@article{f5c4233a7e474a4d992c7c5664c3b81a,
title = "Downregulation of STK4 promotes colon cancer invasion/migration through blocking β-catenin degradation",
abstract = "Mammalian STE20-like kinase 1 (MST1/STK4/KRS2) encodes a serine/threonine kinase that is the mammalian homolog of Drosophila Hippo. STK4 plays an important role in controlling cell growth, apoptosis, and organ size. STK4 has been studied in many cancers with previous studies indicating an involvement in colon cancer lymph node metastasis and highlighting its potential as a diagnostic marker for colon cancer. However, the role of STK4 defect in promoting colon cancer progression is still understudied. Here, we found that STK4 was significantly downregulated in colon cancer and was associated with distal metastasis and poor survival. Furthermore, STK4 knockdown enhanced sphere formation and metastasis in vitro and promoted tumor development in vivo. We found that STK4 colocalized with β-catenin and directly phosphorylated β-catenin resulting in its degradation via the ubiquitin-mediated pathway. This may suggest that STK4 knockdown causes β-catenin phosphorylation failure and subsequently β-catenin accumulation, consequently leading to anchorage-independent growth and metastasis in colon cancer. Our results support that STK4 may act as a potential candidate for the assessment of β-catenin-mediated colon cancer prognosis.",
keywords = "colon cancers, STK4, β-catenin",
author = "Lin, {Cheng Han} and Hsu, {Tai I.} and Chiou, {Pei Yu} and Michael Hsiao and Wang, {Wen Ching} and Chen, {Yu Chia} and Lin, {Jen Tai} and Wang, {Jaw Yuan} and Lin, {Peng Chan} and Lin, {Forn Chia} and Tseng, {Yu Kai} and Cheng, {Hui Chuan} and Chen, {Chi Long} and Lu, {Pei Jung}",
note = "Funding Information: The study was financially supported by the Ministry of Science and Technology, R.O.C. (MOST 106-2320-B-006-066-MY3; MOST 107-2320-B-006-064-MY3), to Pei-Jung Lu; and Chi Mei Medical Center (CMNCKU10415) to Wen-Ching Wang and Pei-Jung Lu. We thank the Proteomics Core Facility of the Clinical Medicine Research Center in National Cheng Kung University Hospital for assistance with protein experiment processing. We are grateful for the support from the Laboratory Animal Center, Medical College, National Cheng Kung University. Funding Information: The study was financially supported by the Ministry of Science and Technology, R.O.C. (MOST 106‐2320‐B‐006‐066‐MY3; MOST 107‐2320‐B‐006‐064‐MY3), to Pei‐Jung Lu; and Chi Mei Medical Center (CMNCKU10415) to Wen‐Ching Wang and Pei‐Jung Lu. We thank the Proteomics Core Facility of the Clinical Medicine Research Center in National Cheng Kung University Hospital for assistance with protein experiment processing. We are grateful for the support from the Laboratory Animal Center, Medical College, National Cheng Kung University. Publisher Copyright: {\textcopyright} 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.",
year = "2020",
month = oct,
day = "1",
doi = "10.1002/1878-0261.12771",
language = "English",
volume = "14",
pages = "2574--2588",
journal = "Molecular Oncology",
issn = "1574-7891",
publisher = "wiley",
number = "10",
}
