scholarly journals Alteration in cardiac PI3K/Akt/mTOR and ERK signaling pathways with the use of growth hormone and swimming, and the roles of miR21 and miR133

2018 ◽  
Author(s):  
Orkide Palabiyik ◽  
Ebru Tastekin ◽  
Zeynep Doganlar ◽  
Pinar Tayfur ◽  
Ayten Dogan ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Signaling Pathways ◽  
Erk Signaling

KCNN4 promotes the progression of lung adenocarcinoma by activating the AKT and ERK signaling pathways

2021 ◽  
pp. 1-15
Author(s):  
Ping Xu ◽  
Xiao Mo ◽  
Ruixue Xia ◽  
Long Jiang ◽  
Chengfei Zhang ◽  
...  
Keyword(s):  
Potassium Channels ◽  
Lung Adenocarcinoma ◽  
Potassium Channel ◽  
Signaling Pathways ◽  
Epithelial To Mesenchymal Transition ◽  
Tumor Biology ◽  
Erk Signaling ◽  
Mesenchymal Transition

BACKGROUND: Potassium channels, encoded by more than seventy genes, are cell excitability transmembrane proteins and become evident to play essential roles in tumor biology. OBJECTIVE: The deregulation of potassium channel genes has been related to cancer development and patient prognosis. The objective of this study is to understand the role of potassium channels in lung cancer. METHODS: We examined all potassium channel genes and identified that KCNN4 is the most significantly overexpressed one in lung adenocarcinoma. The role and mechanism of KCNN4 in lung adenocarcinoma were further investigated by in vitro cell and molecular assay and in vivo mouse xenograft models. RESULTS: We revealed that the silencing of KCNN4 significantly inhibits cell proliferation, migration, invasion, and tumorigenicity of lung adenocarcinoma. Further studies showed that knockdown of KCNN4 promotes cell apoptosis, induces cell cycle arrested in the S phase, and is associated with the epithelial to mesenchymal transition (EMT) process. Most importantly, we demonstrated that KCNN4 regulates the progression of lung adenocarcinoma through P13K/AKT and MEK/ERK signaling pathways. The use of inhibitors that targeted AKT and ERK also significantly inhibit the proliferation and metastasis of lung adenocarcinoma cells. CONCLUSIONS: This study investigated the function and mechanism of KCNN4 in lung adenocarcinoma. On this basis, this means that KCNN4 can be used as a tumor marker for lung adenocarcinoma and is expected to become an important target for a potential drug.

Bufalin induces protective autophagy by Cbl-b regulating mTOR and ERK signaling pathways in gastric cancer cells

2018 ◽  
Vol 43 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Hai-Yan Qi ◽  
Xiu-Juan Qu ◽  
Jing Liu ◽  
Ke-Zuo Hou ◽  
Yi-Bo Fan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Erk Signaling ◽  
Gastric Cancer Cells

Role of extracellular signal-regulated kinase (ERK) signaling in nucleotide excision repair and genotoxicity in response to As(III) and Pb(II)

2008 ◽  
Vol 80 (12) ◽  
pp. 2735-2750
Author(s):  
Ju-Pi Li ◽  
Chun-Yu Wang ◽  
Yen-An Tang ◽  
Yun-Wei Lin ◽  
Jia-Ling Yang
Keyword(s):  
Signaling Pathways ◽  
Nucleotide Excision Repair ◽  
Mammalian Cells ◽  
Excision Repair ◽  
Erk Signaling ◽  
Erk Activation ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Nucleotide Excision

Arsenic and lead can induce genetic injuries and epigenetic signaling pathways in cultured mammalian cells. To test whether signaling pathways affect the extent of genetic injuries, we explored the impacts of extracellular signal-regulated kinase 1 and 2 (ERK) on nucleotide excision repair (NER), cytotoxicity, and genotoxicity following sodium arsenite [As(III)] and lead acetate [Pb(II)]. Sustained ERK activation was observed in human cells exposed to As(III) and Pb(II). As(III) inhibited the cellular NER synthesis capability; conversely, Pb(II) stimulated it. ERK activation contributed to the As(III)-induced NER inhibition and micronucleus formation. In contrast, this signal was required for inducing cellular NER activity and preventing mutagenesis following Pb(II). ERK activation by Pb(II) was dependent on protein kinase C (PKCα) that also exhibited anti-mutagenicity. Enforced expression of ERK signaling markedly elevated the cellular NER activity, which was suppressed by As(III). Nonetheless, ERK activation could counteract the cytotoxicity caused by these two metals. Together, the results indicate that pro-survival ERK signaling exhibits dual and opposing impacts on NER process following As(III) and Pb(II) exposures. The findings also suggest that ERK is an important epigenetic signaling in the determination of metal genotoxicity.

Efficient Induction of Pluripotency in Primordial Germ Cells by Dual Inhibition of TGF-β and ERK Signaling Pathways

2014 ◽  
Vol 23 (10) ◽  
pp. 1050-1061 ◽  
Author(s):  
Farnoosh Attari ◽  
Houri Sepehri ◽  
Hassan Ansari ◽  
Seyedeh-Nafiseh Hassani ◽  
Fereshteh Esfandiari ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Germ Cells ◽  
Primordial Germ Cells ◽  
Erk Signaling ◽  
Efficient Induction ◽  
Dual Inhibition

Quetiapine ameliorates collagen-induced arthritis in mice via the suppression of the AKT and ERK signaling pathways

2018 ◽  
Vol 67 (10) ◽  
pp. 847-861 ◽  
Author(s):  
Yi-Ju Pan ◽  
Wei-Hsun Wang ◽  
Tzu-Yao Huang ◽  
Wei-Hsiang Weng ◽  
Chun-Kai Fang ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Erk Signaling ◽  
Collagen Induced Arthritis

Inhibition of PI3K/Akt and ERK signaling decreases visfatin-induced invasion in liver cancer cells

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Candace Miethe ◽  
Linda Torres ◽  
Megan Zamora ◽  
Ramona S. Price
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Fatty Acid Synthase ◽  
Erk Signaling ◽  
Ros Production ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Liver Cancer Cells ◽  
Phosphorylated Akt ◽  
Erk Inhibition

Abstract Objectives Visfatin is found in adipose tissue and is referred to as nicotinamide phosphoribosyltransferase (Nampt). Visfatin has anti-apoptotic, proliferative, and metastatic properties and may mediate its effects via ERK and PI3K/Akt signaling. Studies have yet to determine whether inhibition of kinase signaling will suppress visfatin-induced liver cancer. The purpose of this study was to determine which signaling pathways visfatin may promote liver cancer progression. Methods HepG2 and SNU-449 liver cancer cells were exposed to visfatin with or without ERK or PI3K/Akt inhibitor, or both inhibitors combined. These processes that were assessed: proliferation, reactive oxygen species (ROS), lipogenesis, invasion, and matrix metalloproteinase (MMP). Results Inhibition of PI3K/Akt and combination of inhibitors suppressed visfatin-induced viability. ERK inhibition in HepG2 cells decreased visfatin-induced proliferation. ERK inhibitor alone or in combination with PI3K inhibitors effectively suppressed MMP-9 secretion and invasion in liver cancer cells. PI3K and ERK inhibition and PI3K inhibition alone blocked visfatin’s ROS production in SNU-449 cells. These results corresponded with a decrease in phosphorylated Akt and ERK, β-catenin, and fatty acid synthase. Conclusions Akt and ERK inhibition differentially regulated physiological changes in liver cancer cells. Inhibition of Akt and ERK signaling pathways suppressed visfatin-induced invasion, viability, MMP-9 activation, and ROS production.

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