Receptor‐type protein tyrosine phosphatase κ (
PTPRK
) is considered to be a candidate tumor suppressor.
PTPRK
dephosphorylates
CD
133, which is a stem cell marker; phosphorylated
CD
133 accelerates xenograft tumor growth of colon cancer cells through the activation of
AKT
, but the functional significance of this has remained elusive. In this study, we have demonstrated that knockdown of
PTPRK
potentiates the pro‐oncogenic
CD
133–
AKT
pathway in colon cancer cells. Intriguingly, depletion of
PTPRK
significantly reduced sensitivity to the anti‐cancer drug oxaliplatin and was accompanied by up‐regulation of phosphorylation of Bad, a downstream target of
AKT
. Together, our present observations strongly suggest that the
CD
133–
PTPRK
axis plays a pivotal role in the regulation of colon cancer progression as well as drug resistance.
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