scholarly journals Mitofusin1 Is a Major Mediator in Glucose-Induced Epithelial-to-Mesenchymal Transition in Lung Adenocarcinoma Cells

2020 ◽  
Vol Volume 13 ◽  
pp. 3511-3523
Author(s):  
Xingyuan Liu ◽  
Chuang Feng ◽  
Guohua Wei ◽  
Wencong Kong ◽  
Hai Meng ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Major Mediator

scholarly journals Ubiquilin proteins regulate EGFR levels and activity in lung adenocarcinoma cells

2020 ◽  
Author(s):  
Zimple Kurlawala ◽  
Kumar Saurabh ◽  
Rain Dunaway ◽  
Parag P. Shah ◽  
Leah J. Siskind ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Family Members ◽  
Growth Factor Receptor ◽  
Human Lung Cancer ◽  
Cell Phenotype ◽  
Mesenchymal Transition ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

AbstractUbiquilin proteins (UBQLNs) are involved in diverse cellular processes like ERAD (endoplasmic reticulum associated degradation), autophagy, apoptosis and epithelial to mesenchymal transition. UBQLNs interact with a variety of substrates, including cell surface receptors, transcription factor regulators, proteasomal machinery proteins, and transmembrane proteins. Additionally, previous work from our lab shows that UBQLN1 interacts with IGFR family members (IGF1R, IGF2R, INSR) and this interaction regulates the activity and proteostasis of IGFR family members. Here, we examined regulation of UBQLN1 with Epidermal Growth Factor Receptor (EGFR) in lung adenocarcinoma cells. Loss of UBQLN1 occurs at high frequency in human lung cancer patient samples and we have shown that loss of UBQLN1 is capable altering processes involved in cell proliferation, migration, invasion and epithelial to mesenchymal transition in lung adenocarcinoma cell lines. Here, we present data that loss of UBQLN1 resulted in increased turnover of total EGFR, whilst increasing the relative amount of active EGFR in lung adenocarcinoma cells, especially in the presence of its ligand EGF. Furthermore, loss of UBQLN1 led to a more invasive cell phenotype as manifested by increased proliferation, migration and speed of movement of these lung adenocarcinoma cells. Taken together, UBQLN1 regulates expression and stability of IGFRs and EGFR, members of the receptor tyrosine kinase family of proteins in lung cancer cells.

scholarly journals miR-218 suppresses epithelial-to-mesenchymal transition by targeting Robo1 and Ecop in lung adenocarcinoma cells

2017 ◽  
Vol 13 (28) ◽  
pp. 2571-2582 ◽  
Author(s):  
Ying-Jie Li ◽  
Wen Zhang ◽  
Hui Xia ◽  
Bao-Shi Zhang ◽  
Ping Chen ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

scholarly journals lncCRLA enhanced chemoresistance in lung adenocarcinoma that underwent epithelial-mesenchymal transition

2021 ◽  
Author(s):  
Weili Min ◽  
Liangzhang Sun ◽  
Burong Li ◽  
Xiao Gao ◽  
Shuqun Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Chemotherapy Resistance ◽  
Metastatic Potential ◽  
Caspase 8 ◽  
Mesenchymal Transition ◽  
Adenocarcinoma Cells ◽  
Signaling Axis ◽  
Lung Adenocarcinoma Cells ◽  
Paclitaxel Liposome

EMT confers increased metastatic potential and the resistance to chemotherapies to cancer cells. However, the precise mechanisms of EMT-related chemotherapy resistance remain unclear. c-Src-mediated Caspase-8 phosphorylation essential for EMT in lung adenocarcinoma cell lines preferentially occurs in cells with the mesenchymal phenotype, resulting in chemoresistance to cisplatin plus paclitaxel inpatients with resectable lung adenocarcinoma and a significantly worse 5-year PFS. Cisplatin killed lung adenocarcinoma cells regardless of Caspase-8. Paclitaxel-triggered necroptosis in lung adenocarcinoma cells was dependent on the phosphorylation or deficiency of Caspase-8, during which FADD interacted with RIPK1 to activateRIPK1/RIPK3/MLKL signaling axis. Accompanied with c-Src-mediated Caspase-8 phosphorylation to trigger EMT, a novel lncRNA named lncCRLA was markedly upregulated and inhibited RIPK1-induced necroptosis by impairing RIPK1-RIPK3 interaction via binding to the intermediate domain of RIPK1. Dasatinib mitigated c-Src-mediated phosphorylation of Caspase-8-induced EMT and enhanced necroptosis in mesenchymal-like lung adenocarcinoma cells treated with paclitaxel, while c-FLIP knockdown predominantly sensitized the mesenchymal-like lung adenocarcinoma cells to paclitaxel+dasatinib. c-Src-Caspase-8 interaction initiates EMT and chemoresistance viaCaspase-8 phosphorylation and lncCRLA expression, to which the dasatinib/paclitaxel liposome+siFLIP regimen was lethal.

scholarly journals Emodin Inhibits ATP-Induced Proliferation and Migration by Suppressing P2Y Receptors in Human Lung Adenocarcinoma Cells

2017 ◽  
Vol 44 (4) ◽  
pp. 1337-1351 ◽  
Author(s):  
Xia Wang ◽  
Long Li ◽  
Ruijuan Guan ◽  
Danian Zhu ◽  
Nana Song ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Lung Adenocarcinoma ◽  
Human Lung ◽  
A549 Cells ◽  
P2y Receptors ◽  
Mesenchymal Transition ◽  
Human Lung Adenocarcinoma ◽  
Adenocarcinoma Cells ◽  
Human Lung Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells

Background/Aims: Extracellular ATP performs multiple important functions via activation of P2 receptors on the cell surface. P2Y receptors play critical roles in ATP evoked response in human lung adenocarcinoma cells (A549 cells). Emodin is an anthraquinone derivative originally isolated from Chinese rhubarb, possesses anticancer properties. In this study we examined the inhibiting effects of emodin on proliferation, migration and epithelial-mesenchymal transition (EMT) by suppressing P2Y receptors-dependent Ca2+ increase and nuclear factor-κB (NF-KB) signaling in A549 cells. Methods: A549 cells were pretreated with emodin before stimulation with ATP for the indicated time. Then, intracellular Ca2+ concentration ([Ca2+]i) was measured by Fluo-8/AM staining. Cell proliferation and cell cycle progression were tested by CCK8 assay and flow cytometry In addition, wound healing and western blot were performed to determine cell migration and related protein levels (Bcl-2, Bax, claudin-1, NF-κB). Results: Emodin blunted ATP/UTP-induced increase of [Ca2+]i and cell proliferation concentration-dependently Meanwhile, it decreased ATP-induced cells accumulation in the S phase. Furthermore, emodin altered protein abundance of Bcl-2, Bax and claudin-1 and attenuated EMT caused by ATP. Such ATP-induced cellular reactions were also inhibited by a nonselective P2Y receptors antagonist, suramin, in a similar way to emodin. Besides, emodin could inhibit activation of NF-κB, thus suppressed ATP-induced proliferation, migration and EMT. Conclusion: Our results demonstrated that emodin inhibits ATP-induced proliferation, migration, EMT by suppressing P2Y receptors-mediated [Ca2+]i increase and NF-κB signaling in A549 cells.

Sign in / Sign up

Export Citation Format

Share Document