effects, establishing flavonoids as ideal candidates for cancer prevention and therapy in the clinic.

scholarly journals Advances and challenges in cancer treatment and nutraceutical prevention: the possible role of dietary phenols in BRCA regulation

2021 ◽  
Author(s):  
Haroon Khan ◽  
Fabiana Labanca ◽  
Hammad Ullah ◽  
Yaseen Hussain ◽  
Nikolay T. Tzvetkov ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Natural Products ◽  
Cancer Treatment ◽  
Clinical Aspects ◽  
Anti Cancer ◽  
Brca 1 ◽  
Brca 2 ◽  
The Impact ◽  
Cancer Activity

AbstractOver the years, the attention towards the role of phytochemicals in dietary natural products in reducing the risk of developing cancer is rising. Cancer is the second primary cause of mortality worldwide. The current therapeutic options for cancer treatment are surgical excision, immunotherapy, chemotherapy, and radiotherapy. Unfortunately, in case of metastases or chemoresistance, the treatment options become very limited. Despite the advances in medical and pharmaceutical sciences, the impact of available treatments on survival is not satisfactory. Recently, natural products are a great deal of interest as potential anti-cancer agents. Among them, phenolic compounds have gained a great deal of interest, thanks to their anti-cancer activity. The present review focuses on the suppression of cancer by targeting BRCA gene expression using dietary polyphenols, as well as the clinical aspects of polyphenolic agents in cancer therapy. They regulate specific key processes involved in cancer progression and modulate the expression of oncogenic proteins, like p27, p21, and p53, which may lead to apoptosis, cell cycle arrest, inhibition of cell proliferation, and, consequently, cancer suppression. Thus, one of the mechanisms underlying the anti-cancer activity of phenolics involves the regulation of tumor suppressor genes. Among them, the BRCA genes, with the two forms (BRCA-1 and BRCA-2), play a pivotal role in cancer protection and prevention. BRCA germline mutations are associated with an increased risk of developing several types of cancers, including ovarian, breast, and prostate cancers. BRCA genes also play a key role in the sensitivity and response of cancer cells to specific pharmacological treatments. As the importance of BRCA-1 and BRCA-2 in reducing cancer invasiveness, repairing DNA damages, oncosoppression, and cell cycle checkpoint, their regulation by natural molecules has been examined.

scholarly journals Taraxerol protects the human hepatic L02 cells from hydrogen peroxide-induced apoptosis

2017 ◽  
Vol 12 (2) ◽  
pp. 20 ◽  
Author(s):  
Xiang-Yang Yao ◽  
Qin Bai
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Caspase 3 ◽  
Protective Agent ◽  
Cytoprotective Effect ◽  
Lactate Dehydrogenase Release ◽  
Anti Cancer ◽  
Induced Apoptosis ◽  
L02 Cells ◽  
Cancer Activity

<p class="Abstract">Taraxerol is known to exhibit anti-inflammatory and anti-cancer activity. However, cytoprotective effect of taraxerol on hepatocytes has not been reported. In the present study, we investigated the hepatoprotective effect of taraxerol in the human hepatic L02 cells injured by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). Taraxerol decreased H<sub>2</sub>O<sub>2</sub>-induced cell viability loss and lactate dehydrogenase release. Taraxerol also inhibited H<sub>2</sub>O<sub>2</sub>-induced cell apoptosis. Further, taraxerol attenuated H<sub>2</sub>O<sub>2</sub>-induced increase in cleaved-caspase-3 and cleaved-PARP. H<sub>2</sub>O<sub>2</sub>-activated p38 and JNK were also inhibited by taraxerol. These data suggest that taraxerol could protect the L02 cells against H<sub>2</sub>O<sub>2</sub>-induced apoptosis via suppression of p38 and JNK. Taraxerol may be an effective protective agent against oxidative stress-induced liver injury.</p>

scholarly journals Role of cell cycle events and apoptosis in mediating the anti-cancer activity of a silver(I) complex of 4-hydroxy-3-nitro-coumarin-bis(phenanthroline) in human malignant cancer cells

2009 ◽  
Vol 602 (2-3) ◽  
pp. 203-214 ◽  
Author(s):  
Bhumika Thati ◽  
Andy Noble ◽  
Bernadette S. Creaven ◽  
Maureen Walsh ◽  
Malachy McCann ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Anti Cancer ◽  
Cancer Activity

scholarly journals Oxidative stress induced by the anti-cancer agents, plumbagin, and atovaquone, inhibits ion transport through Na+/K+-ATPase

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yousef Alharbi ◽  
Arvinder Kapur ◽  
Mildred Felder ◽  
Lisa Barroilhet ◽  
Bikash R. Pattnaik ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ion Transport ◽  
Ovarian Cancer Cell ◽  
Oxygen Radical ◽  
Radical Scavenger ◽  
Patch Clamping ◽  
Cytotoxic Effects ◽  
Ovarian Cancer Cell Lines ◽  
Anti Cancer

Abstract Oxidative stress inhibits Na+/K+-ATPase (NKA), the ion channel that maintains membrane potential. Here, we investigate the role of oxidative stress-mediated by plumbagin and atovaquone in the inhibition of NKA activity. We confirm that plumbagin and atovaquone inhibit the proliferation of three human (OVCAR-3, SKOV-3, and TYKNu) and one mouse (ID8) ovarian cancer cell lines. The oxygen radical scavenger, N-acetylcysteine (NAC), attenuates the chemotoxicity of plumbagin and atovaquone. Whole-cell patch clamping demonstrates that plumbagin and atovaquone inhibit outward and the inward current flowing through NKA in SKOV-3 and OVCAR-3. Although both drugs decrease cellular ATP; providing exogenous ATP (5 mM) in the pipet solution used during patch clamping did not recover NKA activity in the plumbagin or atovaquone treated SKOV-3 and OVCAR-3 cells. However, pretreatment of the cells with NAC completely abrogated the NKA inhibitory activity of plumbagin and atovaquone. Exposure of the SKOV-3 cells to either drug significantly decreases the expression of NKA. We conclude that oxidative stress caused by plumbagin and atovaquone degrades NKA, resulting in the inability to maintain ion transport. Therefore, when evaluating compounds that induce oxidative stress, it is important to consider the contribution of NKA inhibition to their cytotoxic effects on tumor cells.

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