Isoliquiritigenin inhibits cell proliferation and migration through the PI3K/AKT signaling pathway in A549 lung cancer cells

Tian, Tao; Sun, Junying; Wang, Jianxin; Liu, Haitao

doi:10.3892/ol.2018.9344

Cited by 22 publications

(24 citation statements)

References 38 publications

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“…In agreement with our findings, Peng et al reported that treatment of MDA-MB-231 cells with ISL induced cell apoptosis, and they observed an enhancement of the ratio of Bax to Bcl-2 by ISL treatment [37]. Moreover, ISL treatment was also observed to induce cancer cell apoptosis in lung cancer [38], uterine leiomyoma [39], and endometrial cancer [40].…”

Section: Discussionsupporting

confidence: 92%

Dietary Compound Isoliquiritigenin, an Antioxidant from Licorice, Suppresses Triple-Negative Breast Tumor Growth via Apoptotic Death Program Activation in Cell and Xenograft Animal Models

et al. 2020

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Patients with triple-negative breast cancer have few therapeutic strategy options. In this study, we investigated the effect of isoliquiritigenin (ISL) on the proliferation of triple-negative breast cancer cells. We found that treatment with ISL inhibited triple-negative breast cancer cell line (MDA-MB-231) cell growth and increased cytotoxicity. ISL reduced cell cycle progression through the reduction of cyclin D1 protein expression and increased the sub-G1 phase population. The ISL-induced apoptotic cell population was observed by flow cytometry analysis. The expression of Bcl-2 protein was reduced by ISL treatment, whereas the Bax protein level increased; subsequently, the downstream signaling molecules caspase-3 and poly ADP-ribose polymerase (PARP) were activated. Moreover, ISL reduced the expression of total and phosphorylated mammalian target of rapamycin (mTOR), ULK1, and cathepsin B, whereas the expression of autophagic-associated proteins p62, Beclin1, and LC3 was increased. The decreased cathepsin B cause the p62 accumulation to induce caspase-8 mediated apoptosis. In vivo studies further showed that preventive treatment with ISL could inhibit breast cancer growth and induce apoptotic and autophagic-mediated apoptosis cell death. Taken together, ISL exerts an effect on the inhibition of triple-negative MDA-MB-231 breast cancer cell growth through autophagy-mediated apoptosis. Therefore, future studies of ISL as a supplement or alternative therapeutic agent for clinical trials against breast cancer are warranted.

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Section: Discussionsupporting

confidence: 92%

Dietary Compound Isoliquiritigenin, an Antioxidant from Licorice, Suppresses Triple-Negative Breast Tumor Growth via Apoptotic Death Program Activation in Cell and Xenograft Animal Models

et al. 2020

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“…There is mounting evidence suggesting that the PI3K/ AKT signaling pathway plays an indispensable role in the regulation of cellular features such as survival, proliferation, and apoptosis. 37 The research of Tian et al 38 shows the PI3K/AKT pathway is involved in lung cancer cell proliferation and apoptosis. Fang et al 37 reveal that PI3K/ AKT signaling pathway plays an important role in kidney cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

<p>Downregulation of RAGE Inhibits Cell Proliferation and Induces Apoptosis via Regulation of PI3K/AKT Pathway in Cervical Squamous Cell Carcinoma</p>

