Calycosin and Genistein Induce Apoptosis by Inactivation of HOTAIR/p-Akt Signaling Pathway in Human Breast Cancer MCF-7 Cells

Chen, Jian; Chen, Lin; Wang, Yong; Ye, Yu; Huang, Zhichuan

doi:10.1159/000369732

Cited by 116 publications

(76 citation statements)

References 21 publications

(23 reference statements)

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“…It has been found that SGK1 could be regulated by a variety of signaling pathways including PKC, MAPK, and calcium, and enhances survival, invasiveness, motility, epithelial to mesenchymal transition (EMT) and adhesiveness of tumour cells through several kinases and transcription factors [28]. In the latest study, Chen et al demonstrated that genistein inhibited breast cancer cell growth through inactivation of the PI3K/Akt signaling pathway [8]. Similarly, SGK1 induction was also found to be sensitive to the tyrosine kinase inhibitor genistein [10].…”

Section: Discussionmentioning

confidence: 99%

“…Genistein (49,5,7-Trihydroxyisoflavone), a major phytoestrogen constituent of soybeans and soy products, has been shown to exhibit inhibition effects on a variety of malignancies such as CRC [6], prostate cancer [7], breast cancer [8], and lung cancer [9]. Genistein is a protein tyrosine kinase inhibitor and affects cell proliferation, apoptosis, tumor angiogenesis, metastasis and attenuates multidrug resistance through the regulation of key components of signal transduction pathways such as Akt [8], SGK1 [10], EGFR [11], and MAPK [12].…”

Section: Introductionmentioning

confidence: 99%

“…Genistein is a protein tyrosine kinase inhibitor and affects cell proliferation, apoptosis, tumor angiogenesis, metastasis and attenuates multidrug resistance through the regulation of key components of signal transduction pathways such as Akt [8], SGK1 [10], EGFR [11], and MAPK [12]. Akt, also known as protein kinase B (PKB), is a serine/threonine kinase and a major downstream effector of phosphatidylinositide-3-kinase (PI3K).…”

Section: Introductionmentioning

confidence: 99%

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Genistein Inhibits Human Colorectal Cancer Growth and Suppresses MiR-95, Akt and SGK1

Qin

Chen²,

Zhu³

et al. 2015

Cell Physiol Biochem

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Background: Genistein, a major isoflavonoid isolated from dietary soybean, has been shown to suppress the growth of several cancers through modulation of various pathways. However, the molecular mechanisms by which genistein elicit its effects on colorectal cancer (CRC) cells have not been fully elucidated. In this study, we aimed to investigate the anti-tumor activities of genistein on CRC and its potential mechanism. Methods: Effects of genistein on the cell proliferation were tested in HCT-116 cells by MTT assay, and apoptosis was measured by Flow cytometry. Real-time PCR was also used to evaluate the regulation of genistein on miR-95, Akt and SGK1 expression. The protein levels of total Akt (T-Akt), and phosphorylated Akt (P-Akt) were assessed by western blot. A nude mice xenograft model was employed to determine whether genistein could have an anti-tumor effect on CRC in vivo. Results: We found that treatment of HCT-116 cells with genistein caused an inhibition of cell proliferation and induction of apoptosis. Meanwhile, genistein down-regulated the mRNA expression of Akt, SGK1 and miR-95, and inhibited the phosphorylation of Akt in HCT-116 cells. The experiment in vivo also showed that genistein significantly suppressed the growth of mouse xenograft tumor. Conclusion: This study demonstrates that genistein has an inhibitory effect on CRC involved in reducing miR-95, Akt and SGK1, offering novel insights into the mechanisms of genistein therapeutic actions.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Genistein Inhibits Human Colorectal Cancer Growth and Suppresses MiR-95, Akt and SGK1

Qin

Chen²,

Zhu³

et al. 2015

Cell Physiol Biochem

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“…LncRNAs are characterized by a length of more than 200 nt but do not encode any protein [3]. LncRNAs have more diversified molecular mechanisms of expression and regulation, such as activating or inhibiting the expression of target genes by direct binding, or by participating in histone modification and the elevation of regulatory factors; lncRNAs may participate in the regulation of gene expression through two types or all signal molecules, decoy molecules, guidance molecules or scaffolding molecules separately or collectively [4-9]. The dysregulation of lncRNAs has been functionally associated with human cancers.…”

