EGCG Enhances Cisplatin Sensitivity by Regulating Expression of the Copper and Cisplatin Influx Transporter CTR1 in Ovary Cancer

Wang, Xuemin; Jiang, Pan; Wang, Pengqi; Yang, Chung S.; Wang, Xuerong; Feng, Qing

doi:10.1371/journal.pone.0125402

Cited by 59 publications

(58 citation statements)

References 49 publications

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“…Our previous study found that EGCG reversed cDDP-triggered CTR1 degradation in ovarian cancer cells [14], and the present study confirmed this effect in NSCLC cells (Figure 3C–3D). Taken together, these results suggest that EGCG-induced CTR1 expression increased cellular Pt levels.…”

Section: Resultssupporting

confidence: 88%

“…Our previous study demonstrated that the green tea polyphenol, EGCG, induced cDDP transporter CTR1 expression and enhanced cDDP sensitivity in ovarian cancer [14]. In the current study, we confirmed these results in NSCLC in vitro and in vivo and further explored the mechanism of EGCG-mediated CTR1 expression.…”

Section: Discussionsupporting

confidence: 86%

“…Our previous study showed that (−)-epigallocatechin-3-gallate (EGCG), the most abundant and powerful cancer chemopreventive polyphenol in green tea [13], induces CTR1 expression and inhibits its rapid degradation by cDDP in ovarian cancer cells and mouse xenografts [14]. EGCG in combination with cDDP improves cDDP and DNA-platinum adduct accumulation, which enhances ovarian cancer cell sensitivity to the chemotherapeutic agent [14].…”

Section: Introductionmentioning

confidence: 99%

“…EGCG in combination with cDDP improves cDDP and DNA-platinum adduct accumulation, which enhances ovarian cancer cell sensitivity to the chemotherapeutic agent [14]. …”

Section: Introductionmentioning

confidence: 99%

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NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

et al. 2016

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Platinum-based drugs are the firstline of treatment for non-small cell lung cancer (NSCLC), but resistance to these drugs is a major obstacle to effective chemotherapy. Our previous study revealed that the green tea polyphenol, EGCG, induced cisplatin transporter CTR1 (copper transporter 1) and enhanced cisplatin sensitivity in ovarian cancer. In this study, we found that EGCG upregulated CTR1 and increased platinum accumulation in NSCLC (A549, H460 and H1299) cells, cDDP-resistant A549 cells and a nude mouse xenograft model. Cisplatin-induced inhibition of cell growth was enhanced by EGCG treatment in vitro and in vivo. MicroRNA hsa-mir-98-5p appears to suppress CTR1 gene expression, while long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) appears to enhance it. Bioinformatics analysis showed that hsa-mir-98-5p has specific complementary binding sites for NEAT1. In addition, hsa-mir-98-5p was predicted to be a putative CTR1 target. NEAT1 may act as a competing endogenous lncRNA to upregulate EGCG-induced CTR1 by sponging hsa-mir-98-5p in NSCLC. Our findings reveal a novel mechanism how NEAT1 upregulates EGCG-induced CTR1 and enhances cisplatin sensitivity in vitro and in vivo, and suggest EGCG could serve as an effective adjuvant chemotherapeutic in lung cancer treatment.

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Section: Resultssupporting

confidence: 88%

Section: Discussionsupporting

confidence: 86%

Section: Introductionmentioning

confidence: 99%

“…EGCG in combination with cDDP improves cDDP and DNA-platinum adduct accumulation, which enhances ovarian cancer cell sensitivity to the chemotherapeutic agent [14]. …”

Section: Introductionmentioning

confidence: 99%

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NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

et al. 2016

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“…Additionally, EGCG was found to exert its anti-cancer activity by mobilizing increased copper generated in a carcinogen-induced rat model of HCC [48]. In an ovarian cancer xenograft, EGCG was shown to increase copper transporter 1 ( Ctr1 ) expression and sensitize tumors to cisplatin [49]. Administration of EGCG suppressed VEGF levels and increased p-p38 levels to inhibit liver metastasis in a colon carcinoma xenograft model [50].…”

Section: Whole Vs Isolated Compound Entitiesmentioning

confidence: 99%

Food-based natural products for cancer management: Is the whole greater than the sum of the parts?

Hussain

Kumar

Ghosh

2016

Seminars in Cancer Biology

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The rise in cancer incidence and mortality in developing countries together with the human and financial cost of current cancer therapy mandates a closer look at alternative ways to overcome this burgeoning global healthcare problem. Epidemiological evidence for the association between cancer and diet and the long latency of most cancer progression have led to active exploration of whole and isolated natural chemicals from different naturally occurring substances in various preclinical and clinical settings. In general the lack of systemic toxicities of most ‘whole’ and ‘isolated’ natural compounds, their potential to reduce toxic doses and potential to delay the development of drug-resistance makes them promising candidates for cancer management. This review article examines the suggested molecular mechanisms affected by these substances focusing to a large extent on prostate cancer and deliberates on the disparate results obtained from cell culture, preclinical and clinical studies in an effort to highlight the use of whole extracts and isolated constituents for intervention. As such these studies underscore the importance of factors such as treatment duration, bioavailability, route of administration, selection criteria, standardized formulation and clinical end points in clinical trial design with both entities. Overall lack of parallel comparison studies between the whole natural products and their isolated compounds limits decisive conclusions regarding the superior utility of one over the other. We suggest the critical need for rigorous comparative research to identify which one of the two or both entities from nature would be best qualified to take on the mantle of cancer management.

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Copper‐Related Cell Death and the Role of Copper in Head and Neck Squamous Cell Carcinoma and Therapeutic Strategies

Zhang,

Wu,

Wang

et al. 2024

Advanced Therapeutics

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As an essential mineral element for the human body, copper (Cu) is necessary for various physiological functions. Excess or deficiency of copper causes cytotoxicity and damages the body. Thus, strict regulatory mechanisms are required to maintain copper homeostasis. Copper correlates closely to many forms of cell death. A recent study found that copper‐dependent cell death, known as cuproptosis, is different from all other known forms of cell death. This discovery helps us further understand the role of copper in cytotoxicity. Copper dysregulation occurs in a variety of malignancies, including head and neck squamous cell carcinoma (HNSCC), which is the eighth most common malignancy worldwide. This may increase the risk of HNSCC from a population perspective. Further exploring molecular mechanisms of copper in HNSCC will contribute to provide new therapeutic opportunities. Here we review the physiological metabolism and functions of copper, as well as copper‐related cell death. We focus on the research advances of copper in HNSCC, including the epidemiology and molecular mechanisms, as well as therapeutic strategies targeting copper homeostasis.This article is protected by copyright. All rights reserved

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EGCG Enhances Cisplatin Sensitivity by Regulating Expression of the Copper and Cisplatin Influx Transporter CTR1 in Ovary Cancer

Cited by 59 publications

References 49 publications

NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

NEAT1 upregulates EGCG-induced CTR1 to enhance cisplatin sensitivity in lung cancer cells

Food-based natural products for cancer management: Is the whole greater than the sum of the parts?

Copper‐Related Cell Death and the Role of Copper in Head and Neck Squamous Cell Carcinoma and Therapeutic Strategies

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