Cichorins D–F: Three New Compounds from Cichorium intybus and Their Biological Effects

Cichorium intybus L., (chicory) is employed in various traditional medicines to treat a wide range of diseases and disorders. In the current investigation, two new naphthalane derivatives viz., cichorins D (1) and E (2), along with one new anthraquinone cichorin F (3), were isolated from Cichorium intybus. In addition, three previously reported compounds viz., β-sitosterol (4), β-sitosterol β-glucopyranoside (5), and stigmasterol (6) were also isolated from Cichorium intybus. Their structures were established via extensive spectroscopic data, including 1D (1H and 13C) and 2D NMR (COSY, HSQC and HMBC), and ESIMS. Cichorin E (2) has a weak cytotoxic effect on breast cancer cells (MDA-MB-468: IC50: 85.9 µM) and Ewing’s sarcoma cells (SK-N-MC: IC50: 71.1 µM); cichorin F (3) also illustrated weak cytotoxic effects on breast cancer cells (MDA-MB-468: IC50: 41.0 µM and MDA-MB-231: IC50: 45.6 µM), and SK-N-MC cells (IC50: 71.9 µM). Moreover compounds 1–3 did not show any promising anthelmintic effects.

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Glucocorticoid receptor–IRS-1 axis controls EMT and the metastasis of breast cancers

Journal of Molecular Cell Biology ◽

10.1093/jmcb/mjz001 ◽

2019 ◽

Vol 11 (12) ◽

pp. 1042-1055 ◽

Cited By ~ 4

Author(s):

Weiwei Shi ◽

Dongmei Wang ◽

Xinwang Yuan ◽

Yi Liu ◽

Xiaojie Guo ◽

...

Keyword(s):

Breast Cancer ◽

Glucocorticoid Receptor ◽

Cell Survival ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Biological Effects ◽

Ectopic Expression ◽

Metastatic Breast ◽

Mesenchymal Transition ◽

Expression Levels

Abstract Glucocorticoid receptor (GR) is involved in the transcriptional regulation of genes that are important for various biological functions, including tumor growth and metastatic progression. However, the cellular and biological effects of GR remain poorly understood. Here, we investigated the role of GR and its underlying mechanism in mediating breast cancer cell survival and metastasis. We observed that the GR levels were increased in drug-resistant breast cancer cells and in metastatic breast cancer samples. GR promoted tumor cell invasion and lung metastasis in vivo. The GR expression levels were negatively correlated with the survival rates of breast cancer patients. Both ectopic expression and knockdown of GR revealed that GR is a strong inducer of epithelial-to-mesenchymal transition (EMT), which is consistent with its effects on cell survival and metastasis. GR suppressed the expression of insulin receptor substrate 1 (IRS-1) by acting as an IRS-1 transcriptional repressor. In addition, GR has an opposite effect on the expression levels of IRS-2, indicating that GR is able to differentially regulate the IRS-1 and IRS-2 expression. The cellular and biological effects elicited by GR were consistent with the reduced levels of IRS-1 observed in cancer cells, and GR-mediated IRS-1 suppression activated the ERK2 MAP kinase pathway, which is required for GR-mediated EMT. Taken together, our results indicate that GR–IRS-1 signaling axis plays an essential role in regulating the survival, invasion, and metastasis of breast cancer cells.

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554 POSTER The mTOR effector p70 S6 kinase 1 (S6K1): a specific biomarker for the biological effects of the dual HER1/HER2 kinase inhibitor Lapatinib (GW572016) in HER2-overexpressing breast cancer cells

European Journal of Cancer Supplements ◽

10.1016/s1359-6349(06)70559-6 ◽

2006 ◽

Vol 4 (12) ◽

pp. 168 ◽

Cited By ~ 1

Author(s):

A. Vazquez-Martin ◽

R. Colomer ◽

J.A. Menendez

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Kinase Inhibitor ◽

Biological Effects ◽

S6 Kinase ◽

P70 S6 Kinase

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Global transcriptome analysis reveals partial estrogen-like effects of karanjin in MCF-7 breast cancer cells

10.1101/2021.10.28.466373 ◽

2021 ◽

Author(s):

Gaurav Bhatt ◽

Akshita Gupta ◽

Latha Rangan ◽

Anil Mukund Limaye

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Target Genes ◽

Biological Activities ◽

Biological Effects ◽

Dependent Manner ◽

Cell Type ◽

Concentration Dependent Manner ◽

Mcf 7

Karanjin, an abundantly occurring furanoflavonoid in edible and non-edible legumes, exerts diverse biological effects in vivo, and in vitro. Its potential as an anticancer agent is also gaining traction following recent demonstrations of its anti-proliferative, cell cycle inhibitory, and pro-apoptotic effects. However, the universality of its anticancer potential is yet to be scrutinized, particularly so because flavonoids can act as selective estrogen receptor modulators (SERMs). Even the genomic correlates of its biological activities are yet to be examined in hormone responsive cells. This paper presents the early and direct transcriptomic footprint of 10 μM karanjin in MCF-7 breast cancer cells, using next generation sequencing technology (RNA-seq). We show that karanjin-modulated gene-expression repertoire is enriched in several hallmark gene sets, which include early estrogen-response, and G2/M checkpoint genes. Genes modulated by karanjin overlapped with those modulated by 1 nM 17β-estradiol (E2), or 1 μM tamoxifen. Karanjin altered the expression of selected estrogen-regulated genes in a cell-type, and concentration dependent manner. It downmodulated the expression of ERα protein in MCF-7 cells. Furthermore, ERα knockdown negatively impacted karanjins ability to modulate the expression of selected E2 target genes. Our data suggest that karanjin exerts its effects on ERα-positive breast cancer cells, at least in part, via ERα. The apparent SERM-like effects of karanjin pose a caveat to the anticancer potential of karanjin. In-depth studies on cell-type and concentration-dependent effects of karanjin may bring out its true potential in endocrine therapies.

