scholarly journals P2‐5: TGF‐Β‐induced epithelial‐mesenchymal transition and tumor‐promoting effects in CMT64 cells are reflected in the transcriptomic signature of human lung adenocarcinoma

Respirology ◽  
2021 ◽  
Vol 26 (S3) ◽  
pp. 114-115
Keyword(s):  
Lung Adenocarcinoma ◽  
Human Lung ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Human Lung Adenocarcinoma ◽  
Transcriptomic Signature

scholarly journals TGF-β-mediated epithelial–mesenchymal transition and tumor-promoting effects in CMT64 cells are reflected in the transcriptomic signature of human lung adenocarcinoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Naoya Miyashita ◽  
Takayoshi Enokido ◽  
Masafumi Horie ◽  
Kensuke Fukuda ◽  
Hirokazu Urushiyama ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Lung Adenocarcinoma ◽  
Cancer Cells ◽  
Human Lung ◽  
Epithelial Mesenchymal Transition ◽  
Mouse Lung ◽  
Mesenchymal Transition ◽  
Human Lung Adenocarcinoma ◽  
Junction Protein ◽  
Transplantation Model

AbstractEpithelial–mesenchymal transition (EMT) is a cellular process during which epithelial cells acquire mesenchymal phenotypes. Cancer cells undergo EMT to acquire malignant features and TGF-β is a key regulator of EMT. Here, we demonstrate for the first time that TGF-β could elicit EMT in a mouse lung adenocarcinoma cell line. TGF-β signaling activation led to cell morphological changes corresponding to EMT and enhanced the expression of mesenchymal markers and EMT-associated transcription factors in CMT64 lung cancer cells. RNA-sequencing analyses revealed that TGF-β increases expression of Tead transcription factors and an array of Tead2 target genes. TGF-β stimulation also resulted in alternative splicing of several genes including Cd44, tight junction protein 1 (Tjp1), and Cortactin (Cttn). In parallel with EMT, TGF-β enhanced cell growth of CMT64 cells and promoted tumor formation in a syngeneic transplantation model. Of clinical importance, the expression of TGF-β-induced genes identified in CMT64 cells correlated with EMT gene signatures in human lung adenocarcinoma tissue samples. Furthermore, TGF-β-induced gene enrichment was related to poor prognosis, underscoring the tumor-promoting role of TGF-β signaling in lung adenocarcinoma. Our cellular and syngeneic transplantation model would provide a simple and useful experimental tool to study the significance of TGF-β signaling and EMT.

scholarly journals Epithelial-mesenchymal transition promotes reactivity of human lung adenocarcinoma A549 cells to CpG ODN

2016 ◽  
Vol 65 ◽  
pp. S45-S52 ◽  
Author(s):  
Koichi Kobayashi ◽  
Kazuya Koyama ◽  
Maho Suzukawa ◽  
Sayaka Igarashi ◽  
Akira Hebisawa ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Human Lung ◽  
Epithelial Mesenchymal Transition ◽  
A549 Cells ◽  
Cpg Odn ◽  
Mesenchymal Transition ◽  
Human Lung Adenocarcinoma ◽  
Lung Adenocarcinoma A549

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.

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