Quercetin suppresses breast cancer stem cells (CD44 + /CD24 − ) by inhibiting the PI3K/Akt/mTOR-signaling pathway

Li, Xiuli; Zhou, Na; Jin, Wu; Liu, Zhijie; Wang, Xiaohui; Zhang, Qin; Liu, Qing‐Yan; Gao, Lifeng; Wang, Rong

doi:10.1016/j.lfs.2018.01.014

Cited by 132 publications

(80 citation statements)

References 28 publications

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“…Prostate cancer stem cell↓; Breast cancer stem cells↓; Glioblastoma stem cells↓; Gastric cancer stem cells↓; Colorectal cancer stem cells↓; Pancreatic cancer stem↓…”

Section: Introductionmentioning

confidence: 99%

Traditional Chinese medicine as a cancer treatment: Modern perspectives of ancient but advanced science

et al. 2019

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Traditional Chinese medicine (TCM) has been practiced for thousands of years and at the present time is widely accepted as an alternative treatment for cancer. In this review, we sought to summarize the molecular and cellular mechanisms underlying the chemopreventive and therapeutic activity of TCM, especially that of the Chinese herbal medicine‐derived phytochemicals curcumin, resveratrol, and berberine. Numerous genes have been reported to be involved when using TCM treatments and so we have selectively highlighted the role of a number of oncogene and tumor suppressor genes in TCM therapy. In addition, the impact of TCM treatment on DNA methylation, histone modification, and the regulation of noncoding RNAs is discussed. Furthermore, we have highlighted studies of TCM therapy that modulate the tumor microenvironment and eliminate cancer stem cells. The information compiled in this review will serve as a solid foundation to formulate hypotheses for future studies on TCM‐based cancer therapy.

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“…Prostate cancer stem cell↓; Breast cancer stem cells↓; Glioblastoma stem cells↓; Gastric cancer stem cells↓; Colorectal cancer stem cells↓; Pancreatic cancer stem↓…”

Section: Introductionmentioning

confidence: 99%

Traditional Chinese medicine as a cancer treatment: Modern perspectives of ancient but advanced science

et al. 2019

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“…Nobiletin inhibits CD36-dependent tumor angiogenesis, migration, invasion and sphere formation through the CD36/Stat3/Nf-Kb signaling axis [30,31]. Quercetin suppresses breast CSCs through its inhibition of the PI3K/Akt/mTOR signaling pathway [32]. Despite numerous studies, there are no studies on tangeretin-induced antiproliferative and anti-CSC effects.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Tangeretin, a Citrus Peel-Derived Flavonoid, on Breast Cancer Stem Cell Formation through Suppression of Stat3 Signaling

Choi

Liu

et al. 2020

Molecules

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Breast cancer stem cells (BCSCs) are responsible for tumor chemoresistance and recurrence. Targeting CSCs using natural compounds is a novel approach for cancer therapy. A CSC-inhibiting compound was purified from citrus extracts using silica gel, gel filtration and high-pressure liquid chromatography. The purified compound was identified as tangeretin by using nuclear magnetic resonance (NMR). Tangeretin inhibited cell proliferation, CSC formation and tumor growth, and modestly induced apoptosis in CSCs. The frequency of a subpopulation with a CSC phenotype (CD44+/CD24−) was reduced by tangeretin. Tangeretin reduced the total level and phosphorylated nuclear level of signal transducer and activator of transcription 3 (Stat3). Our results in this study show that tangeretin inhibits the Stat3 signaling pathway and induces CSC death, indicating that tangeretin may be a potential natural compound that targets breast cancer cells and CSCs.

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“…When searching for the genes related to ELF5-mediated breast cancer cells effects, we tend to select cancer stem cell marker molecule, especially in breast cancer metastasis. The CD24 phonotype has been reported to express in breast cancer stem cells [23]. Studies have shown that the expression of ELF5 regulates the fate of breast stem/progenitor cells, which let us to explore the possibility of ELF5 regulating CD24 expression.…”

Section: Cd24 Is Transcriptional Regulated By Elf5mentioning

confidence: 99%

ELF5 inhibits migration and invasion of breast cancer cells via regulating CD24 expression

2020

Preprint

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Objective: E74-like factor five (ELF5) is a basic transcriptional factor that plays a key role in breast tissue and glandular development. However, the molecular mechanism by which ELF5 mediates the biological functions of breast cancer cells has not been elucidated. We hypothesize that ELF5 regulate CD24 transcription though an E26 transforming sequence (ETS) cis-element in the CD24 promoter region.Methods: Human breast cancer cell line MCF-7 was transfected with Myc-ELF5 plasmid in over-expression experiment. T47D cells were transfected with ELF5-shRNA plasmid in knockout experiment. The expression level of ELF5 `protein was analyzed by Western blot. MTT assays and Clonal formation assays were used to assess the proliferation properties of cells. Scratch wound-healing assays were performed to determine cell migration and invasive activities. CD24 protein expression was analysis by flow cytometry. Using the bioinformatics tool JASPAR, we identified high-scoring ETS-like sequences in the CD24 gene promoter. To confirm the ETS, Chromatin immunoprecipitation (ChIP) analysis was used. DNA fragments of a putative or mutated ETS-like sequence were synthesized and ligated into a pGL3 basic plasmid to construct the CD24 promoter luciferase reporter systems which was used to detect ELF5 regulation of CD24 transcriptional activity.Results: In this study, we examined the effect of ELF5 on human breast cancer cell lines MCF-7 and T49D, and confirmed that ELF5 act as a suppressor of cell proliferation, migration and invasion. In further research, the interaction between ELF5 and CD24 was characterized in breast cancer cells. We found that CD24 was a target gene of ELF5 through ChIP-Sequence assays, and proved that ELF5 could bind to ETS cis-element on the proximal promoter of CD24 gene. Importantly, experiments verified that CD24 was upregulated after ELF5 overexpression in MCF-7 cells, while knockdown of CD24 expression caused MCF-7 cells to restore cell proliferation, migration and invasion activity in adaptive ELF5 expression.Conclusions: This study not only found that ELF5 can inhibit cell proliferation, migration and invasion in breast cancer cells, but also found that ELF5 induced CD24 expression by binding to the ETS cis element in the CD24 gene promoter sequence. This study provided a molecular mechanism for ELF5 to inhibit breast cancer from a new perspective, and provided further theoretical support for the treatment and prevention of breast cancer.

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Quercetin suppresses breast cancer stem cells (CD44 + /CD24 − ) by inhibiting the PI3K/Akt/mTOR-signaling pathway

Cited by 132 publications

References 28 publications

Traditional Chinese medicine as a cancer treatment: Modern perspectives of ancient but advanced science

Traditional Chinese medicine as a cancer treatment: Modern perspectives of ancient but advanced science

Inhibitory Effects of Tangeretin, a Citrus Peel-Derived Flavonoid, on Breast Cancer Stem Cell Formation through Suppression of Stat3 Signaling

ELF5 inhibits migration and invasion of breast cancer cells via regulating CD24 expression

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