scholarly journals EriB targeted inhibition of microglia activity attenuates MPP+ induced DA neuron injury through the NF-κB signaling pathway

2018 ◽  
Vol 11 (1) ◽  
Author(s):  
Fangfang Dou ◽  
Xinkun Chu ◽  
Bei Zhang ◽  
Liang Liang ◽  
Guoqiang Lu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Targeted Inhibition ◽  
Neuron Injury

scholarly journals Targeting ERK-Hippo Interplay in Cancer Therapy

2020 ◽  
Vol 21 (9) ◽  
pp. 3236 ◽  
Author(s):  
Karel Vališ ◽  
Petr Novák
Keyword(s):  
Cancer Therapy ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Cross Talk ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Mitogen Activated Protein Kinase ◽  
Cancer Therapies ◽  
Anti Cancer ◽  
Targeted Inhibition

Extracellular signal-regulated kinase (ERK) is a part of the mitogen-activated protein kinase (MAPK) signaling pathway which allows the transduction of various cellular signals to final effectors and regulation of elementary cellular processes. Deregulation of the MAPK signaling occurs under many pathological conditions including neurodegenerative disorders, metabolic syndromes and cancers. Targeted inhibition of individual kinases of the MAPK signaling pathway using synthetic compounds represents a promising way to effective anti-cancer therapy. Cross-talk of the MAPK signaling pathway with other proteins and signaling pathways have a crucial impact on clinical outcomes of targeted therapies and plays important role during development of drug resistance in cancers. We discuss cross-talk of the MAPK/ERK signaling pathway with other signaling pathways, in particular interplay with the Hippo/MST pathway. We demonstrate the mechanism of cell death induction shared between MAPK/ERK and Hippo/MST signaling pathways and discuss the potential of combination targeting of these pathways in the development of more effective anti-cancer therapies.

Anti-angiogenic role of microRNA-23b in melanoma by disturbing NF-κB signaling pathway via targeted inhibition of NAMPT

2020 ◽  
Vol 16 (10) ◽  
pp. 541-458 ◽  
Author(s):  
Renrong Lv ◽  
Jing Yu ◽  
Qian Sun
Keyword(s):  
Signaling Pathway ◽  
Tumor Tissues ◽  
Melanoma Treatment ◽  
Melanoma Patients ◽  
Targeted Inhibition ◽  
Nicotinamide Phosphoribosyl Transferase ◽  
Poor Patient Survival

Aim: Melanoma is the major cause of death in patients inflicting skin cancer. We identify miR-23b plays an anti-angiogenic role in melanoma. Materials & methods: We collected tumor tissues from melanoma patients. Experiments in vivo and in vitro were designed to evaluate the role of miR-23b in melanoma. Results & conclusion: miR-23b was found to be downregulated in melanoma tissues, and associated with poor patient survival. Elevating miR-23b inhibited cell viability and colony formation, reduced pro-angiogenetic ability, and accelerated apoptosis in SK-MEL-28 cells. miR-23b targeted NAMPT. Disturbing NF-κB signaling pathway with ammonium pyrrolidinedithiocarbamate (an inhibitor of NF-kB signaling pathway) impeded acquired pro-angiogenetic ability of nicotinamide phosphoribosyl transferase-overexpressed SK-MEL-28 cells. MiR-23b is a prognostic factor in melanoma. This study provides an enhanced understanding of microRNA-based targets for melanoma treatment.

scholarly journals Effect of the PGD2-DP signaling pathway on primary cultured rat hippocampal neuron injury caused by aluminum overload

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Jie Ma ◽  
Qunfang Yang ◽  
Yuling Wei ◽  
Yang Yang ◽  
Chaonan Ji ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hippocampal Neuron ◽  
Neuron Injury

scholarly journals Down-regulated microRNA-183 mediates the Jak/Stat signaling pathway to attenuate hippocampal neuron injury in epilepsy rats by targeting Foxp1

