The findings of the present study support the notion that Wnt/β‑catenin activation may serve a differential role in sarcomas, limiting tumor progression in association with decreased CSC activity.
RNA helicase p68 apart from being a vital player of RNA metabolism acts as a transcriptional coactivator of several oncogenic transcription factors including β-catenin and is highly implicated in cancer progression.
Cripto-1 plays a role in the regulation of different pathways, including TGF-β/Smad and Wnt/β-catenin, which are highly associated with cell migration both during embryonal development and cancer progression.
Sporamin down-regulates the expression and secretion of β-catenin and VEGF in the liver, which subsequently inhibits the transcription of downstream genes involved in cancer progression and angiogenesis.
SIGNIFICANCE: These findings reveal the oncogenic functions of a <i>cis</i>-acting circular RNA in β-catenin activation and cancer progression, with potential value as a therapeutic target for human cancers.
Our present study provided a novel mechanism involved in the inflammation-driven cancer progression through tumor immune escape and downstream gene regulation of WNT/β-catenin pathway-dependent manner.
Under proteasome inhibition, it is further found that SCRIB is associated to the β-catenin destruction complex that is central in Wnt/β-catenin signaling, a conserved pathway regulating embryonic development and cancer progression.
More importantly, downregulation of β-catenin could effectively prevent its enrichment in nuclei and then significantly downregulate the expression of proteins, such as vimentin, Snail, MMP-2, MMP-9, CD44, Nanog, and Oct4 to prevent tumor progression and metastasis.
Overall, our data suggest that β-catenin and Tspan8 are part of a positive feedback loop, which sustains a high Tspan8 expression level, conferring to melanoma cells the invasive properties required for tumor progression and dissemination.
Interestingly, in some sporadic sub-populations, FoxO protein function may also be manipulated by factors such as β-catenin whereby they instead can facilitate cancer progression via maintenance of CSC properties or promoting drug resistance or metastasis and invasion.
Nucleus and/or cytoplasma of β-catenin expression might be associated with tumor progression and could be a possible potential predictive factor of poor prognosis in OC patients.
Upregulation of UBE2Q1 via gene copy number gain in hepatocellular carcinoma promotes cancer progression through β-catenin-EGFR-PI3K-Akt-mTOR signaling pathway.
Mechanistically, C/EBPα exerts its oncogenic role by targeting c-Myc/cyclin D1 mediated by β-catenin involved pathway and we provide evidence indicating that cytoplasmic exclusion of C/EBPα might contribute to its oncogenic function in tumor progression.
The prediction was validated by WB and IP assay that SGK2 could directly bind with β-catenin at protein level to regulate their downstream gene c-Myc expression in bladder cancer to influence tumor progression.
Reduced LIMK2 expression enhanced the nuclear accumulation of β-catenin and activated the Wnt signaling pathway, thus contributing to tumor progression.
Collectively, these results provide unequivocal evidence to establish that SH2B1-IRS1-β-catenin axis is required for promoting EMT, and might prove to be a promising strategy for restraining tumor progression in LADC patients.
The Wnt/β-catenin pathway controls a variety of cellular behaviors, aberrant activation of which are associated with tumor progression in several types of cancer.