scholarly journals Down-regulated microRNA-223 or elevated ZIC1 inhibits the development of pancreatic cancer via inhibiting PI3K/Akt/mTOR signaling pathway activation

Cell Cycle ◽  
2020 ◽  
Vol 19 (21) ◽  
pp. 2851-2865
Author(s):  
Jian Zhu ◽  
Jian Lv ◽  
Jing Chen ◽  
Xuesong Zhang ◽  
Yong Ji
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Pathway Activation

Gemcitabine induces apoptosis and autophagy via the AMPK/mTOR signaling pathway in pancreatic cancer cells

2018 ◽  
Vol 65 (5) ◽  
pp. 665-671 ◽  
Author(s):  
Jinhui Zhu ◽  
Yan Chen ◽  
Yun Ji ◽  
Yuanquan Yu ◽  
Yun Jin ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Pancreatic Cancer Cells

LDLRAD2 promotes pancreatic cancer progression through Akt/mTOR signaling pathway

2021 ◽  
Vol 38 (1) ◽  
Author(s):  
Junhe Li ◽  
Wei Huang ◽  
Qing Han ◽  
Jianping Xiong ◽  
Zhiwang Song
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

Akt/mTOR signaling pathway is crucial for gemcitabine resistance induced by Annexin II in pancreatic cancer cells

2012 ◽  
Vol 178 (2) ◽  
pp. 758-767 ◽  
Author(s):  
Shingo Kagawa ◽  
Shigetsugu Takano ◽  
Hideyuki Yoshitomi ◽  
Fumio Kimura ◽  
Mamoru Satoh ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Annexin Ii ◽  
Mtor Signaling Pathway ◽  
Gemcitabine Resistance ◽  
Pancreatic Cancer Cells

scholarly journals Erzhi Pill® Repairs Experimental Liver Injury via TSC/mTOR Signaling Pathway Inhibiting Excessive Apoptosis

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Bu-gao Zhou ◽  
Hai-mei Zhao ◽  
Xiu-yun Lu ◽  
Xin Wang ◽  
Yong Zou ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Mammalian Target Of Rapamycin ◽  
Liver Weight ◽  
Mtor Signaling ◽  
Hepatoprotective Effect ◽  
Mtor Signaling Pathway ◽  
Gamma Glutamyl Transpeptidase ◽  
Pathway Activation ◽  
Experimental Liver

The present study aimed to investigate the mechanism of hepatoprotective effect of Erzhi Pill (EZP) on the liver injury via observing TSC/mTOR signaling pathway activation. The experimental liver injury was induced by 2-acetylaminofluorene (2-AAF) treatment combined with partial hepatectomy (PH). EZP treated 2-AAF/PH-induced liver injury by the therapeutic and prophylactic administration. After the administration of EZP, the activities of aspartic transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AKP), and gamma-glutamyl transpeptidase (γ-GT) were decreased, followed by the decreased levels of hepatocyte apoptosis and caspase-3 expression. However, the secretion of albumin, liver weight, and index of liver weight were elevated. Microscopic examination showed that EZP restored pathological liver injury. Meanwhile, Rheb and mammalian target of rapamycin (mTOR) activation were suppressed, and tuberous sclerosis complex (TSC) expression was elevated in liver tissues induced by 2-AAF/PHx and accompanied with lower-expression of Bax, Notch1, p70S6K, and 4E-EIF and upregulated levels of Bcl-2 and Cyclin D. Hepatoprotective effect of EZP was possibly realized via inhibiting TSC/mTOR signaling pathway to suppress excessive apoptosis of hepatocyte.

scholarly journals Hypoxia-Related Gene FUT11 Promotes Pancreatic Cancer Progression by Maintaining the Stability of PDK1

2021 ◽  
Vol 11 ◽  
Author(s):  
Wenpeng Cao ◽  
Zhirui Zeng ◽  
Runsang Pan ◽  
Hao Wu ◽  
Xiangyan Zhang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Growth ◽  
Western Blot ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Cell Growth And Migration ◽  
And Migration ◽  
The Stability

BackgroundHypoxia is associated with the development of pancreatic cancer (PC). However, genes associated with hypoxia response and their regulatory mechanism in PC cells were unclear. The current study aims to investigate the role of the hypoxia associated gene fucosyltransferase 11 (FUT11) in the progression of PC.MethodsIn the preliminary study, bioinformatics analysis predicted FUT11 as a key hypoxia associated gene in PC. The expression of FUT11 in PC was evaluated using quantitative real-time PCR (qRT-PCR), Western blot and immunohistochemistry. The effects of FUT11 on PC cells proliferation and migration under normoxia and hypoxia were evaluated using Cell Counting Kit 8, 5-ethynyl-2’-deoxyuridine (EDU) assay, colony formation assay and transwell assay. The effects of FUT11 in vivo was examined in mouse tumor models of liver metastasis and subcutaneous xenograft. Furthermore, Western blot, luciferase assay and immunoprecipitation were performed to explore the regulatory relationship among FUT11, hypoxia-inducible factor 1α (HIF1α) and pyruvate dehydrogenase kinase 1 (PDK1) in PC.ResultsFUT11 was markedly increased of PC cells with hypoxia, upregulated in the PC clinical tissues, and predicted a poor outcome of PC patients. Inhibition of FUT11 reduced PC cell growth and migratory ability of PC cells under normoxia and hypoxia conditions in vitro, and growth and tumor cell metastasis in vivo. FUT11 bound to PDK1 and regulated the expression PDK1 under normoxia and hypoxia. FUT11 interacted with PDK1 and decreased the ubiquitination of PDK1, lead to the activation of AKT/mTOR signaling pathway. FUT11 knockdown significantly increased the degradation of PDK1 under hypoxia, while treatment with MG132 can relieve the degradation of PDK1 induced by FUT11 knockdown. Overexpression of PDK1 in PC cells under hypoxia conditions reversed the suppressive impacts of FUT11 knockdown on PC cell growth and migration. In addition, HIF1α bound to the promoter of FUT11 and increased its expression, as well as co-expressed with FUT11 in PC tissues. Furthermore, overexpression of FUT11 partially rescued the suppressive effects of HIF1α knockdown on PC cell growth and migration in hypoxia condition.ConclusionOur data implicate that hypoxia-induced FUT11 contributes to proliferation and metastasis of PC by maintaining the stability of PDK1, thus mediating activation of AKT/mTOR signaling pathway, and suggest that FUT11 could be a novel and effective target for the treatment of pancreatic cancer.

scholarly journals CSE1L, as a novel prognostic marker, promotes pancreatic cancer proliferation by regulating the AKT/mTOR signaling pathway

2021 ◽  
Vol 12 (10) ◽  
pp. 2797-2806
Author(s):  
Xiao Zhang ◽  
Xiaofei Zhang ◽  
Tiebo Mao ◽  
Haiyan Xu ◽  
Jiujie Cui ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathway ◽  
Prognostic Marker ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Cancer Proliferation
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