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EMT

SNF5, a Core Subunit of SWI/SNF Complex, Regulates Melanoma Cancer Cell Growth, Metastasis, and Immune Escape in Response to Matrix Stiffness

[Translational Oncology] Investigators suggested that stiffer substrate enhanced melanoma development by upregulating SNF5 expression, and SNF5 was a key mediator of stiffer matrix-induced immune evasion of melanoma cancer cells.

Neurokinin-1 Receptor Promotes Non-Small Cell Lung Cancer Progression through Transactivation of EGFR

[Cell Death & Disease] Researchers identified neurokinin-1 as a significantly upregulated GPCR in the transcriptome and tissue array of human lung cancer samples, associated with advanced clinical stages and poor prognosis.

Hsa_circ_0003258 Promotes Prostate Cancer Metastasis by Complexing with IGF2BP3 and Sponging miR-653-5p

[Molecular Cancer] Hsa_circ_0003258 physically binded to insulin like growth factor 2 mRNA binding protein 3 (IGF2BP3) in the cytoplasm and enhanced HDAC4 mRNA stability, in which it activated ERK signaling pathway, then triggered epithelial mesenchymal transformation programming and finally accelerated the metastasis of prostate cancer.

Silencing ESRP1 Expression Promotes Caspase-Independent Cell Death via Nuclear Translocation of AIF in Colon Cancer Cells

[Cellular Signalling] Scientists analyzed Clinical Proteomic Tumor Analysis Consortium, colon tissue microarray, and colon cancer cells to evaluate the ESRP1 expression levels in colorectal cancer subtypes.

FBI-1 Inhibits Epithelial-to-Mesenchymal Transition, Migration, and Invasion in Lung Adenocarcinoma A549 Cells by Downregulating Transforming Growth Factor-β1 Signaling Pathway

[Journal of Cellular Biochemistry] To investigate the function of factor binding inducer of short transcripts-1 (FBI-1) in epithelial-to-mesenchymal transition (EMT) in lung cancer, EMT was measured in FBI-1-deficient or FBI-1-overexpressing cells.

HPV16 E6 Promotes Cell Proliferation, Migration, and Invasion of Human Cervical Cancer Cells by Elevating Both EMT and Stemness Characteristics

[Cell Biology International] HPV16 E6 silence or overexpression were carried out to evaluate the possible mechanisms of HPV16 E6 function in cervical cancer cells with different HPV16 E6 expression background.

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