scholarly journals Epigenetic induction of epithelial to mesenchymal transition by LCN2 mediates metastasis and tumorigenesis, which is abrogated by NF-κB inhibitor BRM270 in a xenograft model of lung adenocarcinoma

2015 ◽  
Vol 48 (1) ◽  
pp. 84-98 ◽  
Author(s):  
RAJ KUMAR MONGRE ◽  
SIMRINDER SINGH SODHI ◽  
NEELESH SHARMA ◽  
MRINMOY GHOSH ◽  
JEONG HYUN KIM ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Xenograft Model ◽  
Mesenchymal Transition

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.

scholarly journals ATP Synthase Subunit Epsilon Overexpression Promotes Metastasis by Modulating AMPK Signaling to Induce Epithelial-to-Mesenchymal Transition and Is a Poor Prognostic Marker in Colorectal Cancer Patients

2019 ◽  
Vol 8 (7) ◽  
pp. 1070 ◽  
Author(s):  
Yan-Jiun Huang ◽  
Yi-Hua Jan ◽  
Yu-Chan Chang ◽  
Hsing-Fang Tsai ◽  
Alexander TH Wu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Atp Synthase ◽  
Distant Metastasis ◽  
Epithelial To Mesenchymal Transition ◽  
Hypoxia Inducible Factor ◽  
Xenograft Model ◽  
Metastatic Colon Cancer ◽  
Mesenchymal Transition ◽  
Ampk Signaling ◽  
Mouse Xenograft Model

Metastasis remains the major cause of death from colon cancer. We intend to identify differentially expressed genes that are associated with the metastatic process and prognosis in colon cancer. ATP synthase epsilon subunit (ATP5E) gene was found to encode the mitochondrial F0F1 ATP synthase subunit epsilon that was overexpressed in tumor cells compared to their normal counterparts, while other genes encoding the ATP synthase subunit were repressed in public microarray datasets. CRC cells in which ATP5E was silenced showed markedly reduced invasive and migratory abilities. ATP5E inhibition significantly reduced the incidence of distant metastasis in a mouse xenograft model. Mechanistically, increased ATP5E expression resulted in a prominent reduction in E-cadherin and an increase in Snail expression. Our data also showed that an elevated ATP5E level in metastatic colon cancer samples was significantly associated with the AMPK-AKT-hypoxia-inducible factor-1α (HIF1α) signaling axis; silencing ATP5E led to the degradation of HIF1α under hypoxia through AMPK-AKT signaling. Our findings suggest that elevated ATP5E expression could serve as a marker of distant metastasis and a poor prognosis in colon cancer, and ATP5E functions via modulating AMPK-AKT-HIF1α signaling.

Abstract 3426: A signature for epithelial to mesenchymal transition in lung adenocarcinoma

2011 ◽  
Author(s):  
Mark Schliekelman ◽  
Ayumu Taguchi ◽  
Hong Wang ◽  
Qing Zhang ◽  
Chee-Hong Wong ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals Adam17, a Target of Mir-326, Promotes Emt-Induced Cells Invasion in Lung Adenocarcinoma

2015 ◽  
Vol 36 (3) ◽  
pp. 1175-1185 ◽  
Author(s):  
Ming Cai ◽  
Zhiqiang Wang ◽  
Jiru Zhang ◽  
Huan Zhou ◽  
Linfang Jin ◽  
...  
Keyword(s):  
Western Blot ◽  
Lung Adenocarcinoma ◽  
Cell Lines ◽  
Epithelial To Mesenchymal Transition ◽  
Luciferase Reporter ◽  
Regulation Mechanism ◽  
Western Blot Assay ◽  
Mesenchymal Transition ◽  
Human A549

Background/Aims: A disintegrin and metalloprotease (ADAM) 17 has been reported to be implicated in cancer cells invasion. Nevertheless, its potential role in lung adenocarcinoma has not been addressed clearly. Methods: RT-PCR and Western blot were used to detect the expression of miR-326 and ADAM17 in lung adenocarcinoma samples (n=73). miR-326 mimics and inhibitor were tansfected in human A549 and SPCA1 cell lines. The transwell assay was used to detect the cell invasive ability. The regulation mechanism was evaluated by luciferase reporter assay. The markers of (epithelial-to-mesenchymal transition) EMT were detected by using Western blot assay. Results: We found increased expression of ADAM17 in lung adenocarcinoma and cell lines. In vitro, up-regulation of ADAM17 promoted cells invasion, while silencing of ADAM17 inhibited cells invasion. Meanwhile, ADAM17 could affect the markers of EMT. Furthermore, we confirmed that ADAM17 is a target of miR-326, which is involved in EMT and cells invasion. Conclusions: These findings revealed that ADAM17, a target of miR-326, promoted EMT-induced cells invasion in lung adenocarcinoma.

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