Calycosin Enhances Some Chemotherapeutic Drugs Inhibition of Akt Signaling Pathway in Gastric Cells

Zhang, Lixia; Wu, Yueming; Guo, Yang; Li, Yanjun; Li, Na; Yang, Yi; Qin, Xue-Yun

doi:10.1080/07357907.2016.1278226

Cited by 15 publications

(13 citation statements)

References 47 publications

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“…Moreover, calycosin inhibited osteosarcoma cell migration and invasion [25]. Calycosin also inhibited in vitro growth and progression of gastric, colorectal, ovarian, and breast cancer cells [26][27][28][29]. In this study, we demonstrated that calycosin inhibited proliferation and progression of breast cancer cells in a dose-and time-dependent manner.…”

Section: Discussionsupporting

confidence: 51%

Calycosin inhibits breast cancer cell migration and invasion by suppressing EMT via BATF/TGF-β1

Zhang

Lin

Wang

et al. 2021

Aging

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In this study, we investigated the effects of calycosin on breast cancer cell progression and their underlying mechanisms. Calycosin dose-and time-dependently inhibited proliferation, migration, and invasion by T47D and MCF-7 breast cancer cells by downregulating basic leucine zipper ATF-like transcription factor (BATF) expression. Moreover, BATF promoted breast cancer cell migration and invasiveness by increasing TGFβ1 mRNA and protein levels. Bioinformatics analysis, dual luciferase reporter assays, and chromatin immunoprecipitation assays confirmed the presence of BATF-binding sites in the promoter sequence of TGFβ1 gene. Calycosin treatment inhibited epithelial-mesenchymal transition (EMT) of breast cancer cells by significantly increasing Ecadherin levels and decreasing N-cadherin, Vimentin, CD147, MMP-2, and MMP-9 levels through downregulation of BATF and TGFβ1. TGFβ1 knockdown reduced the migration and invasiveness of BATFoverexpressing breast cancer cells, whereas incubation with TGFβ1 enhanced the migration and invasiveness of calycosin-treated breast cancer cells. Our findings demonstrated that calycosin inhibited EMT and progression of breast cancer cells by suppressing BATF/TGFβ1 signaling. This suggests calycosin would be a promising therapeutic option for breast cancer patients.

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Section: Discussionsupporting

confidence: 51%

Calycosin inhibits breast cancer cell migration and invasion by suppressing EMT via BATF/TGF-β1

Zhang

Lin

Wang

et al. 2021

Aging

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“…According to a recent report, CA inhibits Akt p-Ser473 and enhances the role of DOX effect on gastric cells (Zhou & Wu, 2017). However, there is a little about whether CA could ameliorate the cardiotoxicity of DOX.…”

Section: Introductionmentioning

confidence: 99%

Calycosin ameliorates doxorubicin‐induced cardiotoxicity by suppressing oxidative stress and inflammation via the sirtuin 1–NOD‐like receptor protein 3 pathway

Zhai

Tao

Zhang

et al. 2019

Phytotherapy Research

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The limitation of doxorubicin (DOX), which is widely used for the treatment of solid tumors and hematologic malignancies, is a vital problem in clinical application. The most serious of limit factors is cardiotoxicity. Calycosin (CA), an isoflavonoid that is the major active component in Radix astragali, has been reported in many bioactivities including antitumor, anti‐inflammatory, and cardioprotection. The aim of the study was to investigate the effects and mechanisms of CA on DOX‐induced cardiotoxicity in vitro and in vivo. CA increased H9c2 cell viability and reduced apoptosis induced by DOX via Bcl‐2, Bax, and the PI3K‐Akt signaling pathway. Moreover, CA prevented DOX‐induced oxidative stress in cells by decreasing the generation of reactive oxygen species. Similarly, oxidative stress was inhibited by CA through the increased activities of antioxidant enzymes such as glutathione peroxidase, catalase, and superoxide dismutase and decreased the levels of aspartate aminotransferase, lactate dehydrogenase, and malondialdehyde in vivo. Furthermore, the levels of sirtuin 1 (Sirt1)–NOD‐like receptor protein 3 (NLRP3) and related proteins were ameliorated by CA in cells and in mice hearts. When H9c2 cells were treated by Ex527 (Sirt1 inhibitor), the effect of CA on expressions of NLRP3 and thioredoxin‐interacting protein was suppressed. In conclusion, the results suggested that CA might be a cotreatment with DOX to ameliorate cardiotoxicity by Sirt1–NLRP3 pathway.

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“…In recent years, research on the effects of Akt on tumor cell drug sensitivity has accumulated. These studies have shown that inhibition of Akt phosphorylation could enhance the sensitivity of gastric cancer cell lines to cisplatin, thereby increasing the therapeutic effect of cisplatin on gastric cancer 36. Mutation of PIK3CA results in overexpression of PIK3CA protein, which leads to an increase in the catalytic activity of PI3K.…”

Section: Discussionmentioning

confidence: 99%

Silencing thePIK3CAGene Enhances the Sensitivity of Childhood Leukemia Cells to Chemotherapy Drugs by Suppressing the Phosphorylation of Akt

Liang

Xin

et al. 2019

Yonsei Med J

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PurposeThis study aimed to investigate the effects of PIK3CA on the sensitivity of acute B lymphocytic leukemia cells (Nalm-6 cells) to chemotherapy drugs.Materials and MethodsChildren's normal B lymphocytes and Nalm-6 cells were cultured. Nalm-6 cells were transfected with PIK3CA siRNA (siPIK3CA group) or its negative control (PIK3CA-Control group). Normal Nalm-6 cells were named Mock group. Nalm-6 cells transfected by PIK3CA siRNA were treated with Akt inhibitor (siPIK3CA+Akti-1/2 group). mRNA and protein expression was detected by qRT-PCR and Western blot. Proliferation and sensitivity to chemotherapeutic drugs was detected by MTT assay. Cell cycle and apoptosis was explored by low cytometry. Transwell assay was performed to test invasion.ResultsPIK3CA mRNA (p=0.008) and protein (p=0.006) expression was higher in Nalm-6 cells than that in normal B lymphocytes. Compared with the Mock group and PIK3CA-Control group, Nalm-6 cells of the siPIK3CA group had lower OD495 values (all p<0.05) and invasion cell numbers (p=0.03 and p=0.025), as well as a higher proportion of G0/G1 phase cells (p=0.020 and p=0.022), percentage of apoptosis (p=0.016 and p=0.022), and inhibition rate (all p<0.05). pAkt expression in the siPIK3CA group (p=0.026 and p=0.031) and siPIK3CA+Akti-1/2 group (p=0.019 and p=0.023) was lower than that in the Mock group.ConclusionPIK3CA silencing inhibited Nalm-6 cell proliferation and invasion, and promoted their apoptosis and sensitivity to chemotherapeutic drugs, potentially through regulation of the PI3K/AKT signaling pathway.

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Calycosin Enhances Some Chemotherapeutic Drugs Inhibition of Akt Signaling Pathway in Gastric Cells

Cited by 15 publications

References 47 publications

Calycosin inhibits breast cancer cell migration and invasion by suppressing EMT via BATF/TGF-β1

Calycosin inhibits breast cancer cell migration and invasion by suppressing EMT via BATF/TGF-β1

Calycosin ameliorates doxorubicin‐induced cardiotoxicity by suppressing oxidative stress and inflammation via the sirtuin 1–NOD‐like receptor protein 3 pathway

Silencing thePIK3CAGene Enhances the Sensitivity of Childhood Leukemia Cells to Chemotherapy Drugs by Suppressing the Phosphorylation of Akt

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