scholarly journals Acquired tumor cell resistance to sunitinib by increased invasion and epithelial-mesenchymal transition in LL/2 murine lung cancer

Oncotarget ◽  
2017 ◽  
Vol 8 (40) ◽  
pp. 68270-68279 ◽  
Author(s):  
Yang Du ◽  
Jia-Qi Liu ◽  
Jie Tang ◽  
Jun Ge ◽  
Ye Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Cell ◽  
Epithelial Mesenchymal Transition ◽  
Cell Resistance ◽  
Mesenchymal Transition ◽  
Murine Lung ◽  
Tumor Cell Resistance

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.

The Means to an End of Tumor Cell Resistance to Chemotherapeutic Drugs Targeting Thymidylate Synthase: Shoot the Messenger

2002 ◽  
Vol 3 (4) ◽  
pp. 297-309 ◽  
Author(s):  
Randal Berg ◽  
Peter Ferguson ◽  
Janice DeMoor ◽  
Mark Vincent ◽  
James Koropatnick
Keyword(s):  
Tumor Cell ◽  
Thymidylate Synthase ◽  
Chemotherapeutic Drugs ◽  
Cell Resistance ◽  
Tumor Cell Resistance

scholarly journals Modulating Tumor Cell Functions by Tunable Nanopatterned Ligand Presentation

Nanomaterials ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 212
Author(s):  
Katharina Amschler ◽  
Michael P. Schön
Keyword(s):  
Extracellular Matrix ◽  
Tumor Cell ◽  
Cell Fate ◽  
Epithelial Mesenchymal Transition ◽  
Model Systems ◽  
Cellular Functions ◽  
Biophysical Parameters ◽  
Ligand Density ◽  
Mesenchymal Transition ◽  
Cell Functions

Cancer comprises a large group of complex diseases which arise from the misrouted interplay of mutated cells with other cells and the extracellular matrix. The extracellular matrix is a highly dynamic structure providing biochemical and biophysical cues that regulate tumor cell behavior. While the relevance of biochemical signals has been appreciated, the complex input of biophysical properties like the variation of ligand density and distribution is a relatively new field in cancer research. Nanotechnology has become a very promising tool to mimic the physiological dimension of biophysical signals and their positive (i.e., growth-promoting) and negative (i.e., anti-tumoral or cytotoxic) effects on cellular functions. Here, we review tumor-associated cellular functions such as proliferation, epithelial-mesenchymal transition (EMT), invasion, and phenotype switch that are regulated by biophysical parameters such as ligand density or substrate elasticity. We also address the question of how such factors exert inhibitory or even toxic effects upon tumor cells. We describe three principles of nanostructured model systems based on block copolymer nanolithography, electron beam lithography, and DNA origami that have contributed to our understanding of how biophysical signals direct cancer cell fate.

scholarly journals Crk and CrkL as Therapeutic Targets for Cancer Treatment

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 739
Author(s):  
Taeju Park
Keyword(s):  
Tumor Cell ◽  
Cancer Treatment ◽  
Epithelial Mesenchymal Transition ◽  
Human Cancer ◽  
Therapeutic Targets ◽  
Viral Oncoprotein ◽  
Mesenchymal Transition ◽  
Chemotherapy Drugs ◽  
Cell Functions

Crk and CrkL are cellular counterparts of the viral oncoprotein v-Crk. Crk and CrkL are overexpressed in many types of human cancer, correlating with poor prognosis. Furthermore, gene knockdown and knockout of Crk and CrkL in tumor cell lines suppress tumor cell functions, including cell proliferation, transformation, migration, invasion, epithelial-mesenchymal transition, resistance to chemotherapy drugs, and in vivo tumor growth and metastasis. Conversely, overexpression of tumor cells with Crk or CrkL enhances tumor cell functions. Therefore, Crk and CrkL have been proposed as therapeutic targets for cancer treatment. However, it is unclear whether Crk and CrkL make distinct or overlapping contributions to tumor cell functions in various cancer types because Crk or CrkL have been examined independently in most studies. Two recent studies using colorectal cancer and glioblastoma cells clearly demonstrated that Crk and CrkL need to be ablated individually and combined to understand distinct and overlapping roles of the two proteins in cancer. A comprehensive understanding of individual and overlapping roles of Crk and CrkL in tumor cell functions is necessary to develop effective therapeutic strategies. This review systematically discusses crucial functions of Crk and CrkL in tumor cell functions and provides new perspectives on targeting Crk and CrkL in cancer therapy.

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