Retraction: microRNA-613 exerts anti-angiogenic effect on nasopharyngeal carcinoma cells through inactivating the AKT signaling pathway by down-regulating FN1

Abstract Background: Nasopharyngeal carcinoma (NPC) is a disease highly sensitive to radiotherapy with the unclear etiology. However, the specific effects of microRNA-613 (miR-613) on NPC still remain elusive. Therefore, the present study probes into the underlying mechanism of miR-613 in NPC via AKT signaling pathway by regulating Fibronectin 1 (FN1). Methods: First, microarray analysis was used to screen differentially expressed genes (DEGs) and regulatory miRs associated with NPC. Next, miR-613 and FN1 expression in NPC cells was determined, followed by verification of target relationship between miR-613 and FN1. With NPC cells exposed to miR-613 mimic, si-FN1 and LY294002 (inhibitor of AKT signaling pathway), the regulatory effects of miR-613 on proliferation, apoptosis, invasion, migration and angiogenesis of NPC cells were detected with ratio of B-cell lymphoma 2/Bcl-2-associated X protein (Bcl-2/Bax), Cleaved-caspase3, matrix metallopeptidase 2 (MMP-2), MMP-9, vascular endothelial growth factor (VEGF), and cell adhesion molecule-1 (CD31) expression measured. Then, tumorigenesis and MVD were determined after Xenograft in nude mice. Results: FN1 modulated by miR-613 was critical for NPC via the AKT signaling pathway. NPC cells exhibited down-regulated miR-613 and up-regulated FN1. Besides, miR-613 was verified to target FN1. Moreover, overexpressed miR-613, silenced FN1 or LY294002 treatment suppressed proliferation, invasion, migration, and angiogenesis in NPC cells, which was indicated by reduced expression of AKT, mTOR, MMP-2, MMP-9, VEGF, and CD31 as well as decreased ratio of Bcl-2/Bax and increased expression of Cleaved-caspase3. Furthermore, cell apoptosis was promoted and tumorigenesis and MVD in nude mice were inhibited with overexpression of miR-613, silenced FN1 or LY294002 treatment. Conclusion: Taken together, miR-613 inhibits angiogenesis in NPC cells through inactivating FN1-dependent AKT signaling pathway.

Download Full-text

Silencing of LMP1 Induces Cell Cycle Arrest and Enhances Chemosensitivity Through Inhibition of AKT Signaling Pathway in EBV-Positive Nasopharyngeal Carcinoma Cells

Cell Cycle ◽

10.4161/cc.6.11.4274 ◽

2007 ◽

Vol 6 (11) ◽

pp. 1379-1385 ◽

Cited By ~ 48

Author(s):

Yu-Ping Mei ◽

Jun-Min Zhou ◽

Yi Wang ◽

He Huang ◽

Rong Deng ◽

...

Keyword(s):

Cell Cycle ◽

Nasopharyngeal Carcinoma ◽

Cell Cycle Arrest ◽

Signaling Pathway ◽

Akt Signaling ◽

Carcinoma Cells ◽

Akt Signaling Pathway ◽

Cycle Arrest

Download Full-text

T63 induces apoptosis in nasopharyngeal carcinoma cells through mitochondrial dysfunction and inhibition of PI3K/Akt signaling pathway

Translational Cancer Research ◽

10.21037/tcr-20-1677 ◽

2020 ◽

Vol 9 (8) ◽

pp. 4635-4645

Author(s):

Qin Liu ◽

Wei Chen ◽

Huiling Yang

Keyword(s):

Nasopharyngeal Carcinoma ◽

Mitochondrial Dysfunction ◽

Signaling Pathway ◽

Akt Signaling ◽

Carcinoma Cells ◽

Akt Signaling Pathway

Download Full-text

Influences of S100A8 and S100A9 on Proliferation of Nasopharyngeal Carcinoma Cells through PI3K/Akt Signaling Pathway

BioMed Research International ◽

10.1155/2021/9917365 ◽

2021 ◽

Vol 2021 ◽

pp. 1-7

Author(s):

Liting Wen ◽

Yu Ding ◽

Xiaodong Chen ◽

Keyong Tian ◽

Danfeng Li ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Signaling Pathway ◽

Akt Signaling ◽

Carcinoma Cells ◽

Akt Pathway ◽

Control Group ◽

Akt Signaling Pathway ◽

Protein Levels ◽

Positive Rate ◽

Sirna Group

Objective. To investigate the effects of S100A8 and S100A9 on proliferation in nasopharyngeal carcinoma cells and the regulatory effects of PI3K/Akt signaling pathway. Methods. Nasopharyngeal carcinoma cells (CNE1) were cultured and randomly divided into three groups: control group, S100A8/S100A9 overexpression group, and siRNA S100A8/S100A9 group. CCK-8 method was used to detect the effect of S100A8 and S100A9 on the viability of nasopharyngeal carcinoma cells. The effects of S100A8 and S100A9 on the colony forming ability of nasopharyngeal carcinoma cells were detected by colony forming assay. The effects of S100A8 and S100A9 on the proliferation of nasopharyngeal carcinoma cells were detected by EdU staining. The mRNA levels of PI3K and Akt were detected by RT-PCR. The expression levels of PI3K and Akt in NPC cells were detected by Western blot. Wortmannin, an inhibitor of PI3K/Akt pathway, was used to inhibit the activation of PI3K/Akt pathway. Results. Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were increased in the overexpression group. Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were decreased in the siRNA group. After inhibiting the activation of PI3K/Akt pathway, the viability of NPC cells in the overexpression group decreased significantly at 48 h and 72 h, while that in the siRNA group increased significantly. Conclusion. SiRNA S100A8 and S100A9 could inhibit the proliferation of nasopharyngeal carcinoma cells, and the underlying mechanism may be related to the inhibition of PI3K/Akt signaling pathway.

Download Full-text