Abstract
Background MET is a receptor tyrosine kinase that is activated by the ligand HGF and this pathway promotes cell survival, migration, and motility. In accordance with its oncogenic role, MET is constitutively active, mutated, or over-expressed in many cancers. Corollary to its impact, inhibition of MET kinase activity causes reduction of the downstream signaling and demise of cells. In myeloma, a B-cell plasma malignancy, MET is neither mutated nor over-expressed, however, HGF is increased in plasma or serum obtained from myeloma patients and this was associated with poor prognosis. The small-molecule, amuvatinib, inhibits MET receptor tyrosine kinase. Based on this background, we hypothesized that targeting the HGF/MET signaling pathway is a rational approach to myeloma therapy and that myeloma cells would be sensitive to amuvatinib.
Highlights
The images used for phospho- and total MET in Fig. 6c were derived from the third replicate of the experiment, but accidentally we used the GAPDH from the second replicate of the experiment
We probed the blot with a rabbit anti-phospho-GSK-3β (S9) antibody followed by the secondary, which was a green fluorescent anti-rabbit antibody
We probed with a mouse anti-totalGSK-3β antibody followed by the secondary, which was a red fluorescent anti-mouse antibody
Summary
Erratum to: Targeting MET kinase with the small-molecule inhibitor amuvatinib induces cytotoxicity in primary myeloma cells and cell lines The images used for phospho- and total MET in Fig. 6c were derived from the third replicate of the experiment, but accidentally we used the GAPDH from the second replicate of the experiment.
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