scholarly journals Pepsin promotes laryngopharyngeal neoplasia by modulating signaling pathways to induce cell proliferation

PLoS ONE ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. e0227408 ◽  
Author(s):  
Kai Niu ◽  
Chunjie Guo ◽  
Shiyong Teng ◽  
Dandan Zhou ◽  
Shuyuan Yu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathways ◽  
Induce Cell Proliferation

111-OR: Pancreatic Elastase Regulates Human Beta-Cell Proliferation via the Focal Adhesion and PAR2 Signaling Pathways

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 111-OR
Author(s):  
GIORGIO BASILE ◽  
AMEDEO VETERE ◽  
KA-CHEUK LIU ◽  
JIANG HU ◽  
OLOV ANDERSSON ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Beta Cell ◽  
Signaling Pathways ◽  
Focal Adhesion ◽  
Beta Cell Proliferation ◽  
Pancreatic Elastase ◽  
Human Beta Cell

Signaling Pathways Involved in Antidepressant-Induced Cell Proliferation and Synaptic Plasticity

2014 ◽  
Vol 20 (23) ◽  
pp. 3776-3794 ◽  
Author(s):  
Fuencisla Pilar-Cuellar ◽  
Rebeca Vidal ◽  
Alvaro Díaz ◽  
Elena Castro ◽  
Severiano Anjos ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Synaptic Plasticity ◽  
Signaling Pathways

scholarly journals The Role of EGFR/PI3K/Akt/cyclinD1 Signaling Pathway in Acquired Middle Ear Cholesteatoma

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Wei Liu ◽  
Hongmiao Ren ◽  
Jihao Ren ◽  
Tuanfang Yin ◽  
Bing Hu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
External Auditory Canal ◽  
Cell Cycle Progression ◽  
Critical Role ◽  
Immunohistochemical Method ◽  
Cycle Progression ◽  
Middle Ear Cholesteatoma

Cholesteatoma is a benign keratinizing and hyper proliferative squamous epithelial lesion of the temporal bone. Epidermal growth factor (EGF) is one of the most important cytokines which has been shown to play a critical role in cholesteatoma. In this investigation, we studied the effects of EGF on the proliferation of keratinocytes and EGF-mediated signaling pathways underlying the pathogenesis of cholesteatoma. We examined the expressions of phosphorylated EGF receptor (p-EGFR), phosphorylated Akt (p-Akt), cyclinD1, and proliferating cell nuclear antigen (PCNA) in 40 cholesteatoma samples and 20 samples of normal external auditory canal (EAC) epithelium by immunohistochemical method. Furthermore,in vitrostudies were performed to investigate EGF-induced downstream signaling pathways in primary external auditory canal keratinocytes (EACKs). The expressions of p-EGFR, p-Akt, cyclinD1, and PCNA in cholesteatoma epithelium were significantly increased when compared with those of control subjects. We also demonstrated that EGF led to the activation of the EGFR/PI3K/Akt/cyclinD1 signaling pathway, which played a critical role in EGF-induced cell proliferation and cell cycle progression of EACKs. Both EGFR inhibitor AG1478 and PI3K inhibitor wortmannin inhibited the EGF-induced EGFR/PI3K/Akt/cyclinD1 signaling pathway concomitantly with inhibition of cell proliferation and cell cycle progression of EACKs. Taken together, our data suggest that the EGFR/PI3K/Akt/cyclinD1 signaling pathway is active in cholesteatoma and may play a crucial role in cholesteatoma epithelial hyper-proliferation. This study will facilitate the development of potential therapeutic targets for intratympanic drug therapy for cholesteatoma.

Activation of adenosine A1receptor-induced neural stem cell proliferation via MEK/ERK and Akt signaling pathways

2008 ◽  
Vol 86 (13) ◽  
pp. 2820-2828 ◽  
Author(s):  
Hideyuki Migita ◽  
Katsuya Kominami ◽  
Mami Higashida ◽  
Rumi Maruyama ◽  
Nobuko Tuchida ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stem Cell ◽  
Signaling Pathways ◽  
Neural Stem Cell ◽  
Akt Signaling ◽  
Stem Cell Proliferation ◽  
Neural Stem Cell Proliferation ◽  
Induced Neural Stem Cell

scholarly journals Adenosine Attenuates Human Coronary Artery Smooth Muscle Cell Proliferation by Inhibiting Multiple Signaling Pathways That Converge on Cyclin D

Hypertension ◽  
2015 ◽  
Vol 66 (6) ◽  
pp. 1207-1219 ◽  
Author(s):  
Raghvendra K. Dubey ◽  
Jürgen Fingerle ◽  
Delbert G. Gillespie ◽  
Zaichuan Mi ◽  
Marinella Rosselli ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cell ◽  
Signaling Pathways ◽  
Muscle Cell ◽  
Smooth Muscle Cell Proliferation ◽  
Cyclin D ◽  
Human Coronary Artery ◽  
Multiple Signaling

Beetroot and leaf extracts present protective effects against prostate cancer cells, inhibiting cell proliferation, migration, and growth signaling pathways

2021 ◽  
Author(s):  
Mariana Camargo Silva Mancini ◽  
Luis Gustavo Saboia Ponte ◽  
Cayo Henrique Rocha Silva ◽  
Isabella Fagundes ◽  
Isadora Carolina Betim Pavan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Protective Effects ◽  
Prostate Cancer Cells ◽  
Leaf Extracts

