Apicobasal polarity and Ras/Raf/MEK/ERK signalling in cancer

Peng, Juan; Gassama‐Diagne, Ama

doi:10.1136/gutjnl-2016-312986

Cited by 17 publications

(10 citation statements)

References 10 publications

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“…The Ras/Raf/MEK/ERK cascade is a key signaling pathway that regulates many cellular functions including proliferation, survival, apoptosis, motility, differentiation, and metabolism [34–36]. Deregulation of the RAS/RAF/MEK/ERK pathway is regarded as a hallmark for driving tumorigenesis in a number of human cancers [37, 38]. Furthermore, it has been shown that RAS/RAF/MEK/ERK pathway is one of the downstream intracellular signals of EGFR [39].…”

Section: Resultsmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits the growth and increases the apoptosis of human thyroid carcinoma cells through suppression of EGFR/RAS/RAF/MEK/ERK signaling pathway

Liu

et al. 2019

Cancer Cell Int

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Background Thyroid cancer is the most common type of endocrine malignancy and the incidence rate is rapidly increasing worldwide. Epigallocatechin-3-gallate (EGCG) could suppress cancer growth and induce apoptosis in many types of cancer cells. However, the mechanism of action of EGCG on the growth of human thyroid carcinoma cells has not been fully illuminated. Methods Cell proliferation and viability were detected by EdU and MTS assays. Cell cycle distribution was measured by flow cytometry. Migration and invasion were evaluated by scratch and transwell assays. Apoptotic levels were detected by TUNEL staining and western blotting. The protein levels of EGFR/RAS/RAF/MEK/ERK signaling pathway were detected by western blotting. The in vivo results were determined by tumor xenografts in nude mice. The in vivo proliferation, tumor microvessel density, and apoptosis were detected by immunohistochemistry. Results EGCG inhibited the proliferation, viability, and cell cycle progression in human thyroid carcinoma cells. EGCG decreased the migration and invasion, but increased the apoptosis of human thyroid carcinoma cells. EGCG reduced the protein levels of phospho (p)-epidermal growth factor receptor (EGFR), H-RAS, p-RAF, p-MEK1/2, and p-extracellular signal-regulated protein kinase 1/2 (ERK1/2) in human thyroid carcinoma cells. EGCG inhibited the growth of human thyroid carcinoma xenografts by inducing apoptosis and down-regulating angiogenesis. Conclusions EGCG could reduce the growth and increase the apoptosis of human thyroid carcinoma cells through suppressing the EGFR/RAS/RAF/MEK/ERK signaling pathway. EGCG can be developed as an effective therapeutic agent for the treatment of thyroid cancer.

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Section: Resultsmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits the growth and increases the apoptosis of human thyroid carcinoma cells through suppression of EGFR/RAS/RAF/MEK/ERK signaling pathway

Liu

et al. 2019

Cancer Cell Int

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“…The differential findings could also be due to inter-laboratory variation in the methods used to measure TL. 11 Most of the studies used single quantitative real-time polymerase chain reaction (qPCR) 66 to measure LTL, 6,12,13,65 only Lynch et al 7 used monochrome multiplex qPCR (MMqPCR). 7 Even among studies that used qPCR, differences in the DNA purity of blood samples or in the methods used to identify, quantify, or normalize the telomeric sequence repeats may affect TL measurements between studies.…”

Section: Association Between Ltl and Pc Riskmentioning

confidence: 99%

“…It is postulated that some of these factors (e.g., tobacco smoking, diabetes, and obesity) modulate PC risk by accelerating the shortening of telomeres or telomere length (TL), 6,7 the non-coding DNA sequence repeats at the ends of eukaryotic chromosomes that protect chromosomal composition from degradation and maintain chromosomal stability during cell replication. 8-10 Findings from studies that have investigated the association between peripheral blood leukocyte telomere length (LTL) and PC risk have been mixed (reviewed in 11 ).However, these studies differ substantially in methods, design, and study population characteristics. Thus, despite inconsistent findings, it remains plausible that LTL may represent a comprehensive biological marker of exposure to risk factors of pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

