Effects of curcumin on stem-like cells in human esophageal squamous carcinoma cell lines

Almanaa, Taghreed N.; Geusz, Michael E.; Jamasbi, Roudabeh J.

doi:10.1186/1472-6882-12-195

Cited by 44 publications

(47 citation statements)

References 77 publications

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“…The spheroid relapse assay provided the first evidence that a subset of DCLK1 +ve cells may be resistant to curcumin, becoming quiescent/dormant for a period of time before re-forming spheroids (Figs 2A,B), which is a hallmark of stem cells. Resistance of a subset of esophageal squamous-carcinoma cells to curcumin has been reported; but the authors concluded that curcumin eliminates CSCs since ALDHA1 +ve /CD44 +ve CSCs were eliminated by curcumin (24). Another dietary agent was reported to significantly target DCLK1 +ve CSCs, via the Notch signaling pathway (34).…”

Section: Discussionmentioning

confidence: 99%

Curcumin Promotes Autophagic Survival of a Subset of Colon Cancer Stem Cells, Which Are Ablated by DCLK1-siRNA

et al. 2014

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Curcumin is known to induce apoptosis of cancer cells by different mechanisms, but its effects on cancer stem-like cells have been less investigated. Here we report that curcumin promotes the survival of DCLK1-positive colon cancer stem-like cells (CSC), potentially confounding application of its anticancer properties. At optimal concentrations, curcumin greatly reduced expression levels of stem cell markers (DCLK1/CD44/ALDHA1/Lgr5/Nanog) in 3D spheroid cultures and tumor xenografts derived from colon cancer cells. However, curcumin unexpectedly induced proliferation and autophagic survival of a subset of DCLK1-positive CSCs. Spheroid cultures were disintegrated by curcumin in vitro but re-grew within 30–40 days of treatment, suggesting a survival benefit from autophagy, permitting long-term persistence of CRC. Notably, RNAi-mediated silencing of DCLK1 triggered apoptotic cell death of colon cancer cells in vitro and in vivo, and abolished CRC survival in response to curcumin; combination of DCLK1-siRNA and curcumin dramatically reversed CSC phenotype, contributing to attenuation of the growth of spheroid cultures and tumor xenografts. Taken together, our findings confirm a role of DCLK1 in colon cancer stem cells and highlight DCLK1 as a target to enhance antitumor properties of curcumin.

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Section: Discussionmentioning

confidence: 99%

Curcumin Promotes Autophagic Survival of a Subset of Colon Cancer Stem Cells, Which Are Ablated by DCLK1-siRNA

et al. 2014

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“…The literature shows a decreased side population (SP) of C6 glioma cells after daily treatment with curcumin. 22 Quinacrine has been used as an antiprotozoal, antirheumatic, and intrapleural sclerosing agent. It has also been used to induce cancer apoptosis through the mitochondrial pathway.…”

Section: Introductionmentioning

confidence: 99%

The functional curcumin liposomes induce apoptosis in C6 glioblastoma cells and C6 glioblastoma stem cells in vitro and in animals

Wang

Xue

et al. 2017

IJN

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Glioblastoma is a kind of malignant gliomas that is almost impossible to cure due to the poor drug transportation across the blood–brain barrier and the existence of glioma stem cells. We prepared a new kind of targeted liposomes in order to improve the drug delivery system onto the glioma cells and induce the apoptosis of glioma stem cells afterward. In this experiment, curcumin was chosen to kill gliomas, while quinacrine was used to induce apoptosis of the glioma stem cells. Also, p -aminophenyl-α-D-mannopyranoside could facilitate the transport of liposomes across the blood–brain barrier and finally target the brain glioma cells. The cell experiments in vitro indicated that the targeted liposomes could significantly improve the anti-tumor effects of the drugs, while enhancing the uptake effects, apoptosis effects, and endocytic effects of C6 glioma cells and C6 glioma stem cells. Given the animal experiments in vivo, we discovered that the targeted liposomes could obviously increase the survival period of brain glioma-bearing mice and inhibit the growth of gliomas. In summary, curcumin and quinacrine liposomes modified with p -aminophenyl-α-D-mannopyranoside is a potential preparation to treat brain glioma cells and brain glioma stem cells.

