Furthermore, PLK4 knockdown inactivated the Wnt/β‑catenin pathway in CRC cells in vitro and in vivo, and suppressed the growth of xenograft tumors in nude mice.
We previously identified the immunoglobulin-like cell adhesion receptor L1 as a target gene of β-catenin/TCF transactivation that is localized at the invasive edge of CRC tissue.
Our data suggested that knockdown of USP6NL in human CRC cell lines (HCT116 and LOVO cells) inhibited cell proliferation, induced G0/G1 cell cycle arrest, and prevented the tumorigenicity of HCT116 cells in nude mice, and which was associated with the prevention of Wnt/β-catenin pathway.
We further confirmed the involvement of β-catenin in Six1-promoted proliferation and migration of CRC cells by activation of Wnt signaling with lithium chloride (LiCl) in Six1 KD CRC cells and results showed that LiCl restores defective β-catenin nuclear localization and proliferation and migration of CRC cells.
However, an inverse gradient of Wnt/β-catenin/TCF7L2 signalling activity during CRC progression has been suggested, with early stage and metastatic tumours displaying high and low Wnt signalling activities, respectively, which lead us to revisit the "just-right" signalling model.
To explore the possibility of a selective small-molecule β-catenin inhibitor, CWP232228, as a potential therapeutic drug in the treatment of colorectal cancer (CRC).
The current findings therefore identified miR-24-1-5p as a potent regulator of β-catenin, and this may provide a novel chemopreventive and therapeutic strategy for β-catenin signalling-driven colorectal cancer.
CRC cells that overexpressed TRIB3 had higher levels of transcription by β-catenin and formed larger spheroids than control CRC cells; knockdown of β-catenin prevented the larger organoid size caused by TRIB3 overexpression.
Thus, DAXX might be considered as a potential regulator of CD24 or β-catenin expression, which might be correlated with proliferative and metastatic potential of CRC.
A discordant pattern of β-catenin and E-cadherin expression between pPDC and cPDC, between main tumor and cPDC, and between primary CRC and LM, confirms that EMT is a dynamic and reversible process in CRC.
This finding indicates that mismatch repair proteins may be combined with β-catenin and GATA-3 to create an immunostaining panel which, in addition to clinical studies, can aid in distinguishing bladder adenocarcinoma from secondary involvement by colorectal carcinoma.
The present study identified that SLP-2 may predict a poor prognosis in CRC patients as a novel marker, and SLP-2 may facilitate the migration and invasion of CRC via regulating Wnt/β-catenin pathway activities.
hTERT may promote CRC by recruiting β-catenin/TCF-4 complex to transactivate CCL2 expression, which is a novel crosstalk mechanism likely involved in the pathogenesis of CRC.
Our results reveal a CD36-GPC4-β-catenin-c-myc signaling axis that regulates glycolysis in CRC development and may provide an intervention strategy for CRC prevention.
These results provided evidence that the downregulation of miR‑183‑5p inhibits CRC proliferation and invasion by regulating the RCN2/Wnt/β‑catenin pathway. miR‑183‑5p and RCN2 may serve an important role in the molecular etiology of CRC and have potential applications in CRC treatment.
Here, we show for the first time that BCL-3 acts as a co-activator of β-catenin/TCF-mediated transcriptional activity in CRC cell lines and that this interaction is important for Wnt-regulated intestinal stem cell gene expression.
This study, therefore, identified five candidate microRNAs, two hub genes (CTNNB1 and epidermal growth factor receptor), and seven significant target genes associated with colorectal cancer.