TACC3 promotes epithelial–mesenchymal transition (EMT) through the activation of PI3K/Akt and ERK signaling pathways

Effects of ginsenoside compound K combined with cisplatin on the proliferation, apoptosis and epithelial mesenchymal transition in MCF-7 cells of human breast cancer

“…Studies have shown that a variety of chemotherapeutic drugs may exert their antitumor effects by blocking this pathway (Zhang et al 2013;Ryu et al 2014). In addition, a number of studies have shown that the activation of PI3K/Akt signalling pathway may promote the occurrence of EMT (Ha et al 2013). Yang et al (2014) confirmed that inhibiting the activation of PI3K/Akt pathway could inhibit the occurrence of EMT in breast cancer MCF-7 and BT-20 cells.…”

MiR-29c mediates epithelial-to-mesenchymal transition in human colorectal carcinoma metastasis via PTP4A and GNA13 regulation of β-catenin signaling

“…The loss of E-cadherin can lead to the accumulation of β-catenin, and stabilized β-catenin in the cytoplasm translocates to the cell nucleus, where it forms a β-catenin-TCF/LEF transcriptional complex and induces the transcription of target genes implicated in EMT and carcinogenesis [24,25]. The Wnt/β-catenin, ERK, and PI3K/AKT signaling pathways have been implicated in the stabilization of β-catenin and EMT induction [26,27]. In present study, the data from the TCF/LEF reporter assay provided evidence for the activation of β-catenin signaling upon miR-29c knockdown in CRC cells; gain-and loss-of-function experiments with PTP4A and GNA13 confirmed that these genes are targets of miR-29c and are mediators of miR-29c effects on cell invasiveness and EMT.…”

Transforming acidic coiled-coil-containing protein 3 (TACC3) overexpression in hepatocellular carcinomas is associated with “stemness” and epithelial-mesenchymal transition-related marker expression and a poor prognosis

“…Therefore, it is still unclear whether TACC3 overexpression helps stabilize HCC cells in spite of the chromosomal instability or whether the overexpression of TACC3 actually has a deleterious effect on HCCs and other mechanisms are needed for the survival of cancer cells and further tumor progression. In addition to the possible role in the evasion of apoptosis of HCC cells with genomic instability, a role for TACC3 in the regulation of EMT has been suggested: it has recently been demonstrated that TACC3 contributes to the EMT process through the activation of phosphatidylinositol 3-kinase (PI3K)/AKT and extracellular signal-regulated protein kinase (ERK) signaling pathways [8], and TACC3 has also been implicated in epidermal growth factor (EGF)-mediated EMT in cervical cancers [7]. We also found that TACC3 expression in HCCs was more frequently associated with the expression of proteins related to EMT (S100A4, ezrin, and uPAR), loss of E-cadherin expression in HCCs, and clinicopathological features of aggressiveness, such as poor histological differentiation, frequent vascular invasion, advanced tumor stage, and poor overall survival, providing additional evidence that TACC3 may be related to EMT in HCCs.…”

“…TACC3 serves an important role in the stabilization of the centrosomal microtubules and regulation of the integrity of centrosomes during mitosis [6], and has also recently been shown to play a role in the regulation of epithelialmesenchymal transition (EMT) of cervical cancer cells [7,8]. While TACC3 expression has been associated with poor prognoses in non-small cell lung cancers and cervical cancers, the expression patterns and the clinicopathological significance of TACC3 protein expression have not yet been studied in HCCs.…”