The use of natural compounds for the targeting and chemoprevention of ovarian cancer

Pistollato, Francesca; Iglesias, Rubén Calderón; Ruíz, R.; Aparicio, Silvia; Crespo, Jorge; López, Luís Alonso Dzul; Giampieri, Francesca; Battino, Maurizio

doi:10.1016/j.canlet.2017.09.050

Cited by 58 publications

(54 citation statements)

References 108 publications

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“…Therefore, CSC‐related molecular changes can enable the development of specific agents for the eradication of tumor‐maintaining CSCs. Natural products, such as EGCG, curcumin, resveratrol, sulforaphane, and withaferin‐A, can diminish the clinically devastating properties of CSCs . For example, curcumin and EGCG can inhibit breast CSCs through downregulating STAT3–NF‐κB signaling .…”

Section: Discussionmentioning

confidence: 99%

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

Jiang

Chen

et al. 2018

J of Cellular Biochemistry

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Non-small-cell lung cancer (NSCLC) appears to be a significant threat to public health worldwide. MicroRNAs have been identified as significant regulators for the development of NSCLC. Previous reports have suggested that hsa-mir-485-5p is dysregulated in various cancers. RXRα, as a kind of nuclear receptor, is an effective target of cancer treatment. Cancer stem cells (CSCs) are recognized as the main cause for tumor metastasis, recurrence, and chemotherapy resistance. However, the mechanism by which hsa-mir-485-5p and RXRα modulate CSCs in NSCLC remains unknown. Here, we found that hsa-mir-485-5p was decreased in serum samples from patients with NSCLC and NSCLC cells. Meanwhile, epigallocatechin-3-gallate (EGCG), an effective anticancer compound extracted from green tea, can enhance hsa-mir-485-5p expression. Hsa-mir-485-5p mimics markedly inhibited NSCLC cell growth and induced cell apoptosis. However, inhibition of hsa-mir-485-5p significantly enriched CSC-like traits. Moreover, bioinformatics analysis predicted the binding correlation between hsa-mir-485-5p and RXRα, which was confirmed by a dual-luciferase reporter assay. We observed that RXRα was increased in NSCLC and EGCG could inhibit RXRα levels dose dependently. In addition, RXRα upregulation or activation expanded the CSC-like properties of NSCLC cells, whereas RXRα inhibition or inactivation could exert a reverse phenomenon. Consistently, in vivo experiments also validated that EGCG could repress the CSC-like characteristics by modulating the hsa-mir-485-5p/RXRα axis. Our findings may reveal a novel molecular mechanism for the treatment of NSCLC.

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Section: Discussionmentioning

confidence: 99%

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

Jiang

Chen

et al. 2018

J of Cellular Biochemistry

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“…8 Natural compounds have aroused increasing attention in the eld of cancer and CSCs due to their high activity and low side effects. [9][10][11] Currently, about 60% of approved anticancer drugs come from unmodied natural products, their semisynthetic derivatives, or molecules synthesized based on natural products. 12,13 18b-glycyrrhetinic acid (GA, 1, Fig.…”

Section: Introductionmentioning

confidence: 99%

Synthesis and discovery of 18β-glycyrrhetinic acid derivatives inhibiting cancer stem cell properties in ovarian cancer cells

Liu

Wang

et al. 2019

RSC Adv.

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“…The potential mechanisms underlying platinum-based chemotherapy involve pharmacological, biochemical, apoptosis and microenvironment resistance (8). Emerging evidences have also indicated that autophagy may be involved in cell survival and chemoresistance mechanisms (9)(10)(11)(12). Macroautophagy (autophagy) is a conserved catabolic pathway in which cytosolic contents, such as damaged organelles, misfolded proteins and bacteria, are transported into lysosomes for degradation (13,14).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of BAG3 attenuates cisplatin resistance by inhibiting autophagy in human epithelial ovarian cancer cells

et al. 2019

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Epithelial ovarian cancer (EOC) is one of the most common malignant gynecological tumors. Interval cytoreductive surgery and cisplatin-based chemotherapy are the standard treatments. However, acquired resistance to cisplatin presents a major challenge for improving the overall survival and prognosis of patients. Recent evidence indicates that cytoprotective functions of autophagy in cancer cells is a potential mechanism for chemoresistance. The present study aimed to investigate the mechanisms responsible for cisplatin resistance in EOC cell lines. The results revealed that cisplatin activated autophagy, measured by an increase in the expression of LC3-II by western blot analysis, protecting ovarian cancer cells from cisplatin toxicity. The present study also identified Bcl-2-associated athanogene 3 (BAG3) as a novel autophagy regulator that serves a role in cisplatin resistance. Treatment with cisplatin was observed to enhance BAG3 expression in parental and cisplatin-resistant ovarian cancer cell lines, and the downregulation of BAG3 blocked cisplatin-induced autophagy, thereby increasing cisplatin sensitivity in the EOC cell lines. In conclusion, BAG3 attenuates cisplatin resistance by inhibiting autophagy, suggesting that downregulation of BAG3 may be a useful therapeutic strategy to overcome cisplatin resistance by preventing cytoprotective autophagy in EOC.

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The use of natural compounds for the targeting and chemoprevention of ovarian cancer

Cited by 58 publications

References 108 publications

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

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

Synthesis and discovery of 18β-glycyrrhetinic acid derivatives inhibiting cancer stem cell properties in ovarian cancer cells

Downregulation of BAG3 attenuates cisplatin resistance by inhibiting autophagy in human epithelial ovarian cancer cells

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