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

Gong, Lijie; Xia, Yingjie; Qian, Zhenyuan; Shi, Jingwei; Luo, Jungang; Song, Guangyuan; Xu, Jianping; Ye, Zai-yuan

doi:10.3892/ol.2018.7944

Cited by 24 publications

(28 citation statements)

References 40 publications

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Zhu

Cai

et al. 2019

Cancer Science

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Hepatocellular carcinoma (HCC) is one of the most common malignancies and the fourth leading cause of cancer‐related death worldwide. Our previous study showed that EYA4 functioned by suppressing growth of HCC tumor cells, but its molecular mechanism is still not elucidated. Based on the results of gene microassay, EYA4 was inversely correlated with MYCBP and was verified in human HCC tissues by immunohistochemistry and western blot. Overexpressed and KO EYA4 in human HCC cell lines confirmed the negative correlation between EYA4 and MYCBP by qRT‐PCR and western blot. Transfected siRNA of MYCBP in EYA4 overexpressed cells and overexpressed MYCBP in EYA4 KO cells could efficiently rescue the proliferation and G2/M arrest effects of EYA4 on HCC cells. Mechanistically, armed with serine/threonine‐specific protein phosphatase activity, EYA4 reduced nuclear translocation of β‐catenin by dephosphorylating β‐catenin at Ser552, thereby suppressing the transcription of MYCBP which was induced by β‐catenin/LEF1 binding to the promoter of MYCBP. Clinically, HCC patients with highly expressed EYA4 and poorly expressed MYCBP had significantly longer disease‐free survival and overall survival than HCC patients with poorly expressed EYA4 and highly expressed MYCBP. In conclusion, EYA4 suppressed HCC tumor cell growth by repressing MYCBP by dephosphorylating β‐catenin S552. EYA4 combined with MYCBP could be potential prognostic biomarkers in HCC.

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Section: Discussionmentioning

confidence: 99%

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

Zhu

Cai

et al. 2019

Cancer Science

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“…In esophageal cancer, miR-26a and miR-26b inhibit tumor cell proliferation by inhibition of MYCBP expression (22). Overexpression of MYCBP binding protein was found to promote the invasion and migration of gastric cancer (23). These findings indicate that MYCBP plays a carcinogenic role in most cancers.…”

Section: Introductionmentioning

confidence: 87%

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Qian

Garg

et al. 2020

Int J Oncol

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Colorectal cancer (CRC) is a tumor type characterized by high patient morbidity and mortality. It has been reported that long non-coding (lncRNA) LUNAR1 (LUNAR1) participates in the regulation of tumor progression, such as diffuse large B-cell lymphoma. However, its role and underlying mechanisms in CRC progression have not been elucidated. The present study was designed to investigate the underlying mechanisms by which LUNAR1 regulates CRC progression. RT-qPCR and Pearson's correlation analysis revealed that LUNAR1 was highly expressed and was negatively associated with the overall survival of CRC patients. Moreover, CCK-8, clone formation, wound-healing migration, Transwell chamber and FACs assay analyses showed that LUNAR1 knockdown inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. Additionally, LUNAR1 was found to function as a sponge of miR-495-3p, which was predicted by TargetScan and confirmed by luciferase reporter assay. Furthermore, functional studies indicated that miR-495-3p overexpression inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. In addition, bioinformatics and luciferase reporter assays showed that miR-495-3p was found to negatively target Myc binding protein (MYCBP), and functional research showed that LUNAR1 accelerated CRC progression via the miR-495-3p/MYCBP axis. In conclusion, LUNAR1 accelerates CRC progression via the miR-495-3p/MYCBP axis, indicating that LUNAR1 may serve as a prognostic biomarker for CRC patients.

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2020

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MicroRNAs (miRs) influence the expression of their target genes post-transcriptionally and serve an important role in multiple cellular processes. The downregulation of miR-22 is associated with a poor prognosis in cervical cancer. However, the mechanisms underlying miR-22-mediated gene regulation and its function are yet to be elucidated. In the present study, the effect of miR-22 expression on the radiosensitivity of cervical cancer was investigated. First, miR-22 was either up-or downregulated to evaluate the regulation of the MYC-binding protein (MYCBP) in four cervical cancer cell lines (C-4I, SKG-II and SiHa). Notably, MYCBP expression was inversely associated with miR-22 induction. A dual-luciferase reporter gene assay revealed that miR-22 directly targets the MYCBP 3'-untranslated region. Subsequently, the level of human telomerase reverse transcriptase component (hTERT; an E-box-containing c-Myc target gene) was analyzed after the up-or downregulation of miR-22. Notably, miR-22-mediated repression of MYCBP reduced hTERT expression. In addition, the influence of miR-22 on radiosensitivity in C-4I, SKG-II and SiHa cells was examined using a clonogenic assay and in mouse xenograft models. Upregulation of miR-22 was associated with increased radiosensitivity. Furthermore, lentiviral transduction of miR-22 reduced the Ki-67 index while increasing the TUNEL index in xenograft tissue. The current findings indicate the potential utility of miR-22 in radiotherapy for cervical cancer.

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

Cited by 24 publications

References 40 publications

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

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

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

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

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