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6,N2-Diaryl-1,3,5-triazine-2,4-diamines: synthesis, antiproliferative activity and 3D-QSAR modeling

RSC Advances ◽

10.1039/d0ra00643b ◽

2020 ◽

Vol 10 (21) ◽

pp. 12135-12144 ◽

Cited By ~ 3

Author(s):

Ahmad Junaid ◽

Felicia Phei Lin Lim ◽

Lay Hong Chuah ◽

Anton V. Dolzhenko

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Antiproliferative Activity ◽

Breast Cancer Cells ◽

Triple Negative ◽

3D Qsar ◽

Qsar Model ◽

Qsar Modeling ◽

New Compounds

New compounds selectively targeting the triple negative MDA-MB231 breast cancer cells were used to build a 3D-QSAR model.

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The N-terminal polypeptide derived from vMIP-II exerts its anti-tumor activity in human breast cancer by regulating lncRNA SPRY4-IT1

Bioscience Reports ◽

10.1042/bsr20180411 ◽

2018 ◽

Vol 38 (5) ◽

Cited By ~ 4

Author(s):

Haihua Wu ◽

Yueyue Wang ◽

Tiantian Chen ◽

Yu Li ◽

Haifeng Wang ◽

...

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Biological Effects ◽

Underlying Mechanism ◽

Vital Role ◽

Inflammatory Protein ◽

Non Coding Rna ◽

Long Non Coding Rna ◽

Anti Tumor Activity

Accumulating evidence demonstrates that long non-coding RNA (lncRNA) sprouty4-intron transcript 1 (lncRNA SPRY4-IT1) plays a vital role in the development of breast cancer. However, the underlying mechanism has not been eventually illuminated. We aimed to explore the biological activity of lncRNA SPRY4-IT1 in breast cancer cells and whether N-terminal polypeptide derived from viral macrophage inflammatory protein II (NT21MP) could exert its anti-tumor effect by regulating lncRNA SPRY4-IT1 and its target gene SKA2. Real-time RT-PCR, Western blotting, wound healing, and invasion assays were used to achieve this goal. We found that lncRNA SPRY4-IT1 was highly expressed in breast cancer cells. Moreover, NT21MP markedly inhibited biological effects of breast cancer cells by regulating lncRNA SPRY4-IT1, which was partially achieved through SKA2. Our findings suggested that lncRNA SPRY4-IT1 could serve as a novel biomarker by NT21MP for breast cancer.

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LncRNA DANCR contributes to tumor progression via targetting miR-216a-5p in breast cancer: lncRNA DANCR contributes to tumor progression

Bioscience Reports ◽

10.1042/bsr20181618 ◽

2019 ◽

Vol 39 (4) ◽

Cited By ~ 12

Author(s):

Weiyang Tao ◽

Chunyang Wang ◽

Bifa Zhu ◽

Guoqiang Zhang ◽

Da Pang

Keyword(s):

Breast Cancer ◽

Cell Proliferation ◽

Tumor Progression ◽

Cancer Cells ◽

Cell Line ◽

Breast Cancer Cells ◽

Biological Effects ◽

Tumor Promoter ◽

Aberrant Expression ◽

Proliferation And Invasion

Abstract Breast cancer, the most frequently occurring malignant tumor, has high mortality rate, especially triple-negative breast cancer (TNBC). LncRNA-differentiation antagonizing non-protein coding RNA (lncRNA DANCR) has been found that its aberrant expression was associated with tumor progression and it was promising to be a potential target for cancer therapy. The goal of the present study was to explore the biological effects and underlying mechanism of DANCR in breast cancer. Our results showed that DANCR was up-regulated in TNBC tissues and breast cancer cells compared with normal breast tissues and cells, and higher DANCR level suggested poorer prognosis, implying that it was promising to be a novel biomarker used for TNBC diagnosis and prognosis. To better research the functions and mechanism of DANCR on breast cancer cells, we selected two cell lines used for next study: one TNBC cell line–MDA-MB-231 and one ER-positive breast cancer cell line–MCF-7. Further study indicated that DANCR overexpression significantly promoted cell proliferation and invasion in vitro and contributed to tumor growth in vivo. To deeply understand its molecular mechanism, miRNA-216a-5p was identified as a target of DANCR by bioinformatic analysis. Experiments demonstrated that miRNA-216a-5p interacted with DANCR and its inhibitor could weaken the influences induced by DANCR knockdown for cancer cells, including cell proliferation and invasion, and the expression of Nanog, SOX2, and OCT4. Therefore, DANCR might act as a tumor promoter by targetting miRNA-216a-5p, which might provide a potential therapy target for breast cancer treatment.

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