Cell Cycle ◽  
2019 ◽  
Vol 18 (22) ◽  
pp. 3206-3222 ◽  
Author(s):  
Xiangyong Feng ◽  
Wei Xiong ◽  
Mingqiong Yuan ◽  
Jian Zhan ◽  
Xiankun Zhu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hippocampal Neuron ◽  
Stat Signaling ◽  
Neuron Injury

scholarly journals Targeted inhibition of KCa3.1 attenuates TGF-β-induced reactive astrogliosis through the Smad2/3 signaling pathway

2014 ◽  
Vol 130 (1) ◽  
pp. 41-49 ◽  
Author(s):  
Zhihua Yu ◽  
Panpan Yu ◽  
Hongzhuan Chen ◽  
Herbert M. Geller
Keyword(s):  
Signaling Pathway ◽  
Reactive Astrogliosis ◽  
Targeted Inhibition

scholarly journals Upregulation of miR-216a-5p by Lentinan Targeted Inhibition of JAK2/STAT3 Signaling Pathway to Reduce Lung Adenocarcinoma Cell Stemness, Promote Apoptosis, and Slow Down the Lung Adenocarcinoma Mechanisms

2021 ◽  
Vol 11 ◽  
Author(s):  
Quan Chen ◽  
Yiming Zheng ◽  
Xia Chen ◽  
Pengfei Ge ◽  
Pengcheng Wang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Control Group ◽  
Inhibitory Effects ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Cell Proliferation Activity ◽  
Targeted Inhibition

To investigate the effect of Lentinan (LNT) on lung adenocarcinoma (LUAD) cell stemness and its mechanism. In this study, we founded that LNT significantly reduce the cell proliferation, activity, migration, invasion, and stemness of LUAD cells, and promote their apoptosis compared with the control group in vitro. Moreover, LNT significantly inhibited the volume and weight of tumors of nude mice in vivo. At the same time, LNT can significantly up-regulate miR-216a-5p levels and reduce the protein expression of phospho-JAK2 (Y1007/1008) and phospho-STAT3 (Tyr705), thereby inhibiting the JAK2/STAT3 signaling pathway. Interfering with miR-216a-5p expression and activating the JAK2/STAT3 signaling pathway can significantly reverse LNT inhibitory effects on LUAD. Collectively, LNT can inhibit the JAK2/STAT3 signaling pathway by up-regulating miR-216a-5p, reducing stemness, and promoting LUAD cells apoptosis, then slow down LUAD occurrence and development, providing concepts and experimental foundation treating patients with LUAD.

scholarly journals NLRP3 Inflammasome Activation of Mast Cells by Estrogen via the Nuclear-Initiated Signaling Pathway Contributes to the Development of Endometriosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Xinyue Guo ◽  
Xinxin Xu ◽  
Tiantian Li ◽  
Qin Yu ◽  
Jianzhang Wang ◽  
...  
Keyword(s):  
Mast Cells ◽  
Signaling Pathway ◽  
Nlrp3 Inflammasome ◽  
Estrogen Signaling ◽  
Inflammasome Activation ◽  
Pyrin Domain ◽  
Nlrp3 Inflammasome Activation ◽  
Estrogen Responsive Element ◽  
Targeted Inhibition ◽  
Responsive Element

Endometriosis is an estrogen-dependent gynecological disease. The pathogenesis of endometriosis remains controversial, although it is generally accepted that the inflammatory immune response plays a crucial role in this process. Mast cells (MCs) are multifunctional innate immune cells that accumulate in endometriotic lesions. However, the molecular mechanism by which estrogen modulates MCs in the development of endometriosis is not well understood. Here we report that estrogen can induce the expression of NOD-like receptor family pyrin domain containing 3 (NLRP3) through estrogen receptor (ER)-α via the estrogen responsive element (ERE) in MCs. Such transcriptional regulation is necessary for the activation of NLRP3 inflammasome and the production of mature interleukin (IL)-1β in MCs. Targeted inhibition of NLRP3 significantly restrained lesion progression and fibrogenesis in a mouse model of endometriosis. Collectively, these findings suggest that MCs contribute to the development of endometriosis through NLRP3 inflammasome activation mediated by nuclear-initiated estrogen signaling pathway.

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