RETRACTED: Silencing of Prrx1b suppresses cellular proliferation, migration, invasion and epithelial–mesenchymal transition in triple‐negative breast cancer

Abstract

Triple-negative breast cancer (TNBC) is a highly aggressive tumour subtype associated with poor prognosis. The mechanisms involved in TNBC progression remains largely unknown. To date, there are no effective therapeutic targets for this tumour subtype. Paired-related homeobox 1b (Prrx1b), one of major isoforms of Prrx1, has been identified as a new epithelial-mesenchymal transition (EMT) inducer. However, the function of Prrx1b in TNBC has not been elucidated. In this study, we found that Prrx1b was significantly up-regulated in TNBC and associated with tumour size and vascular invasion of breast cancer. Silencing of Prrx1b suppressed the proliferation, migration and invasion of basal-like cancer cells. Moreover, silencing of Prrx1b prevented Wnt/b-catenin signaling pathway and induced the mesenchymal-epithelial transition (MET). Taken together, our data indicated that Prrx1b may be an important regulator of EMT in TNBC cells and a new therapeutic target for interventions against TNBC invasion and metastasis.

Silencing of Prrx2 Inhibits the Invasion and Metastasis of Breast Cancer both In Vitro and In Vivo by Reversing Epithelial-Mesenchymal Transition

“…After washing, biotin labeled secondary antibody against rabbit immunoglobulin was applied for 30 min at room temperature. The results were evaluated as described previously [12]. …”

“…After 42 days, the mice were killed, and the tumors were weighed. The tumor volumes were determined as described previously [12]. 2 × 10 6 cells were injected into the tail vein to establish a lung metastatic model of breast cancer (n=8).…”

“…Prrx1/Prrx2 double-deficient mice particularly demonstrate the important roles performed by these factors in craniofacial and limb morphogenesis. We previously reported that silencing of Prrx1b repression of Wnt/β-catenin signaling pathway and inhibited the proliferation, invasive and migration in triple-negative breast cancer by reversing the EMT phenotypes [12]. A recent study reported that Prrx2 as a TGF-β-induced factor that enhances invasion and migration in breast cancer [13].…”

Alpha B‐crystallin promotes the invasion and metastasis of gastric cancer via NF‐κB‐induced epithelial‐mesenchymal transition

“…As numerous genetic changes are in relation to cancer cell invasion and metastasis,14, 19, 20, 21, 22 great efforts have been made in the identification of novel key regulators and the potential mechanisms involved in this process over the years. Interestingly, recent studies have revealed that CRYAB is aberrantly overexpressed in various types of cancer, and its expression could promote cell invasion and metastasis 8, 9, 10.…”

FL118, a novel camptothecin analogue, suppressed migration and invasion of human breast cancer cells by inhibiting epithelial-mesenchymal transition <i>via</i> the Wnt/β-catenin signaling pathway

“…EMT is a biological process that allows a polarized epithelial cell, which normally interacts with the basement membrane via its basal surface, to undergo multiple biochemical changes that enable it to assume a mesenchymal cell phenotype, which includes enhanced migratory and invasive capacities (10). Studies have reported that Wnt/β-catenin is among the main pathways that regulate EMT, which may be the key mechanism that mediates breast cancer progression (11,12). Agents that target Wnt/β-catenin and downstream molecules such as survivin and cyclin D1 have a potent inhibitory effect on cell proliferation, invasion, and metastasis in…”