The proliferative effects of ghrelin on human gastric cancer AGS cells

Tian, Peng; Fan, Xuemei

doi:10.1111/j.1751-2980.2012.00616.x

Cited by 16 publications

(22 citation statements)

References 28 publications

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“…The results of this study provide the first evidence that ghrelin does not affect cancer progression in lung adenocarcinoma. Although a considerable body of in vitro researches indicated that ghrelin might affect cancer progression via several signaling pathways, e.g., PI3K/Akt [9] and Erk1/2 [10], our findings demonstrate that ghrelin treatment did not influence biological activities, viability, proliferation, or resistance to apoptosis in human lung adenocarcinoma HLC-1 cells. In normal cells, ghrelin promotes proliferation by stimulating the PI3K/AKT pathway and MAPK pathways [11], and also increases resistance to apoptosis [12].…”

Section: Discussioncontrasting

confidence: 72%

Ghrelin does not influence cancer progression in a lung adenocarcinoma cell line

et al. 2017

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Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor (GHSR), is produced in the human stomach. Although ghrelin has therapeutic potential for cancer cachexia, ghrelin treatment may have a concern about accelerating cancer progression. Here, using the human lung adenocarcinoma cell line HLC-1, we investigated the effects of ghrelin on molecular mechanisms linked to cancer progression, including cell viability, proliferation, resistance to apoptosis, and mitochondrial activity. Both types of mouse alveolar epithelial cells (types I and II) expressed the GHSR, as did the human normal airway cell lines BEAS-2B and HLC-1. Treatment with ghrelin (10, 10, 1, 10 μM) did not affect cell viability or proliferation. Pretreatment of HLC-1 cells with ghrelin (10 μM) did not affect resistance to paclitaxel-induced apoptosis. The parameters of mitochondrial respiration, including basal respiration, proton leak, ATP production, maximal respiration, spare respiratory capacity, and non-mitochondrial respiration, of the HLC-1 cells pretreated with or without ghrelin were unchanged. Taken together, ghrelin does not influence cancer progression in lung adenocarcinoma cells.

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Section: Discussioncontrasting

confidence: 72%

Ghrelin does not influence cancer progression in a lung adenocarcinoma cell line

et al. 2017

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“…Several factors mediate the metastatic capacity of gastric carcinoma through the PI3K/Akt/mTOR pathway [ 61 , 62 , 63 , 64 , 65 ]. Administration of 2-methoxyestradiol, a metabolite of estradiol-17b, decreased cell invasion and metastasis of gastric carcinoma through attenuation of Akt activity [ 66 ].…”

Section: The Role Of the Pi3k/akt/mtor Pathway In The Biological Pmentioning

confidence: 99%

The Role of PI3K/Akt/mTOR Signaling in Gastric Carcinoma

Matsuoka

Yashiro

2014

Cancers

178

121

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The phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway is one of the key signaling pathways induced by various receptor-tyrosine kinases. Accumulating evidence shows that this pathway is an important promoter of cell growth, metabolism, survival, metastasis, and resistance to chemotherapy. Genetic alterations in the PI3K/Akt/mTOR pathway in gastric carcinoma have often been demonstrated. Many kinds of molecular targeting therapies are currently undergoing clinical testing in patients with solid tumors. However, with the exception of the ErbB2-targeting antibody, targeting agents, including PI3K/Akt/mTOR inhibitors, have not been approved for treatment of patients with gastric carcinoma. This review summarizes the current knowledge on PI3K/Akt/mTOR signaling in the pathogenesis of gastric carcinoma and the possible therapeutic targets for gastric carcinoma. Improved knowledge of the PI3K/Akt/mTOR pathway in gastric carcinoma will be useful in understanding the mechanisms of tumor development and for identifying ideal targets of anticancer therapy for gastric carcinoma.

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“…The highest levels of ghrelin are found in the small intestine, pancreatic islet cells, gallbladder, liver, spleen and immune cells (10). Recent evidence has demonstrated that ghrelin has dual proliferative effects, according to the type of cell or tissue, via mechanisms that are dependent on or independent of GHS-R1a (11). In addition, ghrelin has possible antioxidant and anti-inflammatory effects (7,12).…”

Section: Introductionmentioning

confidence: 99%

Effects of ghrelin, leptin and melatonin on the levels of reactive oxygen species, antioxidant enzyme activity and viability of the HCT 116 human colorectal carcinoma cell line

Bułdak

Pilc-Gumuła

Bułdak

et al. 2015

Molecular Medicine Reports

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Obesity is associated with an increased risk of certain types of cancer, including colon cancer. Adipose tissue is an endocrine organ that produces biologically active substances, such as leptin and ghrelin. Recent research has suggested that adipose-derived hormones may be associated with mechanisms linked to tumorigenesis and cancer progression. Furthermore, previous studies have demonstrated that pineal gland-derived melatonin possesses important oncostatic and antioxidant properties. The present study aimed to determine the effects of the adipokines ghrelin and leptin, and the melatonin on intracellular levels of reactive oxygen species (ROS) and the activity of selected antioxidant enzymes, such as superoxide dismutase, catalase (CAT) and glutathione peroxidase. The effects of these compounds were also determined on the viability of HCT 116 human colorectal carcinoma cells in vitro. The pro-oxidant and growth inhibitory effects of melatonin resulted in an accumulation of ROS and decreased antioxidant capacity in melatonin-treated cells. Ghrelin administration alone caused a significant decrease in the levels of ROS, due to an increased activity of CAT in the HCT 116 cells. In addition, the present study observed increased lipid peroxidation following melatonin treatment, and decreased levels of malondialdehyde following ghrelin or leptin treatment. In conclusion, ghrelin, leptin and melatonin have various influences on the antioxidant capacity of HCT 116 cells. Compared with the adipokines, treatment with melatonin increased ROS levels and decreased cellular viability.

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The proliferative effects of ghrelin on human gastric cancer AGS cells

Abstract: Ghrelin and des-acyl ghrelin stimulate the proliferation of gastric cancer cells via the activation of the ERK1/2 and PI3K/Akt pathway.

Cited by 16 publications

References 28 publications

Ghrelin does not influence cancer progression in a lung adenocarcinoma cell line

Ghrelin does not influence cancer progression in a lung adenocarcinoma cell line

The Role of PI3K/Akt/mTOR Signaling in Gastric Carcinoma

Effects of ghrelin, leptin and melatonin on the levels of reactive oxygen species, antioxidant enzyme activity and viability of the HCT 116 human colorectal carcinoma cell line

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