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These results suggest the role of JAM-A as a negative regulator of migration in breast cancer cells.
Finally, we demonstrate that FXR agonists do not stimulate migration in breast cancer cell lines, an important potential adverse effect.
Many studies indicated that PI3K/Akt/mTOR inhibitors and Hh inhibitors displayed synergistic effects, and the combination of the two signaling drugs could delay drug resistance and inhibit cancer migration in breast cancer.
Also, HSPCs encapsulating siMDR1 knockdowned 99.4% MDR1 gene with up to 6 times of enhancement compared to naked siMDR1, increased the doxorubicin accumulation, down-regulated P-glycoprotein (P-gp) expression and suppressed cellular migration in breast cancer MCF-7/ADR cells.
It has been previously shown that activating c-CBL mutation downregulates EGFR signaling and decreases cellular proliferation and migration in breast cancer cell lines [34].
HPGD plays important role in epithelial-mesenchymal transition and migration in breast cancer cells [ 26].
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Our results provide evidence of the involvement of ACSL4 in the mechanism responsible for the increase in proliferation, invasion and migration shown in breast cancer cells.
We found that blockade of CXCR4 pathway by GST-NT21MP decreased SDF-1-induced cell growth, adhesion and migration capacities in breast cancer cells.
Tiam1 protein expression also correlates with migration capacity in breast tumor cell lines [ 23], and a close correlation has been observed between increased Tiam1 expression and tumor grade [ 29].
More striking, Nup153 depletion induces a dramatic cytoskeletal rearrangement that impairs cell migration in human breast carcinoma cells.
To investigate whether ROS generation leads to LPA-induced activation of the PI3K/PAK1/ERK signaling pathway and cell migration in cultured breast cancer cells, N-acetyl-L-cysteine (NAC), a known scavenger of ROS, was used and its effect on LPA-induced PI3K/PAK1/ERK activation was examined.
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