Section: Introductionmentioning

confidence: 99%

“…The dysregulation of lncRNAs is correlated with promoted proliferation, chemoresistance, invasion and metastasis [10-14]. For example, HOTAIR accelerates such cancer biology in pan-cancers, including breast cancer, glioblastoma, gastric cancer, pancreatic cancer, thyroid cancer, ovarian cancer and lung cancer [4, 15]. Thus, the identification and validation of lncRNAs that act as HOTAIR in pan-cancer is essential and may remain a huge challenge for us to accomplish.…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA Linc00152 Functions as a Tumor Propellant in Pan-Cancer

Wan

Yin

et al. 2017

Cell Physiol Biochem

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Background/Aims: The oncogenic role of linc00152 in pan-cancer is unclear. Methods: In this study, RNA-Seq of 33 breast specimens was performed, and the expression of linc00152 was validated by qPCR using 50 paired breast cancer tissues and adjacent normal tissues. This result combined with the expression of linc00152 in pan-cancer was revalidated by Gene Expression Omnibus and The Cancer Genome Atlas data. Next, the oncogenic roles of linc00152 in view of prognosis, chemoresistance, genomic and epigenetic regulation, including DNA methylation and histone modification, potential biological function enrichment, and basic molecular function in pan-cancer, were also evaluated in vitro and in vivo. Results: Linc00152 is upregulated in pan-cancer, especially in progressive cancer, and the high expression of linc00152 may lead to a worse prognosis and chemoresistance in pan-cancer patients. Amplification, DNA hypomethylation, promoter-like lncRNA characteristics and super-enhancer regulation are the drivers that lead to the upregulation of linc00152 in pan-cancer. Meanwhile, linc00152 was involved in cancer-related pathways, infection and immune response-associated pathways by enriched analysis using TCGA data. Finally, linc00152 was confirmed to promote the proliferation, migration and invasion in MDA-MB-231, SGC-7901 and 786-O. Moreover, RIP and RNA pull-down assays indicated that linc00152 can bind to EZH2 directly. Conclusion: All of the results indicated that linc00152 acted as an oncogenic propellant from various perspectives, and it may be an effective therapy target in pan-cancer.

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Unveiling the potential anti‐cancer activity of calycosin against multivarious cancers with molecular insights: A promising frontier in cancer research

Sohel,

Zahra Shova,

shuvo

et al. 2024

Cancer Medicine

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BackgroundCalycosin may be a potential candidate regarding chemotherapeutic agent, because already some studies against multivarious cancer have been made with this natural compound.AimThis review elucidated a brief overview of previous studies on calycosin potential effects on various cancers and its potential mechanism of action.MethodologyData retrieved by systematic searches of Google Scholar, PubMed, Science Direct, Web of Science, and Scopus by using keywords including calycosin, cancer types, anti‐cancer mechanism, synergistic, and pharmacokinetic and commonly used tools are BioRender, ChemDraw Professional 16.0, and ADMETlab 2.0.ResultsBased on our review, calycosin is available in nature and effective against around 15 different types of cancer. Generally, the anti‐cancer mechanism of this compound is mediated through a variety of processes, including regulation of apoptotic pathways, cell cycle, angiogenesis and metastasis, oncogenes, enzymatic pathways, and signal transduction process. These study conducted in various study models, including in silico, in vitro, preclinical and clinical models. The molecular framework behind the anti‐cancer effect is targeting some oncogenic and therapeutic proteins and multiple signaling cascades. Therapies based on nano‐formulated calycosin may make excellent nanocarriers for the delivery of this compound to targeted tissue as well as particular organ. This natural compound becomes very effective when combined with other natural compounds and some standard drugs. Moreover, proper use of this compound can reverse resistance to existing anti‐cancer drugs through a variety of strategies. Calycosin showed better pharmacokinetic properties with less toxicity in human bodies.ConclusionCalycosin exhibits excellent potential as a therapeutic drug against several cancer types and should be consumed until standard chemotherapeutics are available in pharma markets.

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Calycosin and Genistein Induce Apoptosis by Inactivation of HOTAIR/p-Akt Signaling Pathway in Human Breast Cancer MCF-7 Cells

Cited by 116 publications

References 21 publications

Genistein Inhibits Human Colorectal Cancer Growth and Suppresses MiR-95, Akt and SGK1

Genistein Inhibits Human Colorectal Cancer Growth and Suppresses MiR-95, Akt and SGK1

Long Noncoding RNA Linc00152 Functions as a Tumor Propellant in Pan-Cancer

Unveiling the potential anti‐cancer activity of calycosin against multivarious cancers with molecular insights: A promising frontier in cancer research

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