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Tytuł pozycji:

PTPRK suppresses progression and chemo-resistance of colon cancer cells via direct inhibition of pro-oncogenic CD133.

Tytuł:
PTPRK suppresses progression and chemo-resistance of colon cancer cells via direct inhibition of pro-oncogenic CD133.
Autorzy:
Matsushita M; Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Japan.
Mori Y; Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Japan.; Laboratory of Oncogenomics, Chiba Cancer Center Research Institute, Japan.
Uchiumi K; Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Japan.
Ogata T; Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Japan.
Nakamura M; Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Japan.
Yoda H; Laboratory of Cancer Genetics, Chiba Cancer Center Research Institute, Japan.
Soda H; Department of Esophago-Gastrointestinal Surgery, Chiba Cancer Center Hospital, Japan.
Takiguchi N; Department of Esophago-Gastrointestinal Surgery, Chiba Cancer Center Hospital, Japan.
Nabeya Y; Department of Esophago-Gastrointestinal Surgery, Chiba Cancer Center Hospital, Japan.
Shimozato O; Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Japan.; Laboratory of Oncogenomics, Chiba Cancer Center Research Institute, Japan.
Ozaki T; Laboratory of DNA Damage Signaling, Chiba Cancer Center Research Institute, Japan.; Laboratory of Oncogenomics, Chiba Cancer Center Research Institute, Japan.
Źródło:
FEBS open bio [FEBS Open Bio] 2019 May; Vol. 9 (5), pp. 935-946. Date of Electronic Publication: 2019 Apr 18.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: Jan. 2016- : West Sussex : John Wiley & Sons Ltd.
Original Publication: Amsterdam : Elsevier, 2011-
MeSH Terms:
AC133 Antigen/*genetics
Antineoplastic Agents/*pharmacology
Carcinogenesis/*genetics
Cell Proliferation/*genetics
Oxaliplatin/*pharmacology
Receptor-Like Protein Tyrosine Phosphatases, Class 2/*genetics
AC133 Antigen/metabolism ; Carcinogenesis/drug effects ; Cell Line, Tumor ; Disease Progression ; Drug Resistance ; HEK293 Cells ; HT29 Cells ; Humans ; Phosphorylation ; Receptor-Like Protein Tyrosine Phosphatases, Class 2/metabolism ; Signal Transduction
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Contributed Indexing:
Keywords: PTPRK; CD133; colon carcinoma; drug resistance; protein tyrosine phosphatase
Substance Nomenclature:
0 (AC133 Antigen)
0 (Antineoplastic Agents)
0 (PROM1 protein, human)
04ZR38536J (Oxaliplatin)
EC 3.1.3.48 (PTPRK protein, human)
EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 2)
Entry Date(s):
Date Created: 20190405 Date Completed: 20191112 Latest Revision: 20200309
Update Code:
20240104
PubMed Central ID:
PMC6487712
DOI:
10.1002/2211-5463.12636
PMID:
30947381
Czasopismo naukowe
Receptor-type protein tyrosine phosphatase κ (PTPRK) is considered to be a candidate tumor suppressor. PTPRK dephosphorylates CD133, which is a stem cell marker; phosphorylated CD133 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 CD133-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 CD133-PTPRK axis plays a pivotal role in the regulation of colon cancer progression as well as drug resistance.
(© 2019 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.)

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