Biological Effects of Gyrophoric Acid and Other Lichen Derived Metabolites, on Cell Proliferation, Apoptosis and Cell Signaling pathways

2022 ◽  
Vol 351 ◽  
pp. 109768
Author(s):  
Mahshid Mohammadi ◽  
Leila Bagheri ◽  
Amr Badreldin ◽  
Pedram Fatehi ◽  
Leila Pakzad ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Signaling ◽  
Signaling Pathways ◽  
Biological Effects ◽  
Cell Signaling Pathways ◽  
Gyrophoric Acid

AKIP1 promotes cell proliferation, invasion, stemness and activates PI3K-Akt, MEK/ERK, mTOR signaling pathways in prostate cancer

2021 ◽  
Author(s):  
Jiabin Zhao ◽  
Binjiahui Zhao ◽  
Limin Hou
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Signaling Pathways ◽  
Cancer Patients ◽  
Rna Sequencing ◽  
Mtor Signaling ◽  
Sequencing Analysis ◽  
Lncap Cells ◽  
Oncogenic Signaling ◽  
Interacting Protein

Abstract Background: The study aimed to examine the molecular mechanism and clinical significance of A-kinase interacting protein 1 (AKIP1) in prostate cancer. Methods: The effect of AKIP1 on cell proliferation, migration, invasion, apoptosis and stemness was determined by overexpressing and knocking down AKIP1 in LNCaP and 22Rv1 cells via lentivirus infection. Furthermore, differentially expressed genes (DEGs) by AKIP1 modification were determined using RNA sequencing. Besides, the correlation of AKIP1 with clinicopathological features and prognosis in 130 prostate cancer patients was assessed. Results: AKIP1 expression was increased in VCaP, LNCaP, DU145 cells while similar in 22Rv1 cells compared with RWPE-1 cells. Furthermore, AKIP1 overexpression promoted 22Rv1 and LNCaP cell proliferation, invasion, but inhibited apoptosis; meanwhile, AKIP1 overexpression increased CD133+ cell rate and enhanced spheres formation efficiency in 22Rv1 and LNCaP cells. Reversely, AKIP1 knockdown exhibited the opposite effect in 22Rv1 and LNCaP cells. Further RNA sequencing analysis exhibited that AKIP1-modified DEGs were enriched in the oncogenic signaling pathways related to prostate cancer, such as PI3K-Akt, MEK/ERK, mTOR signaling pathways. The following western blot indicated that AKIP1 overexpression activated while its knockdown blocked PI3K-Akt, MEK/ERK, mTOR signaling pathways in prostate cancer cells. Clinically, AKIP1 was upregulated in the prostate tumor tissues compared with paired adjacent tissues, and its tumor high expression correlated with increased pathological T, pathological N stage and poor prognosis in prostate cancer patients. Conclusion: AKIP1 promotes cell proliferation, invasion, stemness, activates PI3K-Akt, MEK/ERK, mTOR signaling pathways and correlates with worse tumor features and prognosis in prostate cancer.

scholarly journals MicroRNA-3666 inhibits lung cancer cell proliferation, migration, and invasiveness by targeting BPTF

2019 ◽  
Vol 97 (4) ◽  
pp. 415-422 ◽  
Author(s):  
Linqing Pan ◽  
Zhipeng Tang ◽  
Lina Pan ◽  
Ranran Tang
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Signaling Pathways ◽  
Histological Grade ◽  
Clinical Stage ◽  
Luciferase Reporter ◽  
Advanced Clinical Stage ◽  
Mesenchymal Transition ◽  
Adenocarcinoma Cell

A previous study by our group indicted that overexpression of bromodomain PHD-finger transcription factor (BPTF) occurs in lung adenocarcinoma, and is closely associated with advanced clinical stage, higher numbers of metastatic lymph nodes, the occurrence of distant metastasis, low histological grade, and poor prognosis. Down-regulation of BPTF inhibited lung adenocarcinoma cell proliferation and promoted lung adenocarcinoma cell apoptosis. The purpose of this study is to identify valuable microRNAs (miRNAs) that target BPTF to modulate lung adenocarcinoma cell proliferation. In our results, we found that miR-3666 was notably reduced in lung adenocarcinoma tissues and cell lines. Using an miR-3666 mimic, we discovered that cell proliferation, migration, and invasiveness were suppressed by miR-3666 overexpression, but these were all enhanced when the expression of miR-3666 was reduced. Moreover, bioinformatics analysis using the TargetScan database and miRanda software suggested a putative target site in BPTF 3′-UTR. Furthermore, using a luciferase reporter assay, we verified that miR-3666 directly targets the 3′-UTR of BPTF. Using Western blot we discovered that overexpression of miR-3666 negatively regulates the protein expression of BPTF. Finally, we identified that the PI3K–AKT and epilthelial–mesenchymal transition (EMT) signaling pathways were inhibited by miR-3666 overexpression in lung cancer cells. In conclusion, our data indicate that miR-3666 could play an essential role in cell proliferation, migration, and invasiveness by targeting BPTF and partly inhibiting the PI3K–AKT and EMT signaling pathways in human lung cancers.

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