Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway

Bai, Ruixia; Wang, W.P.; Zhao, Pengwei; Li, C.B.

doi:10.1590/1414-431x20155043

Cited by 26 publications

(23 citation statements)

References 18 publications

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“…It has been reported that ghrelin promotes prostate cancer cell proliferation and oral tumor cell proliferation through the regulation of glucose metabolism . However, ghrelin also inhibits cancer cell proliferation . Lin and Hsiao suggested that these discrepancies might be partially due to the ghrelin concentrations used to treat cancer cell lines .…”

Section: Discussionmentioning

confidence: 99%

Expression of the ghrelin/growth hormone secretagogue receptor axis and its functional role in promoting tumor growth in primary central nervous system lymphomas

et al. 2020

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Ghrelin and its receptor, growth hormone secretagogue receptor (GHS‐R), have been found in a variety of malignant tumor tissues, suggesting a biological function of the ghrelin/GHS‐R axis in tumor growth and progression. Among central nervous system tumors, primary central nervous system lymphomas (PCNSLs) are relatively rare and characterized by a rapid progression and poor prognosis. In order to clarify ghrelin expression and its functional role in promoting tumor growth and progression in PCNSLs, we undertook an immunohistochemical investigation for ghrelin and GHS‐R expression in 43 patients and tested the effect of ghrelin inhibition on lymphoma cells. Furthermore, we investigated the expression of CD105, a marker for tumor angiogenesis, to explore its association with the ghrelin/GHS‐R axis. The Kaplan–Meier method and Cox's proportional hazards regression model were used to determine the association of ghrelin/GHS‐R expression with overall survival rate. The immunohistochemical study showed moderate/strong immunostaining of cells for ghrelin and GHS‐R in 40 patients (93.0%) and 39 patients (90.7%), respectively. A ghrelin inhibitor did not affect tumor cell proliferation in vitro. Expression levels of ghrelin and GHS‐R were divided into high and low groups by the rate of moderate‐strong staining cells to tumor cells. The survival rate was significantly lower in patients with high GHS‐R expression (P = 0.0368 by log‐rank test; P = 0.0219 by Wilcoxon test). In addition, multivariate analysis of overall survival using Cox's proportional hazards regression model indicated that GHS‐R was a significant independent prognostic factor (P = 0.0426). CD105 expression on tumor vessels was positive in 33 patients (33/37, 89.2%). There was a positive correlation between the moderate‐strong staining rate of ghrelin and CD105‐positive vessel count. These results indicated that the ghrelin/GHS‐R axis plays a potential role in promoting tumor growth and progression through neoangiogenesis, rather than the proliferation of tumor cells.

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Section: Discussionmentioning

confidence: 99%

Expression of the ghrelin/growth hormone secretagogue receptor axis and its functional role in promoting tumor growth in primary central nervous system lymphomas

et al. 2020

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“…In squamous cell carcinoma cells, MEK/ERK signaling has been demonstrated to support cell survival by inducing the anti-apoptotic protein Bcl-2 (28). Previous studies have shown that alteration of the MEK/ERK pathway is also strongly implicated in ovarian cancer pathogenesis (29)(30)(31)(32)(33)(34)(35)(36)(37). Al-Ayoubi et al (38) reported that signaling via the MEK/ERK pathway helps cells escape anoikis and maintain anchorage-independent growth in several ovarian cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

SPARCL1 suppresses the proliferation and migration of human ovarian cancer cells via the MEK/ERK signaling

2018

Exp Ther Med

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Ovarian cancer is the most lethal gynecological malignancy worldwide and is one of the five leading causes of cancer-associated mortality in women. There is an urgent requirement to obtain a greater understanding of the molecular mechanism underlying ovarian cancer progression in order to identify novel drug targets and biomarkers. Secreted protein acidic and rich in cysteine-like protein 1 (SPARCL1) has been suggested as a candidate tumor suppressor in various types of human cancers. However, the potential role of SPARCL1 for ovarian cancer has not yet been clearly established. In the present study, lower protein expression levels of SPARCL1 were detected in ovarian cancer tissues when compared with adjacent normal tissues. Overexpression of SPARCL1 significantly suppressed the proliferation and migration of cells from the ovarian cancer cell line SKOV-3, whereas knockdown of SPARCL1 significantly increased cell growth and migration. Furthermore, the results revealed that SPARCL1 overexpression significantly suppressed the activation of the mitogen-activated protein kinase kinase (MEK)/extracellular signal-related kinase (ERK) signaling pathway. Collectively, these results indicated that SPARCL1 may suppress the proliferation and migration of ovarian cancer cells by downregulating signaling via the MEK/ERK pathway.

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“…A number of studies have shown that MAPKs (jNK1/2, ERK1/2, and p38) are involved in the growth, migration, and alterations in MMPs activity (24,25) in various cancers including lung, prostate, colorectal and ovarian cancer (26)(27)(28)(29)(30). Furthermore, the ERK signaling pathway in addition to the p38 signaling pathway may regulate numerous factors that are associated with cancer progression and poor prognosis in NSCLC (31)(32)(33).…”

Section: Discussionmentioning

confidence: 99%

Fibroblast growth factor 18 promotes proliferation and migration of H460 cells via the ERK and p38 signaling pathways

et al. 2016

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Abstract.Recently, fibroblast growth factor 18 (FGF18) expression was reported to be upregulated in colon cancer and ovarian cancer, and increased expression of FGF18 mRNA and protein is associated with tumor progression and poor overall survival in patients; however, its role in lung cancer remains to be explored. In the present study, the effect and underlying molecular mechanisms of FGF18 on H460 cells were investigated. Cell proliferation and cell cycle alterations were detected using a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and flow cytometry. A wound healing assay was conducted to detect cell migration. Reverse transcription-quantitative polymerase chain reaction and western blotting were performed to measure extracellular signal-regulated kinase (ERK), p38 and matrix metalloproteinase 26 (MMP26) expression. Knockdown of FGF18 using short interfering RNA (siRNA-FGF18) suppressed H460 cell proliferation, inhibited cell migration via the downregulation of MMP26 levels, with siRNA-FGF18 additionally inhibiting the ERK and p38 signaling pathway. The present study indicates that FGF18 serves an essential role in the growth and migration of non-small cell lung cancer (NSCLC) cells by regulating the ERK, p38 signaling pathways and MMP26 protein levels, suggesting that FGF18 may be a potential molecular drug target for the treatment NSCLC.

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Ghrelin attenuates the growth of HO-8910 ovarian cancer cells through the ERK pathway

Cited by 26 publications

References 18 publications

Expression of the ghrelin/growth hormone secretagogue receptor axis and its functional role in promoting tumor growth in primary central nervous system lymphomas

Expression of the ghrelin/growth hormone secretagogue receptor axis and its functional role in promoting tumor growth in primary central nervous system lymphomas

SPARCL1 suppresses the proliferation and migration of human ovarian cancer cells via the MEK/ERK signaling

Fibroblast growth factor 18 promotes proliferation and migration of H460 cells via the ERK and p38 signaling pathways

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