L-norleucine interacted with hnRNPA2/B1 protein to inhibit the expressions of Twist1 and Snail, two inhibitors of E-cadherin, and promote the E-cadherin expression, leading to the inhibition of tumor metastasis.
The TWIST gene was silenced by short hairpins in chordoma cell line MUG-Chor1 and effects on metastasis were investigated by wound healing/gap closure and invasion assays.
TWIST1 is an important transcription factor in EMT, which is present under both physiologic (embryogenesis) and pathologic (metastasis) conditions, and enhances the invasiveness and migration ability of cells.
Importantly, we find that lung BEAS-2B cells expressing GHRP495T display increased expression of transcripts associated with tumour proliferation, epithelial-mesenchymal transition and metastases (TWIST1, SNAI2, EGFR, MYC and CCND1) at 2 h after a GH pulse.
We found that ETV5 is critical for PTC cell growth, is expressed downstream of the MAPK pathway, and directly upregulates the transcription factor TWIST1, a known marker of intravasation and metastasis.
Twist1 is a key transcription factor, which confers tumor cells with cancer stem cell (CSC)-like characteristics and enhances epithelial-mesenchymal transition in pathological conditions including tumor malignancy and metastasis.
Overall, this study provides the first evidence to show that the high expression of TWIST1 increases the expression of miR-214 to promote the EMT process and metastasis in LAD.
Functional studies showed that specific down-regulation of either HIF1α or TWIST1 inhibited the ability of CPEB2B to induce the acquisition of anoikis resistance and drive metastasis.
To this end, we have investigated the unique WR domain of the transcription factor TWIST1, which has been shown to play a role in driving metastasis and drug resistance.
The present study aimed to explore the role of the combination of Twist1 expression in metastasized ALN and the serum level of CA15‑3 in evaluating the prognosis of patients with breast cancer. cluster of differentiation (CD)44, CD24, aldehyde dehydrogenase (ALDH)1 and Twist1 expression in normal and metastasized ALN from 102 patients with breast cancer were detected using laser confocal microscopy and the expression of the genes evaluated by reverse transcription‑quantitative polymerase chain reaction; E‑cadherin, N‑cadherin and vimentin expression was also tested by western blotting.
Here we demonstrate that Chk2 induction proficiently abrogates invasion, cell scattering and invadopodia formation ability of p53-mutated invasive cells by suppressing Twist1, indicating Chk2 confers vital role in metastasis prevention.
The transcription factor TWIST1 plays an important role in the epithelial-mesenchymal transition (EMT) process and in the migration, invasion and metastasis of cancer cells.
There is evidence to indicate that Twist expression plays a role in breast tumor formation and metastasis, but the role of Twist in dysregulating pathways that drive the metastatic cascade is unclear.
This platform has potential application for overcoming the clinical challenges of metastasis and chemoresistance in EOC and other TWIST overexpressing cancers.
Because cathepsin expression is higher in peritoneal tumors than underlying peritoneum, the hand-held cathepsin-based fluorescent imaging system could be useful for intraoperative detection of microscopic peritoneal metastasis during CRS-HIPEC and clinical trial is warranted.