scholarly journals KrasG12D-LOH promotes malignant biological behavior and energy metabolism of pancreatic ductal adenocarcinoma cells through the mTOR signaling pathway

Neoplasma ◽  
2018 ◽  
Vol 65 (01) ◽  
pp. 81-88 ◽  
Author(s):  
X. SHEN ◽  
L.G. CHANG ◽  
M.Y. HU ◽  
D. YAN ◽  
L.N. ZHOU ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Biological Behavior ◽  
Ductal Adenocarcinoma ◽  
Mtor Signaling Pathway ◽  
Adenocarcinoma Cells

scholarly journals EPHA2 Promotes the Invasion and Migration of Human Tongue Squamous Cell Carcinoma Cal-27 Cells by Enhancing AKT/mTOR Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Fengqin Wang ◽  
Hanzhong Zhang ◽  
Zhigang Cheng
Keyword(s):  
Cell Cycle ◽  
Signaling Pathway ◽  
Mtor Inhibitor ◽  
Mtor Signaling ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Akt Inhibitor ◽  
Invasion And Migration ◽  
And Migration

EPHA2 is a member of the ephrin receptor tyrosine kinase family and is closely related to the malignant tumor progression. The effect of EPHA2 on OSCC is not clear. This study explored the role of EPHA2 and AKT/mTOR signaling pathways in Cal-27 cell invasion and migration. The expression of EPHA2 and EPHA4 in human OSCC and normal oral tissue was detected by immunohistochemistry. EPHA2-overexpressing and EPHA2-knockdown Cal-27 cells were established, and the cells were treated with an AKT inhibitor (MK2206) and mTOR inhibitor (RAD001). The expression of EPHA2 was detected by qRT-PCR, cell proliferation was evaluated by MTT assay, cell migration and invasion were examined by scratch and Transwell assay, and cell morphology and apoptosis were assessed by Hoechst 33258 staining. Western blot was performed to detect the expression of proteins related to AKT/mTOR signaling, cell cycle, and pseudopod invasion. EPHA2 and EPHA4 were highly expressed in clinical human OSCC. Overexpression of EPHA2 promoted the proliferation, migration, and invasion of Cal-27 cells, inhibited cell cycle blockage and apoptosis, and enhanced the activity of the AKT/mTOR signaling pathway. MK2206 (AKT inhibitor) and RAD001 (mTOR inhibitor) reversed the effect of EPHA2 overexpression on the biological behavior of Cal-27 cells. EPHA2 promotes the invasion and migration of Cal-27 human OSCC cells by enhancing the AKT/mTOR signaling pathway.

scholarly journals Effect of activation of the Akt/mTOR signaling pathway by EEF1A2 on the biological behavior of osteosarcoma

2021 ◽  
Vol 9 (2) ◽  
pp. 158-158
Author(s):  
Jianing Yang ◽  
Jun Tang ◽  
Juan Li ◽  
Ying Cen ◽  
Junjie Chen ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Mtor Signaling ◽  
Biological Behavior ◽  
Mtor Signaling Pathway

scholarly journals Bee Pollen Improves Muscle Protein and Energy Metabolism in Malnourished Old Rats through Interfering with the Mtor Signaling Pathway and Mitochondrial Activity

Nutrients ◽  
2014 ◽  
Vol 6 (12) ◽  
pp. 5500-5516 ◽  
Author(s):  
Jérôme Salles ◽  
Nicolas Cardinault ◽  
Véronique Patrac ◽  
Alexandre Berry ◽  
Christophe Giraudet ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Signaling Pathway ◽  
Muscle Protein ◽  
Mtor Signaling ◽  
Mitochondrial Activity ◽  
Mtor Signaling Pathway ◽  
Bee Pollen ◽  
Old Rats

scholarly journals Regulatory Mechanism of mTOR Signaling Pathway on Cell Energy Metabolism

2015 ◽  
Vol 45 (11) ◽  
pp. 1124-1131
Author(s):  
BiE TAN ◽  
FangYuan SHAO ◽  
YuLong YIN ◽  
Hao XIAO ◽  
MiaoMiao WU
Keyword(s):  
Energy Metabolism ◽  
Signaling Pathway ◽  
Regulatory Mechanism ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Cell Energy ◽  
Cell Energy Metabolism

