miR‑125b‑5p inhibits cell proliferation by targeting ASCT2 and regulating the PI3K/AKT/mTOR pathway in an LPS‑induced intestinal mucosa cell injury model

Objective This study aimed to evaluate the efficacy of Pycnogenol (PYC) and its antioxidant and antiapoptotic effect in an experimental hypoxic-ischemic (HI) rat model. Study Design A total of 24 Wistar albino rats who were on the seventh postnatal day were divided into three groups with developed HI brain injury model under the sevoflurane anesthesia: 40 mg/kg PYC was given to Group A, saline was given to Group B, and the sham group was Group C. Neuronal apoptosis was investigated by terminal deoxynucleotidyl transferase dUTP nick end labeling and immunohistochemically stained manually with primer antibodies of tumor necrosis factor-α and interleukin-1β. Results The neuronal cell injury was statistically lower in the PYC treatment group. Conclusion This is the first study that investigates the role of PYC in the HI brain injury model. PYC reduces apoptosis and neuronal injury in the cerebral tissue of the rats. PYC may be a protective agent against hypoxic-ischemic encephalopathy. Key Points

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Arctigenin upregulates apoptosis through the AKT/MTOR pathway, inhibiting the proliferation of glioma

10.21203/rs.2.18701/v1 ◽

2019 ◽

Author(s):

jiang yongan ◽

Liu Jia yu ◽

Hong Wangwang ◽

Fei Xiaowei ◽

Liu ru'en

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Glioma Cells ◽

Mtor Pathway ◽

Migration And Invasion ◽

Glioblastoma Cell ◽

Caspase 9 ◽

Arctium Lappa ◽

Dose Dependent ◽

Glioblastoma Cell Lines

Abstract Arctigenin (ARG) is a natural lignan compound extracted from arctium lappa and has displayed anticancer functions and effective treatments in a variety of cancers.Studies had shown that Arctigenin(ARG) inhibits tumors through the AKT/MTOR pathway and mediates autophagy.However,the role in glioma cellshave not still fully understood.This study was designed to investigate whether Arctigenin(ARG) can mediateAKT/mTOR pathway in glioma to regulate autophagy,and affected glioma cells growth and survival.We found that the dose-dependent downregulation of Arctigenin(ARG),reducing cell proliferation,migration and invasion in two human glioblastoma cell lines (U87, T98G),These phenomena were reversed after the administration of the AKT agonist (SC79). Arctigenin(ARG) also affected other autophagy markers such as p62, LC3B.In addition, the apoptotic molecules cleaved-PARP,caspase-9, and cleaved-caspase3 were also dose-dependently altered.

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Knocking down FAM83B inhibits endometrial cancer cell proliferation and metastasis by silencing the PI3K/AKT/mTOR pathway

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2019.108939 ◽

2019 ◽

Vol 115 ◽

pp. 108939 ◽

Cited By ~ 7

Author(s):

Qiongyan Lin ◽

Hui Chen ◽

Minfen Zhang ◽

Hanzhen Xiong ◽

Qingping Jiang

Keyword(s):

Cell Proliferation ◽

Endometrial Cancer ◽

Cancer Cell ◽

Mtor Pathway ◽

Cancer Cell Proliferation ◽

Endometrial Cancer Cell ◽

Proliferation And Metastasis ◽

Cell Proliferation And Metastasis

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Effects of epidermal growth factor on diamine oxidase expression and cell growth in Caco-2 cells

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1991.261.4.g669 ◽

1991 ◽

Vol 261 (4) ◽

pp. G669-G676 ◽

Cited By ~ 3

Author(s):

B. Daniele ◽

A. Quaroni

Keyword(s):

Cell Proliferation ◽

Growth Factor ◽

Epidermal Growth Factor ◽

Dna Synthesis ◽

Intestinal Mucosa ◽

Diamine Oxidase ◽

Small Intestinal Mucosa ◽

Cell Proliferation And Differentiation ◽

Proliferation And Differentiation ◽

Epidermal Growth

To investigate the role of diamine oxidase (DAO) in the intestinal mucosa, we compared its expression with cell proliferation and differentiation in the human colon carcinoma cell line Caco-2. DAO synthesis was evaluated in subconfluent and confluent cultures and in the presence of epidermal growth factor (EGF), a polypeptide hormone known to have specific trophic effects on the small intestinal mucosa. EGF stimulated DNA synthesis, significantly increased cellular DAO activity and the amount of enzyme secreted into the culture medium, but decreased expression of dipeptidyl peptidase IV, a marker of cell differentiation in confluent Caco-2 cells. Immunoprecipitation of DAO from cells labeled metabolically with [35S]methionine failed to demonstrate an increased enzyme synthesis in EGF-treated cells, suggesting that this hormone acted primarily at a posttranslational level by reducing DAO degradation before intracellular storage or secretion. A possible relationship between changes in cellular DAO activity and cell proliferation was also investigated by using aminoguanidine, a specific and potent DAO inhibitor. Although DAO activity was markedly suppressed, aminoguanidine had no significant effects on the rate of DNA synthesis. These results demonstrated that in Caco-2 cells EGF stimulated DNA synthesis and DAO expression; however, cell proliferation and differentiation were not correlated with the levels of cellular DAO, suggesting that this enzyme does not play a major role in the regulation of intestinal epithelial cell turnover.

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