The Role of Curcumin in Cancer Treatment

Zoi, Vasiliki; Galani, Vasiliki; Lianos, Georgios D; Voulgaris, Spyridon; Kyritsis, Athanassios P.; Alexiou, George Α.

doi:10.3390/biomedicines9091086

Cited by 132 publications

(56 citation statements)

References 151 publications

(149 reference statements)

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“…CUR is an effective scavenger of ROS, which are generated in excess due to environmental influences [ 28 ]. In contrast to its antioxidant activity, higher than micro-molar concentrations of CUR inducing ROS were documented with significant anticancer activities in many in vitro models of cancer cells as well as in animal models and clinical trials [ 9 , 29 ]. Therefore, CUR can both decrease and increase the cellular levels of ROS that may rely on its concentration at the target site and the affected cells.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Induces Apoptosis of Chemoresistant Lung Cancer Cells via ROS-Regulated p38 MAPK Phosphorylation

Huang

Chiu

et al. 2022

IJMS

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This study aimed to challenge chemoresistance by curcumin (CUR) with drug-selected human lung cancer A549 sublines that continuously proliferate in the present of docetaxel (DOC) and vincristine (VCR). Their sensitivities to CUR were measured by MTT assay and the particular intracellular reactive oxygen species (ROS) was detected by fluorescence activated cell sorting (FACS) analysis. Apoptosis was analyzed by Annexin V assay of the flow cytometry. Inhibitors and RNA interference were used to examine the signaling pathway regulated by the kinases. The obtained data demonstrated that CUR induces chemoresistant cell apoptosis by generating ROS and application of N-acetylcysteine (NAC) blocks ROS production, resulting in apoptosis suppression. Phosphorylation of extracellular regulated kinase (ERK), p38 MAPK, and eIF-2α were increased but c-Jun N-terminal kinase (JNK) did not increase when chemoresistant cells were treated with CUR. Downregulation of ERK and p38 MAPK phosphorylation by their inhibitors had no effect on CUR-induced apoptosis. Interestingly, the knockdown of p38 MAPK with shRNA significantly reduced CUR-induced apoptosis on the chemoresistant sublines. Phosphorylation of the eIF-2α protein was inhibited when p38 MAPK was knocked down in DOC-resistant A549 cells, but a high level of phosphorylated eIF-2α protein remained on the VCR-resistant A549 cells when p38 MAPK was knocked down. These data confirmed that CUR-augmented ROS potently induced apoptosis via upregulated p38 MAPK phosphorylation. Therefore, activated p38 MAPK is considered a pro-apoptotic signal for CUR-induced apoptosis of chemoresistant human lung cancer cells.

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Section: Discussionmentioning

confidence: 99%

Curcumin Induces Apoptosis of Chemoresistant Lung Cancer Cells via ROS-Regulated p38 MAPK Phosphorylation

Huang

Chiu

et al. 2022

IJMS

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“…We have previously described the importance of hypoxia in treatment response. Several studies have explored the effect of hypoxic radiosensitizer to overcome the radioresistence mechanisms induced by low oxygen levels inside the tumour mass [ 53 , 54 , 55 , 56 , 57 ]. Among them, the DAHANCA 5 trial tested the hypoxia modifier nimorazole in combination with radiotherapy on HNSCC patients [ 58 , 59 ].…”

Section: Hncs Clinical Approachesmentioning

confidence: 99%

Precision Medicine in Head and Neck Cancers: Genomic and Preclinical Approaches

Miserocchi

Spadazzi

Calpona

et al. 2022

JPM

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Head and neck cancers (HNCs) represent the sixth most widespread malignancy worldwide. Surgery, radiotherapy, chemotherapeutic and immunotherapeutic drugs represent the main clinical approaches for HNC patients. Moreover, HNCs are characterised by an elevated mutational load; however, specific genetic mutations or biomarkers have not yet been found. In this scenario, personalised medicine is showing its efficacy. To study the reliability and the effects of personalised treatments, preclinical research can take advantage of next-generation sequencing and innovative technologies that have been developed to obtain genomic and multi-omic profiles to drive personalised treatments. The crosstalk between malignant and healthy components, as well as interactions with extracellular matrices, are important features which are responsible for treatment failure. Preclinical research has constantly implemented in vitro and in vivo models to mimic the natural tumour microenvironment. Among them, 3D systems have been developed to reproduce the tumour mass architecture, such as biomimetic scaffolds and organoids. In addition, in vivo models have been changed over the last decades to overcome problems such as animal management complexity and time-consuming experiments. In this review, we will explore the new approaches aimed to improve preclinical tools to study and apply precision medicine as a therapeutic option for patients affected by HNCs.

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“…A half maximal HDAC inhibitory concentration was reported at a level of micromolar (IC 50 : 115 µM) [14]. Previous reports showed that CU induced cytotoxicity in NSCLCs via the inhibition of cell proliferation and differentiation, induction of apoptosis, induction of cell cycle arrest at G2/M phases, and induction of ROS production, contributing to the activation of the DNA damage signaling pathway [15]. Nevertheless, the clinical applications of CU are limited by its poor water solubility, rapid metabolism, and high toxicity in non-cancer cells.…”

Section: Introductionmentioning

confidence: 99%

HDAC Inhibitory and Anti-Cancer Activities of Curcumin and Curcumin Derivative CU17 against Human Lung Cancer A549 Cells

et al. 2022

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Previous research reported that the curcumin derivative (CU17) inhibited several cancer cell growths in vitro. However, its anticancer potential against human lung cancer cells (A549 cell lines) has not yet been evaluated. The purpose of this research was to examine the HDAC inhibitory and anti-cancer activities of CU17 compared to curcumin (CU) in A549 cells. An in vitro study showed that CU17 had greater HDAC inhibitory activity than CU. CU17 inhibited HDAC activity in a dose dependent manner with the half-maximal inhibitory concentration (IC50) value of 0.30 ± 0.086 µg/mL against HDAC enzymes from HeLa nuclear extract. In addition, CU17 could bind at the active pockets of both human class I HDACs (HDAC1, 2, 3, and 8) and class II HDACs (HDAC4, 6, and 7) demonstrated by molecular docking studies, and caused hyperacetylation of histone H3 (Ac-H3) in A549 cells shown by Western blot analysis. MTT assay indicated that both CU and CU17 suppressed A549 cell growth in a dose- and time-dependent manner. Besides, CU and CU17 induced G2/M phase cell cycle arrest and p53-independent apoptosis in A549 cells. Both CU and CU17 down-regulated the expression of p53, p21, Bcl-2, and pERK1/2, but up-regulated Bax expression in this cell line. Although CU17 inhibited the growth of lung cancer cells less effectively than CU, it showed less toxicity than CU for non-cancer cells. Accordingly, CU17 is a promising agent for lung cancer treatment. Additionally, CU17 synergized the antiproliferative activity of Gem in A549 cells, indicating the possibility of employing CU17 as an adjuvant treatment to enhance the chemotherapeutic effect of Gem in lung cancer.

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The Role of Curcumin in Cancer Treatment

Cited by 132 publications

References 151 publications

Curcumin Induces Apoptosis of Chemoresistant Lung Cancer Cells via ROS-Regulated p38 MAPK Phosphorylation

Curcumin Induces Apoptosis of Chemoresistant Lung Cancer Cells via ROS-Regulated p38 MAPK Phosphorylation

Precision Medicine in Head and Neck Cancers: Genomic and Preclinical Approaches

HDAC Inhibitory and Anti-Cancer Activities of Curcumin and Curcumin Derivative CU17 against Human Lung Cancer A549 Cells

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