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In addition, histological transition in lung EGFR mutant tumor also contributes to drug resistance: on one hand, ADC can transdifferentiate into SCC which is resistant to EGFR inhibitor; on the other hand, ADC can also transform into SCLC with decreased EGFR expression and resistance to EGFR inhibitor.
In turn, ER stress can induce epithelial-to-mesenchymal transition in lung epithelial cells [ 24].
Furthermore, DDR2 mutation could induce Epithelial-to-Mesenchymal Transition in lung SCC cells by downregulating E-cadherin expression.
To investigate whether BRF2 regulates the EMT transition in lung cancer cells, we examined the expression of the key EMT markers E cadherin and N-cadherin in BRF2 knocked down lung cancer cells by western blotting analysis.
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We have previously reported that ACL KD reverses epithelial mesenchymal transition (EMT) in lung cancer cells.
However, the role of epithelial mesenchymal transition (EMT) in lung fibrosis is just beginning to be understood.
Jayachandran and colleagues [ 29] found that Snail transcription factors mediate the epithelial-mesenchymal transition (EMT) in lung fibrosis.
Immunocytofluorescence data clearly demonstrated that magnolin abolished the epithelial-to-mesenchymal transition in A549 lung cancer cells (Fig. 4b).
This finding was in accordance with the results reported by Milara et al., which showed that M1 and M3 mAChRs were involved in carbachol- or TGF-β1-induced fibroblast to myofibroblast transition in human lung fibroblasts [ 12].
Our recent studies have shown that the water extract and flavonoids from Korean S. baicalensis G. inhibits cell cycle G1/S transition in A549 lung cancer cells [ 18] and inhibited inflammatory signaling pathways in RAW 264.7 Cells, respectively [ 19].
The nitrosamine NNK, a tobacco-specific lung carcinogen, is associated with GC → AT transitions in rodent lung tumours [ 18].
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