[Corrigendum] ANXA1‑derived peptides suppress gastric and colon cancer cell growth by targeting EphA2 degradation.

Following the publication of the above article, the authors have realized that one of the data panels featured in Fig. 5D was selected incorrectly. Specifically, the wrong image was selected for the A1 (28‑30), HCT116 experiment.

ANXA1‑derived peptides suppress gastric and colon cancer cell growth by targeting EphA2 degradation.

EphA2 (EPH receptor A2) (erythropoietin‑producing hepatocellular receptor tyrosine kinase subtype A2) plays a crucial role in human cancers, and is a promising target for the development of new anticancer drugs. In this study, we showed that the interaction of Annexin A1 (ANXA1) and EphA2 increased EphA2 stability by inhibiting its proteasome degradation in gastric cancer (GC) and colon cancer (CC) cells, and the amino acid residues 20‑30 and 28‑30 of ANXA1 N terminal were responsible for binding and stabilizing EphA2. Based on the amino acid residues of ANXA1 responsible for binding EphA2, we developed ANXA1‑derived 3 amino acid‑long (SKG) and 11 amino acid‑long peptides (EYVQTVKSSKG) in fusion to cell‑penetrating peptide, named as A1(28‑30) and A1(20‑30) respectively, and found that A1(28‑30) and A1(20‑30) blocked the binding of ANXA1 with EphA2, targeted EphA2 degradation, and suppressed the growth of GC and CC cells in vitro and in mice.

Y772 phosphorylation of EphA2 is responsible for EphA2-dependent NPC nasopharyngeal carcinoma growth by Shp2/Erk-1/2 signaling pathway.

EphA2 is an important oncogenic protein and emerging drug target, but the oncogenic role and mechanism of ligand-independent phosphorylation of EphA2 at tyrosine 772 (pY772-EphA2) is unclear. In this study, we established nasopharyngeal carcinoma (NPC) cell lines with stable expression of exogenous EphA2 and EphA2-Y772A (phosphorylation inactivation) using endogenous EphA2-knockdown cells, and observed that pY772A EphA2 was responsible for EphA2-promoting NPC cell proliferation and anchorage-independent and in vivo growth in mice. Mechanistically, EphA2-Y772A mediated EphA2-activating Shp2/Erk-1/2 signaling pathway in the NPC cells, and Gab1 (Grb2-associated binder 1) and Grb2 (growth factor receptor-bound protein 2) were involved in pY772-EphA2 activating this signaling pathway.

ANXA1 Binds and Stabilizes EphA2 to Promote Nasopharyngeal Carcinoma Growth and Metastasis.

Overexpression of ANXA1 and EphA2 has been linked to various cancers and both proteins have attracted considerable attention for the development of new anticancer drugs. Here we report that ANXA1 competes with Cbl for binding EphA2 and increases its stability by inhibiting Cbl-mediated EphA2 ubiquitination and degradation in nasopharyngeal carcinoma (NPC). Binding of ANXA1 to EphA2 promoted NPC cell growth and metastasis and by elevating EphA2 levels and increasing activity of EphA2 oncogenic signaling (pS897-EphA2).

HDAC7 promotes the oncogenicity of nasopharyngeal carcinoma cells by miR-4465-EphA2 signaling axis.

HDAC7 plays a crucial role in cancers, and is the main drug target of several HDAC inhibitors. However, the role and mechanism of HDAC7 in nasopharyngeal carcinoma (NPC) are still unclear. In this study, we observed that HDAC7 was significantly upregulated in the NPC tissues relative to normal nasopharyngeal mucosa (NNM) tissues, HDAC7 expression levels were positively correlated with NPC progression and negatively correlated with patient prognosis, and HDAC7 knockdown dramatically inhibited the in vitro proliferation, migration, and invasion of NPC cells, and the growth of NPC xenografts in mice, indicating the HDAC7 promotes the oncogenicity of NPC.

Heterozygous p53-R280T Mutation Enhances the Oncogenicity of NPC Cells Through Activating PI3K-Akt Signaling Pathway.

A heterozygous point mutation of p53 gene at codon 280 from AGA to ACA (R280T) frequently occurs in nasopharyngeal carcinoma (NPC) cell lines, and about 10% NPC tissues. However, the role of this mutation in the pathogenesis of NPC remains unclear. In this study, we generated p53 knockout (KO) NPC cell lines from CNE2 cells carrying heterozygous p53 R280T (p53-R280T) mutation and C666-1 cells carrying wild-type p53 by CRISPR-Cas9 gene editing system, and found that KO of heterozygous p53-R280T significantly decreased NPC cell proliferation and increased NPC cell apoptosis, whereas KO of wild-type p53 had opposite effects on NPC cell proliferation and apoptosis.

Targeted Inhibitory Effect of Nasopharyngeal Carcinoma Cells by Hre.Grp78 Chimeric Promoter Regulating Fusion Gene .

Objective: To construct plasmids with Hre.Grp78 chimeric promoter regulating fusion gene and elaborate the effects of overexpressed on nasopharyngeal carcinoma cells.

Methods: Four plasmids were constructed, including pcDNA3.

[Killing effect improved by fusion gene HRE1.Egr-1. yCDglyTK on gene-radio therapy of nasopharyngeal cancer in vitro].

Objective: To construct hypoxia/radiation inducible promotor HRE1.Egr-1, and to observe its promotive effect on the expression of yCDglyTK gene in nasopharyngeal cancer HNE-1 cells and the anti-tumor effect of yCDglyTK and to lay an experimental foundation for further exploration of new gene-radio therapy of nasopharyngeal cancer.

Methods: pcDNA3.

[Killing effect of VP3 on human nasopharyngeal carcinoma cell line CNE-2 cells].

Objective: To investigate the killing effects of VP(3) on nasopharyngeal carcinoma cell line CNE-2.

Methods: Plasmid expression vector pcDNA3.1(-) CMV.

[Clinical analysis of pneumomediastinum or pneumothorax during the removal of brochial foreign bodies].

Objective: To discuss the etiology, diagnosis, treatment, and prevention of pneumomediastinum or pneumothorax during the removal of bronchial foreign bodies in children.

Methods: We analyzed the clinical data of 10 cases of pneumomediastinum or pneumothorax during the removal of bronchial foreign bodies in children.

Results: Two patients died and the other 8 were cured.