Leukocyte Telomere Length and Pancreatic Cancer Risk

Antwi¹,

Petersen²

2018

Pancreas

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Many risk factors have been firmly established for pancreatic cancer (PC), but the molecular processes by which known risk factors influence susceptibility to PC are not clear. There has been a recent upsurge of interest in the role of telomere length (TL), the protective DNA sequence repeats at chromosome ends, in pancreatic carcinogenesis. Given this heightened interest, we performed an in-depth, focused, and up-to-date review of the epidemiological evidence linking leukocyte TL (LTL) with PC risk. We searched MEDLINE, Embase, and the Cochrane Library databases for all published studies on LTL and PC risk, up to May 2017. Five studies were identified for review: 4 nested case-control studies and 1 retrospective case-control study. Two studies found opposite associations between LTL and PC risk: 1 found a dose-response positive association and the other found a dose-response inverse association. Two studies also found a "U-shaped" association, whereas another reported a weak nonlinear relationship. We offer potential reasons for the conflicting findings including variation in study design, biospecimen characteristics, and differences in interlaboratory measurements of TL. Future studies should carefully control for risk factors of PC that are associated also with telomere attrition and investigate the role of genetic variation in TL maintenance.

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“…The RAS/RAF/MEK/ERK cascade is a key intracellular signaling pathway that regulates many physiological functions and cellular processes, including proliferation, apoptosis, survival, motility, differentiation, and metabolism [39–41]. Hyperactivation of the RAS/RAF/MEK/ERK signaling pathway has been regarded as a hallmark for driving tumorigenesis in a high percentage of human cancers [42, 43]. As shown in Figure 7, treatment with 25–50 μ M NaHS increased the protein levels of H-RAS, p-RAF, p-MEK1/2, and p-ERK1/2.…”

Section: Resultsmentioning

confidence: 99%

Exogenous Hydrogen Sulfide Regulates the Growth of Human Thyroid Carcinoma Cells

Zhang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Hydrogen sulfide (H2S) is involved in the development and progression of many types of cancer. However, the effect and mechanism of H2S on the growth of human thyroid carcinoma cells remain unknown. In the present study, we found that the proliferation, viability, migration, and invasion of human thyroid carcinoma cells were enhanced by 25–50 μM NaHS (an H2S donor) and inhibited by 200 μM NaHS. However, H2S showed no obvious effects on the proliferation, viability, and migration of human normal thyroid cells. Administration of 50 μM NaHS increased the expression levels of CBS, SQR, and TST, while 200 μM NaHS showed reverse effects in human thyroid carcinoma cells. After treatment with 25-50 μM NaHS, the ROS levels were decreased and the protein levels of p-PI3K, p-AKT, p-mTOR, H-RAS, p-RAF, p-MEK1/2, and p-ERK1/2 were increased, whereas 200 μM NaHS exerted opposite effects in human thyroid carcinoma cells. Furthermore, 1.4-2.8 mg/kg/day NaHS promoted the tumor growth and blood vessel formation in human thyroid carcinoma xenograft tumors, while 11.2 mg/kg/day NaHS inhibited the tumor growth and angiogenesis. In conclusion, our results demonstrate that exogenous H2S regulates the growth of human thyroid carcinoma cells through ROS/PI3K/Akt/mTOR and RAS/RAF/MEK/ERK signaling pathways. Novel H2S-releasing donors/drugs can be designed and applied for the treatment of thyroid cancer.

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Apicobasal polarity and Ras/Raf/MEK/ERK signalling in cancer

Cited by 17 publications

References 10 publications

Epigallocatechin-3-gallate inhibits the growth and increases the apoptosis of human thyroid carcinoma cells through suppression of EGFR/RAS/RAF/MEK/ERK signaling pathway

Epigallocatechin-3-gallate inhibits the growth and increases the apoptosis of human thyroid carcinoma cells through suppression of EGFR/RAS/RAF/MEK/ERK signaling pathway

Leukocyte Telomere Length and Pancreatic Cancer Risk

Exogenous Hydrogen Sulfide Regulates the Growth of Human Thyroid Carcinoma Cells

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