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“…Possible therapeutic potential of curcumin was revealed in the last decades. Different studies have explained its efficacy against various types of cancers such as chemo resistant colon cancer cells, esophageal cancers, thyroid carcinomas, skin cancer (2) and as a potent anti-inflammatory agent (3). Curcumin regulates various growth factors, protein kinases, inflammatory cytokines and transcription factors to suppress the metastases and proliferation of human tumors (4).…”

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confidence: 99%

Curcumin: Synthesis optimization andin silicointeraction with cyclin dependent kinase

et al. 2017

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Curcumin: Synthesis optimization and in silico interaction with cyclin dependent kinaseCurcumin is a natural product with enormous biological potential. In this study, curcumin synthesis was revisited using different reaction solvents, a catalyst (n-butylamine) and a water scavenger [(n-BuO) 3 B], to develop the optimal procedure for its rapid acquisition. During synthesis, solvent choice was found to be an important parameter for better curcumin yield and high purity. In a typical reaction, acetyl acetone was treated with boron trioxide, followed by condensation with vanillin in the presence of tri-n-butyl borate as water scavenger and n-butylamine as catalyst at 80 °C in ethyl acetate to afford curcumin. Moreover, curcumin was also extracted from turmeric powder and spectroscopic properties such as IR, MS, 1 H NMR and 13 C NMR with synthetic curcumin were established to identify any impurity. The purity of synthetic and extracted curcumin was also checked by TLC and HPLC-DAD. To computationally assess its therapeutic potential against cyclin dependent kinases (CDKs), curcumin was docked in different isoforms of CDKs. It was observed that it did not dock at the active sites of CDK2 and CDK6. However, it could enter into weak interactions with CDK4 protein.Keywords: curcumin synthesis, CDKs, molecular docking Curcumin (C) is a phenolic compound that is considered to be a bioactive component of turmeric. Since ancient times it has been an integral part of ancient herbal medicine. Nowadays, it is widely used in medicine and in diet supplements. Structurally, curcumin exists in keto and enol tautomeric forms due to intra-molecular hydrogen bonding between keto carbonyl oxygen and an enolic hydrogen atom (1). Possible therapeutic potential of curcumin was revealed in the last decades. Different studies have explained its efficacy against various types of cancers such as chemo resistant colon cancer cells, esophageal cancers, thyroid carcinomas, skin cancer (2) and as a potent anti-inflammatory agent (3). Curcumin regulates various growth factors, protein kinases, inflammatory cytokines and transcription factors to suppress the metastases and proliferation of human tumors (4). Other than anticancer and antitumor activities, it has also shown its effects against a variety of diseases such as respiratory tract infection, hepatic steatosis, skin photoageing, Parkinson's disease, pathogenesis of obesity, diabetes, HIV-associated diarrhea and Alzheimer's disease, through inhibition of amyloid beta oligomer formation (5-8). The structure-activity relationship studies of curcumin molecule against different biological targets have indicated that the presence of two phenyl rings with a C-7 linker with ketoenol function (C=O groups as hydrogen acceptors and C-4 as a hydrogen donor) are most important for its biological activities. However, unsaturation in the linker (conformational flexibility) is important for its antitumor/anticancer activity but not for redox regulatory or apoptotic activities (9). Synthetic methodology to...

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Effects of curcumin on stem-like cells in human esophageal squamous carcinoma cell lines

Cited by 44 publications

References 77 publications

Curcumin Promotes Autophagic Survival of a Subset of Colon Cancer Stem Cells, Which Are Ablated by DCLK1-siRNA

Curcumin Promotes Autophagic Survival of a Subset of Colon Cancer Stem Cells, Which Are Ablated by DCLK1-siRNA

The functional curcumin liposomes induce apoptosis in C6 glioblastoma cells and C6 glioblastoma stem cells in vitro and in animals

Curcumin: Synthesis optimization andin silicointeraction with cyclin dependent kinase

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