Epigallocatechin‐3‐gallate inhibited cancer stem cell–like properties by targeting hsa‐mir‐485‐5p/RXRα in lung cancer

Jiang, Pan; Xu, Chuyue; Chen, Lijun; Chen, Aochang; Wu, Xiaoyue; Zhou, Ming; Haq, Ijaz ul; Mariyam, Zahula; Feng, Qing

doi:10.1002/jcb.27117

Cited by 57 publications

(29 citation statements)

References 41 publications

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“…It was reported that hsa-mir-485-5p was decreased in serum samples from patients with cancer cells. In the meantime, epigallocatechin-3-gallate played a role in the enhancement of hsa-mir-485-5p expression and Hsa-mir-485-5p mimics noticeably induced cell apoptosis and inhibited cancer cell growth [ 136 ]. The treatment of cancer cells with epigallocatechin-3-gallate -induced apoptosis through increased the expression of cleaved caspase-3 and Bax, whereas decreased the expression of Bcl-xL [ 137 ].…”

Section: Role Of Egcg In Inhibition and Prevention Of Various Typementioning

confidence: 99%

Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer

et al. 2020

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Epigallocatechin-3-gallate (EGCG), an active compound of green tea and its role in diseases cure and prevention has been proven. Its role in diseases management can be attributed to its antioxidant and anti-inflammatory properties. The anti-cancer role of this green tea compound has been confirmed in various types of cancer and is still being under explored. EGCG has been proven to possess a chemopreventive effect through inhibition of carcinogenesis process such as initiation, promotion, and progression. In addition, this catechin has proven its role in cancer management through modulating various cell signaling pathways such as regulating proliferation, apoptosis, angiogenesis and killing of various types of cancer cells. The additive or synergistic effect of epigallocatechin with chemopreventive agents has been verified as it reduces the toxicities and enhances the anti-cancerous effects. Despite its effectiveness and safety, the implications of EGCG in cancer prevention is certainly still discussed due to a poor bioavailability. Several studies have shown the ability to overcome poor bioavailability through nanotechnology-based strategies such as encapsulation, liposome, micelles, nanoparticles and various other formulation. In this review, we encapsulate therapeutic implication of EGCG in cancer management and the mechanisms of action are discussed with an emphasis on human clinical trials.

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Section: Role Of Egcg In Inhibition and Prevention Of Various Typementioning

confidence: 99%

Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer

et al. 2020

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“…miR-485-5p directly targeted RXRα in drug-resistant lung cancer cells. EGCG repressed CSC-like properties via modulation of the miR-485-5p/RXRα axis [62]. miR-155 is a tumor suppressor miRNA reportedly involved in enhancing drug sensitivity of cancer cells [63].…”

Section: Tumor Suppressor Mirnasmentioning

confidence: 99%

EGCG Mediated Targeting of Deregulated Signaling Pathways and Non-Coding RNAs in Different Cancers: Focus on JAK/STAT, Wnt/β-Catenin, TGF/SMAD, NOTCH, SHH/GLI, and TRAIL Mediated Signaling Pathways

Farooqi

Pinheiro

Granja

et al. 2020

Cancers

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Decades of research have enabled us to develop a better and sharper understanding of multifaceted nature of cancer. Next-generation sequencing technologies have leveraged our existing knowledge related to intra- and inter-tumor heterogeneity to the next level. Functional genomics have opened new horizons to explore deregulated signaling pathways in different cancers. Therapeutic targeting of deregulated oncogenic signaling cascades by products obtained from natural sources has shown promising results. Epigallocatechin-3-gallate (EGCG) has emerged as a distinguished chemopreventive product because of its ability to regulate a myriad of oncogenic signaling pathways. Based on its scientifically approved anticancer activity and encouraging results obtained from preclinical trials, it is also being tested in various phases of clinical trials. A series of clinical trials associated with green tea extracts and EGCG are providing clues about significant potential of EGCG to mechanistically modulate wide ranging signal transduction cascades. In this review, we comprehensively analyzed regulation of JAK/STAT, Wnt/β-catenin, TGF/SMAD, SHH/GLI, NOTCH pathways by EGCG. We also discussed most recent evidence related to the ability of EGCG to modulate non-coding RNAs in different cancers. Methylation of the genome is also a widely studied mechanism and EGCG has been shown to modulate DNA methyltransferases (DNMTs) and protein enhancer of zeste-2 (EZH2) in multiple cancers. Moreover, the use of nanoformulations to increase the bioavailability and thus efficacy of EGCG will be also addressed. Better understanding of the pleiotropic abilities of EGCG to modulate intracellular pathways along with the development of effective EGCG delivery vehicles will be helpful in getting a step closer to individualized medicines.

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“…Epigallocatechin-3-gallate (EGCG) inhibited cancer stem cells characteristics through regulating RXRα/miR-485-5p axis. 36 Du Moreover, elevated expression of miR-485-3p decreased the ki-67…”

Section: Discussionmentioning

confidence: 99%

MiR‐485‐3p modulates neural stem cell differentiation and proliferation via regulating TRIP6 expression

Shao

et al. 2019

J Cellular Molecular Medi

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Recent references have showed crucial roles of several miRNAs in neural stem cell differentiation and proliferation. However, the expression and role of miR‐485‐3p remains unknown. In our reference, we indicated that miR‐485‐3p expression was down‐regulated during NSCs differentiation to neural and astrocytes cell. In addition, the TRIP6 expression was up‐regulated during NSCs differentiation to neural and astrocytes cell. We carried out the dual‐luciferase reporter and found that overexpression of miR‐485‐3p decreased the luciferase activity of pmirGLO‐TRIP6‐wt but not the pmirGLO‐TRIP6‐mut. Ectopic expression of miR‐485‐3p decreased the expression of TRIP6 in NSC. Ectopic miR‐485‐3p expression suppressed the cell growth of NSCs and inhibited nestin expression of NSCs. Moreover, elevated expression of miR‐485‐3p decreased the ki‐67 and cyclin D1 expression in NSCs. Furthermore, we indicated that miR‐485‐3p reduced proliferation and induced differentiation of NSCs via targeting TRIP6 expression. These data suggested that a crucial role of miR‐485‐3p in self‐proliferation and differentiation of NSCs. Thus, altering miR‐485‐3p and TRIP6 modulation may be one promising therapy for treating with neurodegenerative and neurogenesis diseases.

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Epigallocatechin‐3‐gallate inhibited cancer stem cell–like properties by targeting hsa‐mir‐485‐5p/RXRα in lung cancer

Cited by 57 publications

References 41 publications

Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer

Potential Therapeutic Targets of Epigallocatechin Gallate (EGCG), the Most Abundant Catechin in Green Tea, and Its Role in the Therapy of Various Types of Cancer

EGCG Mediated Targeting of Deregulated Signaling Pathways and Non-Coding RNAs in Different Cancers: Focus on JAK/STAT, Wnt/β-Catenin, TGF/SMAD, NOTCH, SHH/GLI, and TRAIL Mediated Signaling Pathways

MiR‐485‐3p modulates neural stem cell differentiation and proliferation via regulating TRIP6 expression

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