RETRACTED ARTICLE: TRIM29 facilitates the epithelial-to-mesenchymal transition and the progression of colorectal cancer via the activation of the Wnt/β-catenin signaling pathway

Abstract

Background Tripartite Motif 29 (TRIM29) has been newly identified as being implicated in cancer progression. However, the biological role and molecular mechanism of TRIM29 in the invasion and metastasis of colorectal cancer (CRC) remain to be determined. Methods The expression levels of TRIM29 and β-catenin in CRC patient specimens were detected by immunohistochemistry. Recombinant lentivirus vectors containing the TRIM29 gene and its small hairpin interfering RNAs were constructed and transduced into CRC cells. Wound-healing and Transwell assays were performed to evaluate the migration and invasion abilities of CRC cells in vitro. Hepatic metastasis models in nude mice were established to validate the function of TRIM29 in vivo. Moreover, the expressions of epithelial-to-mesenchymal transition (EMT)-associated proteins were detected by qRT-PCR and Western blotting in CRC cells. Finally, Western blotting, qRT-PCR, luciferase reporter assays, and immunofluorescence assays were used to explore the molecular mechanisms of TRIM29 in CRC progression. Results Increased TRIM29 expression positively correlated with lymph node metastasis and β-catenin expression in patient CRC tissues. Overexpression of TRIM29 promoted invasion and metastasis of CRC cells in vitro and in vivo by regulating EMT, whereas the knockdown of TRIM29 had the opposite effect. Further mechanistic studies suggest that TRIM29 can activate the Wnt/β-catenin signaling pathway via up-regulating CD44 expression in colorectal cancer. Conclusions TRIM29 induces EMT through activating the Wnt/β-catenin signaling pathway via up-regulating CD44 expression, thus promoting invasion and metastasis of CRC.

ATDC promotes the growth and invasion of hepatocellular carcinoma cells by modulating GSK‐3β/Wnt/β‐catenin signalling

“…of Wnt/β-catenin signalling during tumour progression has been highlighted in recent years. Multiple sources of evidence have demonstrated that ATDC promoted the activation of Wnt/β-catenin signalling in various cancers, including non-small-cell lung cancer, cervical cancer, colorectal cancer, pancreatic cancer and glioma 25,29,[47][48][49]. Consistent with these findings, our results demonstrate that ATDC contributes to the activation of Wnt/β-catenin signalling in HCC cells.…”

<p>PFND1 Predicts Poor Prognosis of Gastric Cancer and Promotes Cell Metastasis by Activating the Wnt/β-Catenin Pathway</p>

“…It's widely acceptable that Wnt/β-catenin signaling pathway is involved in cancer migration and invasion. 11 Herein, we found that PFDN1 expression was positively correlated with β-catenin expression in GC tissues. Hence, we reasoned that Wnt/β-catenin signaling may be involved in PFDN1-induced GC cell migration and invasion.…”

“…Firstly, previous studies have confirmed that the blockade of the Wnt/β-catenin signaling suppressed EMT, migration and metastasis of cancer cells. 11,18 Β-catenin, a central molecule of the Wnt/βcatenin signaling, could activate the downstream targets (including c-myc, cyclin D1, and survivin) and subsequently cause tumor metastasis. 19 Notably, we found not only that PFDN1 expression significantly correlated with β-catenin expression in GC specimens, but also that PFDN1 silencing decreased the expressions of the Wnt/βcatenin signaling targets, whereas PFDN1 overexpression achieved the opposite outcomes.…”

Mortalin contributes to colorectal cancer by promoting proliferation and epithelial–mesenchymal transition

“…There are many signaling pathways involved in CRC occurrence and progression, including the Akt/mTOR pathway, the CDK4 pathway, and the Notch pathway . Recent reports emphasized that EMT played an important role in CRC dependence on the Wnt/β‐catenin pathway . Here, we focused on the mortalin‐activated Wnt/β‐catenin signaling pathway and EMT progression.…”

“…32 Recent reports emphasized that EMT played an important role in CRC dependence on the Wnt/β-catenin pathway. [33][34][35][36] Here, we focused on the mortalin-activated Wnt/β-catenin signaling pathway and EMT progression. Mortalin suppression inhibited CRC cell proliferation and EMT via deregulating the levels of β-catenin, Survivin, c-Myc, and Cyclin-D1.…”