MiR-186 serves as a tumor suppressor in lung adenocarcinoma cells by down-regulation of Shp2 gene and inhibiting PI3K/Akt/mTOR signaling pathway

2020 ◽  
Author(s):  
Shao-Hui Yan ◽  
Shu-Feng Xu ◽  
Lei Zheng ◽  
Li-Ying Kang ◽  
Jun-Li Cao ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Signaling Pathway ◽  
Tyrosine Phosphatase ◽  
Negative Control ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Blank Group ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

Abstract Background The study aimed to investigate the effect and mechanism of miR-186, which targets protein tyrosine phosphatase (Shp2) PI3K/Akt/mTOR signaling pathway, on the biological characteristics of lung adenocarcinoma cells. Methods In this experimental study, Human lung adenocarcinoma cell line SPC-A-1 was grouped as Blank group, negative control (NC) group, miR-186 mimic group, miR-186 inhibitor group, si-Shp2 group and miR-186 inhibitor+si-Shp2 group. Results The results showed that miR-186 can target and down-regulate the expression of Shp2 gene. Compared with the Blank group, levels of Shp2, N-cadherin and Bcl-2 and level of PI3K/p-PI3K, Akt/P-Akt, mTOR/p-mTOR as well as cell proliferation, migration and invasion ability and the proportion of cells in S phase significantly decreased in the miR-186 mimic group and the si-Shp2 group, while the levels of E-cadherin and Bax as well as the proportion of cells in G1 phase and cell gene and mediates apoptosis rate increased significantly (all P < 0.05). Compared with the miR-186 inhibitor group, the miR-186 inhibitor + si-Shp2 group showed similar trend in all parameters with the comparison above (all P < 0.05). Conclusions The overexpression of miR-186 can down-regulate Shp2 gene expression, further inhibit the proliferation, invasion and migration and promote apoptosis of lung adenocarcinoma cells by inhibiting the activation of PI3K/Akt/mTOR signaling pathway.

scholarly journals ID2 Inhibits Lung Adenocarcinoma Cell Malignant Behaviors Through Inhibiting the Activation of the PI3K/AKT/mTOR Signaling Pathway

2021 ◽  
Author(s):  
Wenzhong Peng ◽  
Jia Chen ◽  
Ruoxi He ◽  
Yongjun Tang ◽  
Juan Jiang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Candidate Gene ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Tissue Samples ◽  
Adenocarcinoma Cell ◽  
Protein Levels ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

Abstract Background: Lung cancer is the most common cancer and one of the main causes of cancer-related deaths, and it manifests as metastatic disease in most cases. Considering frequent gene mutation and/or signaling deregulation in lung adenocarcinoma, identifying novel factors or agents targeting these signaling pathways might be promising strategies for lung adenocarcinoma therapy. Methods: GEO datasets were analyzed to identify differentially expressed genes (DEGs) in lung adenocarcinoma. The specific effects of candidate gene overexpression or knockdown on lung adenocarcinoma cell phenotypes were examined. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) are used to connect the genomic and functional information of DEGs. The dynamic effects of candidate gene and signaling pathway agonist on lung adenocarcinoma malignant behaviors were investigated. Finally, clinical lung adenocarcinoma and adjacent non-cancerous tissues were collected and the levels of candidate gene were examined in tissue samples.Results: Inhibitor of DNA binding 2 (ID2) was identified as an aberrantly downregulated gene in lung adenocarcinoma. ID2 overexpression suppressed lung adenocarcinoma cell viability, colony formation capacity, and migration. ID2 overexpression also reduced the protein levels of N-cadherin, MMP2, MMP9, and the phosphorylation of AKT and mTOR. The PI3K/AKT/mTOR signaling agonist exerted opposite effects on lung adenocarcinoma cells to those of ID2 overexpression, and partially reversed the effects of ID2 overexpression. In tissue samples, ID2 protein levels and mRNA expression were also downregulated compared with those in adjacent non-cancerous tissues. Conclusion: ID2 exerts its tumor-suppressive effects on lung adenocarcinoma cell malignant behaviors through inhibiting the activation of the PI3K/AKT/mTOR signaling pathway. Restoring ID2 expression in lung adenocarcinoma cells might improve the curative effect of lung adenocarcinoma therapies.

Sign in / Sign up

Export Citation Format

Share Document