Overexpression of MYC binding protein promotes invasion and migration in gastric cancer

Abstract

Abstract. Gastric cancer (GC) is the second leading cause of cancer-associated mortality worldwide. Although the mortality rate of patients with GC has improved, it remains a significant health issue. The MYC proto-oncogene protein serves key roles in cellular proliferation, differentiation, transformation and apoptosis. Previous studies have identified the abnormal expression of MYC-binding protein (MYCBP) during tumorigenesis in multiple types of cancer. Furthermore, evidence demonstrates that the abnormal expression of MYCBP contributes to the invasion and migration of human cancer types, including colon cancer and glioma; however, its influence on GC remains unclear. In the present study, the expression of MYCBP in GC cells and tissues was analyzed by reverse transcription-quantitative polymerase chain reaction. Additionally, GC cell lines were transfected with small interfering RNAs against MYCBP or lymphoid enhancer-binding factor 1 (LEF-1) and assessed by in vitro transwell migration and invasion assays. The results indicated that the expression of MYCBP in GC cells and tissues was markedly increased compared with a normal gastric epithelial cell line and adjacent normal gastric mucosal tissues, respectively. Furthermore, MYCBP downregulation notably inhibited the metastatic capacity of GC cells, and LEF-1 knockdown was found to downregulate the expression of MYCBP. On the basis of the findings of the present study, MYCBP may be a direct target of the β-catenin/LEF-1 pathway via binding LEF-1, and could potentially be used as a biomarker for the diagnosis and prognosis of GC.

EYA4 inhibits hepatocellular carcinoma by repressing MYCBP by dephosphorylating β‐catenin at Ser552

“…In order to verify the correlation between EYA4 and MYCBP, MYCBP was reported as a direct target of the β-catenin/LEF-1 pathway. 15,22 EYA4 was shown to mediate the Wnt pathway by dephosphorylating β-catenin Ser675 in pancreatic cancer. 15,23 Therefore, we hypothesized that EYA4 may mediate MYCBP by dephosphorylating β-catenin.…”

“…15,22 EYA4 was shown to mediate the Wnt pathway by dephosphorylating β-catenin Ser675 in pancreatic cancer. 15,23 Therefore, we hypothesized that EYA4 may mediate MYCBP by dephosphorylating β-catenin. β-Catenin is one of the core proteins in the Wnt signaling pathway, and it was shown that phosphorylation at Ser552 and Ser675 of β-catenin could activate the β-catenin mediated signaling pathway.…”

“…13 Recently published papers showed that MYCBP played an important role in lung cancer, gastric cancer, glioma, esophageal squamous cancer and acute myeloid leukaemia. [14][15][16][17][18] However, it still remains unknown as to whether MYCBP plays a role in HCC.…”

MicroRNA‑22 enhances radiosensitivity in cervical cancer cell lines via direct inhibition of c‑Myc binding protein, and the subsequent reduction in hTERT expression

“…Previous studies have suggested that MYCBP is an important regulator affecting the progression and development of tumors; for example, in glioma cells, the MYCBP mRNA expression increased along with the malignant grade (36). Moreover, in gastric cancer, Gong et al (37) reported that MYCBP mRNA expression was markedly increased compared with that in normal gastric tissues and knockdown of MYCBP inhibited the metastatic capacity. However, the influence of MYCBP on radiosensitivity is yet to be elucidated.…”

Whole slide images reflect DNA methylation patterns of human tumors

“…Overexpression of this gene was shown to promote invasion and migration in gastric cancer. 27 Both genes are involved in the cell cycle progression and the methylation states of them are well-predicted by morphometric features in the glioma samples. Both CDK4 and MYCBP have an AUC score over 0.94 and F1 score over 0.84 under logistic regression, support vector machines, and neural network models.…”