MiR-597 Targeting 14-3-3σ Enhances Cellular Invasion and EMT in Nasopharyngeal Carcinoma Cells

Abstract

Background: Alterations in microRNAs (miRNAs) are related to the occurrence of nasopharyngeal carcinoma (NPC) and play an important role in the molecular mechanism of NPC. Our previous studies show low expression of 14-3-3σ (SFN) is related to the metastasis and differentiation of NPC, but the underlying molecular mechanisms remain unclear. Methods: Through bioinformatics analysis, we find miR-597 is the preferred target miRNA of 14-3-3σ. The expression level of 14-3-3σ in NPC cell lines was detected by Western blotting. The expression of miR-597 in NPC cell lines was detected by qRT-PCR. We transfected miR-597 mimic, miR-597 inhibitor and 14-3-3σ siRNA into 6-10B cells and then verified the expression of 14-3-3σ and EMT related proteins, including E-cadherin, N-cadherin and Vimentin by western blotting. The changes of migration and invasion ability of NPC cell lines before and after transfected were determined by wound healing assay and Transwell assay. Results: miR-597 expression was upregulated in NPC cell lines and repaired in related NPC cell lines, which exhibit a potent tumor-forming effect. After inhibiting the miR-597 expression, its effect on NPC cell line was obviously decreased. Moreover, 14-3-3σ acts as a tumor suppressor gene and its expression in NPC cell lines is negatively correlated with miR-597. Here 14-3-3σ was identified as a downstream target gene of miR-597, and its downregulation by miR-597 drives epithelial-mesenchymal transition (EMT) and promotes the migration and invasion of NPC. Conclusion: Based on these findings, our study will provide theoretical and experimental evidences for molecular targeted therapy of NPC.

IGHG1 induces EMT in gastric cancer cells by regulating TGF-β/SMAD3 signaling pathway

“…A large number of studies have found that the occurrence of EMT biological behavior plays an important role in the metastasis of malignant tumors [16][17][18]. In gastric cancer, many signaling pathways were involved in the regulation of EMT, and signaling pathways such as PI3K/AKT [19], MEK/ERK [20], and WNT/β-Catenin [21], especially TGF-β/ SMAD [22,23] play important roles.…”

Silencing circRNA_001937 may inhibit cutaneous squamous cell carcinoma proliferation and induce apoptosis by preventing the sponging of the miRNA‑597‑3p/FOSL2 pathway

“…miRNA-597-3p is located on the 8p23.1 chromosome ( 21 ). Xie et al ( 22 ) reported that miR-597 targeting 14-3-3σ enhances cellular invasion and the epithelial-mesenchymal transition in nasopharyngeal carcinoma cells, whilst Zhang et al ( 23 ) revealed that a low expression of miR-597 is correlated with tumor stage and a poor outcome in breast cancer. FOSL2 is a member of the AP-1 transcription factor family ( 24 ).…”

<p>MicroRNA-379-5p/YBX1 Axis Regulates Cellular EMT to Suppress Migration and Invasion of Nasopharyngeal Carcinoma Cells</p>

“…For example, miR-9-3p suppressed the EMT process via downregulating FN1, ITGB1, ITGAV expression to reduce the proliferation and metastases of NPC; 26 miR-BART8 -3p involved in EMT of NPC cells through directly targeting RNF38 to activate NF-κB and Erk1/2 signaling axis, thereby promoting NPC progression and metastasis; 27 miR-597 promoted cellular EMT to enhance the migration and invasion of NPC cells by targeting 14-3-3σ (SFN). 28 In this study, we found that the ectopic expression of miR-379-5p obviously suppressed the EMT program, thereby inhibiting the migration and invasion of NPC cells, whereas the inhibition of miR-379-5p exerted the opposite effect. These data implicate that miR-379-5p is an important regulator of EMT in NPC.…”