Curcumin Exerts Cytotoxicity Dependent on Reactive Oxygen Species Accumulation in Non-Small-Cell Lung Cancer Cells

Wang, Cuijuan; Song, Xingguo; Shang, Ming; Zou, Wei; Zhang, Mengping; Wei, Haiyan; Shao, Hua

doi:10.2217/fon-2018-0708

Cited by 51 publications

(35 citation statements)

References 31 publications

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“…Radiation‐induced ROS leads to the accumulation of misfolded or abnormal proteins in the ER, which causes ER stress. Because ER stress is a critical inducer of apoptosis, previous studies focused on the link between ER stress and the enhanced radiosensitivity of cancer cells . Of note, Matsuo et al .…”

Section: Discussionmentioning

confidence: 99%

“…Because ER stress is a critical inducer of apoptosis, previous studies focused on the link between ER stress and the enhanced radiosensitivity of cancer cells. [15][16][17][18] Of note, Matsuo et al found that overexpression of TMXs in 293 cells significantly attenuated ER stress and delayed the onset of ER stress-induced cell death. 13 These findings suggest that TMX1 and TMX2 might protect NSCLC against radiationinduced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

et al. 2020

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Background Radioresistance of some non‐small cell lung cancer (NSCLC) types increases the risk of recurrence or metastasis in afflicted patients, following radiotherapy. As such, further improvements to NSCLC radiotherapy are needed. The expression of oncogene TP53‐regulated inhibitor of apoptosis 1 (TRIAP1) in NSCLC is increased following irradiation. Furthermore, gene set enrichment analysis (GSEA) has suggested that TRIAP1 might be involved in maintaining redox homeostasis. This in turn might enhance cell radioresistance. Methods In this study we irradiated human NSCLC cell lines (A549 and H460), while knocking down TRIAP1, to determine whether a disrupted redox homeostasis could attenuate radioresistance. Results Irradiation notably increased both mRNA and protein levels of TRIAP1. In addition, TRIAP1 knockdown decreased the expression of several antioxidant proteins, including thioredoxin‐related transmembrane protein (TMX) 1, TMX2, thioredoxin (TXN), glutaredoxin (GLRX) 2, GLRX3, peroxiredoxin (PRDX) 3, PRDX4, and PRDX6 in A549 and H460 cells. In addition, silencing TRIAP1 impaired the radiation‐induced increase of the aforementioned proteins. Continuing along this line, we observed a radiation‐induced reduction of cell viability and invasion, as well as increased apoptosis and intracellular reactive oxygen species following TRIAP1 knockdown. Conclusions In summary, we identified TRIAP1 as a key contributor to the radioresistance of NSCLC by maintaining redox homeostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

et al. 2020

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“…A monocarbonyl analog of curcumin (Wz35) has the capability of stimulation of apoptotic cell death in NSCLC cells. During ER stress, unfolded protein response (UPR) is activated via the induction of eukaryotic initiation factor 2α (elF2α) phosphorylation (C. Wang et al, 2019, 2020). Then ATF4 undergoes upregulation that subsequently triggers CHOP and ER stress‐mediated apoptosis (E.‐S.…”

Section: Curcumin and Lung Cancermentioning

confidence: 99%

Versatile role of curcumin and its derivatives in lung cancer therapy

Ashrafizadeh

Najafi

Makvandi

et al. 2020

Journal Cellular Physiology

104

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Lung cancer is a main cause of death all over the world with a high incidence rate. Metastasis into neighboring and distant tissues as well as resistance of cancer cells to chemotherapy demand novel strategies in lung cancer therapy. Curcumin is a naturally occurring nutraceutical compound derived from Curcuma longa (turmeric) that has great pharmacological effects, such as anti‐inflammatory, neuroprotective, and antidiabetic. The excellent antitumor activity of curcumin has led to its extensive application in the treatment of various cancers. In the present review, we describe the antitumor activity of curcumin against lung cancer. Curcumin affects different molecular pathways such as vascular endothelial growth factors, nuclear factor‐κB (NF‐κB), mammalian target of rapamycin, PI3/Akt, microRNAs, and long noncoding RNAs in treatment of lung cancer. Curcumin also can induce autophagy, apoptosis, and cell cycle arrest to reduce the viability and proliferation of lung cancer cells. Notably, curcumin supplementation sensitizes cancer cells to chemotherapy and enhances chemotherapy‐mediated apoptosis. Curcumin can elevate the efficacy of radiotherapy in lung cancer therapy by targeting various signaling pathways, such as epidermal growth factor receptor and NF‐κB. Curcumin‐loaded nanocarriers enhance the bioavailability, cellular uptake, and antitumor activity of curcumin. The aforementioned effects are comprehensively discussed in the current review to further direct studies for applying curcumin in lung cancer therapy.

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“…Another synthetic nanomaterial, chitosan nanoparticles loaded with demethoxycurcumin in combination with cisplatin, downregulates the expression levels of thymidine phosphorylase required for DNA self-repairing pyrimidine salvage pathways and induces apoptosis in non-small cell lung cancer (NSCLC) cell lines (38). Moreover, Wang et al (27) demonstrated that in NSCLC, curcumin decreases the mitochondrial transmembrane potential and increases the accumulation of reactive oxygen species (ROS) in cells, inducing DNA and mitochondrial damage-mediated apoptosis (39).…”

Section: Curcumin and Tumor Proliferation Previous Studies Havementioning

confidence: 99%

The roles of curcumin in regulating the tumor immunosuppressive microenvironment (Review)

et al. 2020

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Cancer is a harmful threat to human health. In addition to surgery, a variety of anticancer drugs are increasingly used in cancer therapy; however, despite the developments in multimodality treatment, the morbidity and mortality of patients with cancer patients are on the increase. The tumor-specific immunosuppressive microenvironment serves an important function in tumor tolerance and escape from immune surveillance leading to tumor progression. Therefore, identifying new drugs or foods that can enhance the tumor immune response is critical to develop improved cancer prevention methods and treatment. Curcumin, a polyphenolic compound extracted from ginger, has been shown to effectively inhibit tumor growth, proliferation, invasion, metastasis and angiogenesis in a variety of tumors. Recent studies have also indicated that curcumin can modulate the tumor immune response and remodel the tumor immunosuppressive microenvironment, indicating its potential in the immunotherapy of cancer. In this review, a brief introduction to the effects of curcumin on the tumor immune response and tumor immune microenvironment is provided and recent clinical trials investigating the potential of curcumin in cancer therapy are discussed.

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Curcumin Exerts Cytotoxicity Dependent on Reactive Oxygen Species Accumulation in Non-Small-Cell Lung Cancer Cells

Cited by 51 publications

References 31 publications

TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

TRIAP1 knockdown sensitizes non‐small cell lung cancer to ionizing radiation by disrupting redox homeostasis

Versatile role of curcumin and its derivatives in lung cancer therapy

The roles of curcumin in regulating the tumor immunosuppressive microenvironment (Review)

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