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Gao S, Lin Z, Li C, Wang Y, Yang L, Zou B, et al. TFPI2AS1, a novel lncRNA that inhibits cell proliferation and migration in lung cancer.
Furthermore, we also evaluated whether PM014 was capable of inhibiting fibroblast migration in lung fibroblasts from healthy donor and IPF patient (Fig. S8).
Taken together, our findings indicate that because miR-19a/b and MTUS1 exhibit contrasting expression patterns and exert contrasting biological effects in lung cancer cells, it is very possible that miR-19a/b synergistically modulate cell proliferation and migration in lung cancer cells by silencing MTUS1.
Owen et al. described that the membrane-bound form of this enzyme regulates neutrophil migration in lung tissue [47].
We next investigated whether miR-205 would modify cell migration in lung cancer cells.
These data indicate that TGF β1 and mir-200c participate in complementary pathways for migration in lung cells.
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To examine the direct role of OPN for neutrophil migration in lungs, we injected rmOPN in lungs intratracheally and assessed neutrophil infiltration in lung tissues.
In conclusion, we have clearly demonstrated the protective role of anti-OPN Ab against ALI after sepsis in mice by inhibiting neutrophil migration in lungs.
Interestingly, our in vivo finding demonstrating excessive neutrophil migration in lungs as a result of intratracheal rmOPN injection provided direct involvement of OPN-mediated induction of ALI, which might in turn be reversed by administrating neutralizing Ab against OPN to attenuate lung neutrophil migration in sepsis-induced ALI.
The inhibition of the ERK signaling pathway restores the beneficial effects of ATRA, reduces proliferation, increases apoptosis, and blocks the cell migration process in lung cancer cells.
In addition, ursolic acid also suppressed expression of MMP-2, as well as declined invasion and migration in these lung and gastric cancer cells (Hussain et al. 2017).
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