scholarly journals Lentinan Attenuated the PM2.5 Exposure-Induced Inflammatory Response, Epithelial–Mesenchymal Transition and Migration by Inhibiting the PVT1/miR-199a-5p/caveolin1 Pathway in Lung Cancer

2021 ◽  
Author(s):  
He Qi ◽  
Ying Liu ◽  
Nan Wang ◽  
Chunling Xiao
Keyword(s):  
Lung Cancer ◽  
Inflammatory Response ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Pm2.5 Exposure ◽  
And Migration

scholarly journals Alectinib and lorlatinib function by modulating EMT-related proteins and MMPs in NSCLC metastasis

2020 ◽  
Author(s):  
Xu Feng ◽  
En-Shi Xu
Keyword(s):  
Lung Cancer ◽  
Matrix Metalloproteinases ◽  
Brain Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Underlying Mechanism ◽  
Dependent Manner ◽  
Mesenchymal Transition ◽  
Protein Levels ◽  
Anaplastic Lymphoma ◽  
And Migration

Most advanced non-small cell lung cancer (NSCLC) patients are accompanied by brain metastasis which is the major cause of increased mortality. The fusion rearrangement of anaplastic lymphoma kinase (ALK) gene is an important feature of brain metastasis in lung cancer. The novel ALK inhibitors alectinib and lorlatinib are shown to be effective against NSCLC brain metastasis, while their underlying mechanism of action is unclear. Epithelial–mesenchymal transition (EMT) proteins and matrix metalloproteinases (MMPs) play important roles in brain metastasis by regulating the blood-brain barrier (BBB). To reveal the molecular function of alectinib and lorlatinib, we explored their effects on the cellular levels of EMT markers: VIM and FN1 and the matrix metalloproteinases MMP-9 and MMP-7. The mRNA and protein levels of VIM, FN1, MMP-9, and MMP-7 were elevated in H3122 cells. However, upon alectinib and lorlatinib treatment the levels were significantly reduced. Similar results were obtained when these experiments were performed either in a dose dependent or time dependent manner. Furthermore, alectinib and lorlatinib also inhibited the cell viability and migration of H3122 cells. Interestingly, in comparison to individual drugs, the combination of alectinib and lorlatinib was found to be substantially more effective. Overall, these results suggest that alectinib and lorlatinib possibly function via the downregulation of MMPs and EMT in NSCLC metastasis.

Silencing LINC00511 inhibits cell proliferation, migration, and epithelial–mesenchymal transition via the PTEN–AKT–FOXO1 signaling pathway in lung cancer

2019 ◽  
pp. 1-8 ◽  
Author(s):  
Lianyong Jiang ◽  
Xiao Xie ◽  
Fangbao Ding ◽  
Ju Mei ◽  
Rui Bi
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Expression Levels ◽  
H460 Cells ◽  
Pten Mrna ◽  
And Migration

Lung cancer is the most common cause of cancer-related death worldwide. Long noncoding RNAs (lncRNAs) are longer than 200 nt transcripts and are not translated into proteins. Increasing evidence has shown that lncRNAs are associated with several biological processes in cancer. However, the roles of LINC00511 in lung cancer progression remain unknown. In the present study, we confirmed that LINC00511 knockdown significantly inhibited cell proliferation and migration in A549, SPCA1, and H460 cells. Western blot results showed that silencing LINC00511 inhibited epithelial–mesenchymal transition (EMT), which resulted in decreased expression levels of ZEB2, N-cadherin, and vimentin and increased expression levels of E-cadherin. Additionally, silencing LINC00511 significantly upregulated PTEN mRNA and protein expression, increased FOXO1, and inactivated AKT. Furthermore, we found that PTEN knockdown reversed the inhibition of cell migration and proliferation induced by LINC00511 siRNA, markedly reduced p-FOXO1 expression, and promoted p-AKT expression and EMT in A549 and H460 cells. Therefore, these findings revealed that LINC00511 functions as an oncogene through the PTEN–AKT–FOXO1 signaling pathway in lung cancer, providing a potential target of metastasis in lung cancer.

scholarly journals MicroRNA-484 promotes cell migration and invasion in non-small cell lung cancer

2020 ◽  
Author(s):  
Xiaoning Yang ◽  
Junfeng Ma ◽  
Fanghua Gong ◽  
Yu Liu
Keyword(s):  
Lung Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Small Cell ◽  
Tumor Cell Invasion ◽  
Small Cell Lung ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration

Abstract Background Lung cancer is one of the most common causes of cancer-related deaths in the world, and non-small cell lung cancer (NSCLC) accounts for 85% of it. Studies have reported that microRNA-484 (miR-484) plays an important regulatory role in carcinogenesis and cancer development. Methods 25 clinical NSCLC samples were collected for microRNA array. The funvtion of miR-484 was investigated through Transwell and Mitgration assays. The expression levers of epithelial-mesenchymal transition (EMT) related factors were assessed by Western blot. Results miR-484 was up-regulated in tissues from NSCLC patients relative to tumor-adjacent normal tissues. Knocking-down miR-484 expression in A549 cells significantly suppressed tumor cell invasion and migration, suppressed epithelial-mesenchymal transition (EMT) process by increasing the expression of E-cadherin, and decreasing the expression of N-cadherin, vimentin, and MMP2. Upregulation of miR-484 expression in BEAS-2B normal lung epithelial cells significantly promoted tumor cell invasion and migration, decreased E-cadherin expression levels, and increased N-cadherin, vimentin, and MMP2 expression levels Conclusion miR-484 can promote tumor cell invasion and migration in NSCLC and may be a new target for NSCLC treatment.

scholarly journals Baicalin Inhibits EMT through PDK1/AKT Signaling in Human Nonsmall Cell Lung Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Jia Chen ◽  
Cheng-Bo Yuan ◽  
Bo Yang ◽  
Xuan Zhou
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cell Lung Cancer ◽  
Epithelial Mesenchymal Transition ◽  
Nonsmall Cell Lung Cancer ◽  
Dependent Manner ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
And Migration ◽  
Human Nsclc

Background. Baicalin is a naturally occurring compound with anticancer, antioxidant, and anti-inflammatory properties. However, the mechanism underlying its anticancer activity on nonsmall cell lung cancer (NSCLC) remains unclear. Methods. The effects of baicalin on the progression and metastasis of experimental NSCLC cell lines were studied in vitro and in vivo. Wound-healing and transwell assays were performed to evaluate the potency of baicalin and the motility and migration ability of NCI-H460 cells. Immunofluorescence assay, western blot assay, and immunohistochemistry test were conducted to investigate the inhibiting effect of baicalin on the epithelial-mesenchymal transition (EMT) of NSCLC. Results. Baicalin inhibited the proliferation and migration of NCI-H446 human NSCLC cells in a dose-dependent manner, reduced the expression levels of phospho-3-phosphoinositide-dependent protein kinase 1 (p-PDK1) and phosphor-serine/threonine-protein kinase (p-AKT), reversed the levels of EMT markers, and inhibited the migration of NSCLC cells. Conclusions. Baicalin impedes EMT by inhibiting the PDK1/AKT pathway in human NSCLC and thus may be an effective alternative treatment for carcinoma and a new candidate antimetastasis drug.

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