Li¹,

Song²,

Zhou³

et al. 2020

OTT

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Aim: The receptor for advanced glycation endproducts (RAGE) expression has been reported to be implicated with cancer development. In this study, the role of RAGE in the regulation of cervical squamous cancer cell proliferation, apoptosis and the mechanism of RAGE involved in the biological behaviors were explored. Methods: The RAGE expression was overexpressed or downregulated by lentivirus transfection. The effect of RAGE expression on cell proliferation was explored by CCK-8, MTT, and BrdU assay, and the effect of RAGE on tumor development was confirmed by the xenograft mouse model along with the immunohistochemistry stain of proliferating cell nuclear antigen (PCNA). Apoptosis was investigated by flow cytometry and TUNEL assay. Western blotting was performed to investigate the expression of possible proteins, including Bax, Bcl-2, PI3K, p-PI3K, AKT, and p-AKT. Results: Overexpression of RAGE promoted proliferation of cervical squamous cancer cell and increased PCNA expression. In the meantime, RAGE overexpression inhibited cell apoptosis along with a decrease of Bax/Bcl-2 ratio, and induction of PI3K/AKT activation. The in vivo results showed that overexpression of RAGE enhanced tumor growth. Conversely, knockdown of RAGE exhibited opposed effects on cervical cancer cells and xenograft mouse model. Furthermore, RAGE inhibitor FPS-ZM1 effectively inhibited SiHa cell viability and PCNA expression, and increased cell apoptosis and Bax/Bcl-2 ratio. Moreover, PI3K inhibitor LY294002 effectively inhibited activation of PI3K and AKT, and further repressed RAGE overexpression-induced cell proliferation and apoptosis inhibition. Conclusion: RAGE promotes the growth ability of cervical squamous cell carcinoma by inducing PCNA expression and inhibiting cell apoptosis via inactivation of the PI3K/AKT pathway.

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“…As a result, this signaling network could be a major target in cancer inhibition. An imbalance in the PI3K/AKT pathway make an important contribution in the arrangement and growth of lung cancer, and the activation of the PI3K/AKT pathway can stimulate the transduction of many downstream signals and assist the growth of NSCLC [ 10 , 11 , 12 ]. Targeting such intracellular pathways that modulate proliferation, apoptosis, metastasis and resistance to chemotherapy shows a significant therapeutic approach for lung cancer.…”

Section: Introductionmentioning

confidence: 99%

Vibrational spectra, Hirshfeld surface analysis, molecular docking studies of (RS)-N,N-bis(2-chloroethyl)-1,3,2-oxazaphosphinan-2-amine 2-oxide by DFT approach

Govindammal

Prasath

2020

Heliyon

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The Cyclophosphamide (CYC) is used as an anti cancer agent. It is chemically known as (RS)-N,N-bis(2-chloroethyl)-1,3,2-oxazaphosphinan-2-amine 2-oxide. The vibrational assignments survey of the CYC was implemented by employing FT-IR and FT-Raman spectroscopic investigation and the results are compared with theoretical features. The optimized geometrical parameters, IR intensity and Raman Activity of the vibrational bands of CYC were determined from the B3LYP functional with 6–311++G (d, p) level of theory. In the current work, quantum chemical calculations were adopted to contemplate the vibrational assignments of CYC and the outcomes are compared with experimental findings. Molecular Electrostatic Potential (MEP) and HOMO-LUMO energies are very effective in the examination of charge transfer and distribution of the molecular structure. The molecular orbital contributions were evaluated by using the Total Density of States (TDOS). The analysis of Natural Bond Orbital (NBO), Mulliken population and Fukui function studies were done. Intermolecular interaction of the title compound was examined through Hirshfeld surface analysis. The evaluation of drug-likeness was accomplished in accordance with Lipinski's Rule of Five and molecular descriptors were utilized to predict the ADMET profiles of the CYC molecule. The recent research studies reports that the structural and bio-activity of the CYC was affirmed by the docking analysis of CYC with protein PI3K/AKT inhibitor, it acts as anti-lung cancer agent.

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Isoliquiritigenin inhibits cell proliferation and migration through the PI3K/AKT signaling pathway in A549 lung cancer cells

Cited by 22 publications

References 38 publications

Dietary Compound Isoliquiritigenin, an Antioxidant from Licorice, Suppresses Triple-Negative Breast Tumor Growth via Apoptotic Death Program Activation in Cell and Xenograft Animal Models

Dietary Compound Isoliquiritigenin, an Antioxidant from Licorice, Suppresses Triple-Negative Breast Tumor Growth via Apoptotic Death Program Activation in Cell and Xenograft Animal Models

<p>Downregulation of RAGE Inhibits Cell Proliferation and Induces Apoptosis via Regulation of PI3K/AKT Pathway in Cervical Squamous Cell Carcinoma</p>

Vibrational spectra, Hirshfeld surface analysis, molecular docking studies of (RS)-N,N-bis(2-chloroethyl)-1,3,2-oxazaphosphinan-2-amine 2-oxide by DFT approach

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