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Oncogenic receptor tyrosine kinase signaling is driven by the Golgi protein GOLPH3 and its interaction with MYO18A
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DOI：10.1126/scisignal.aed1622.png)
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Abstract
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Many cancers are driven by signaling mediated by receptor tyrosine kinases (RTKs) upon activation by growth factors. Starost et al. found that RTK signaling was enhanced by the Golgi-localized oncoprotein GOLPH3 and its binding partner MYO18A. Together, these proteins were required for the delivery of EGFR (which is frequently mutated in lung cancer), insulin receptor, and other RTKs to the plasma membrane and for the responsiveness of different cell types to growth factors. These findings identify growth factor signaling as a potential mechanism underlying the oncogenicity of GOLPH3. Moreover, they provide a possible alternate targeting strategy for limiting the growth of RTK-driven cancers that have developed resistance to RTK inhibitors. —Wei Wong
Keywords:
GOLPH3
MYO18A
receptor tyrosine kinase
EGFR
oncogenic signaling
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