MYBL2 is a Potential Prognostic Marker that Promotes Cell Proliferation in Gallbladder Cancer

Liang, Hai Bin; Yang, Cao; Ma, Qiang; Shu, Yi; Wang, Zheng; Zhang, Fei; Ye, Yuan Yuan; Li, Huai Feng; Xiang, Shufen; Song, Xiao; Xu, Yi; Zhang, Yi Chi; Bao, Run Fa; Rui, Yuan; Zhang, Yi Jian; Hu, Yun; Jiang, Lin; Li, Mao Lan; Wang, Xu An; Wu, Xiang; Wu, Wen; Zhao, Shuai; Fand, Yong; Cui, Xiao; Yun, Lingsong; Zhou, Jian; Li, Zheng; Gong, Wei; Liu, Ying Bin

doi:10.1159/000475454

Cited by 22 publications

(19 citation statements)

References 35 publications

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“…MYBL2 is upregulated in various cancer types and has been implicated in cancer pathogenesis 8–12. Previous studies have found that MYBL2 promotes tumor-cell proliferation in breast cancer and gallbladder cancer 17,18. In our study, elevated MYBL2 expression was observed in ESCC tissue when compared to corresponding nontumor tissue in ESCC patients.…”

Section: Discussionsupporting

confidence: 59%

<p>Prognostic implications and oncogenic roles of MYBL2 protein expression in esophageal squamous-cell carcinoma</p>

Qin

Zhang

et al. 2019

OTT

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BackgroundThe MYBL2 gene, a highly conserved member of the Myb transcription-factor family, has been implicated in the genesis and progression of many types of tumors.MethodsWe analyzed the expression of MYBL2 and Ki67 in tissue samples of esophageal squamous-cell carcinoma (ESCC) patients by immunohistochemistry. We further analyzed the effect of MYBL2 on cell proliferation and DNA replication using a CCK8 assay, 5-ethynyl-2′-deoxyuridine–retention assay, flow-cytometry analysis, real-time quantitative PCR, Western blot, and a xenograft model of ESCC cells in nude mice.ResultsMYBL2 expression was significantly higher in ESCC tissue when compared to the adjacent normal tissue (P=0.007). MYBL2 was found to be positively correlated with Ki67 (γ=0.286, P=0.003). Furthermore, Kaplan–Meier curves indicated that MYBL2 expression in ESCC tissue was associated with poor patient outcome (P<0.001), with MYBL2-positive patients who exhibited high Ki67 expression in ESCC tissue showing the worst prognosis for overall survival (P=0.003). Our in vitro results showed that downregulation of MYBL2 in ESCC cell lines inhibited cell proliferation and DNA replication (P<0.05 for both). We also found that loss of MYBL2 caused a reduction in levels of cell cycle-related G2/M proteins CDK1 and cyclin B1 in ESCC cells. In contrast, overexpression of MYBL2 caused an increase in these proteins. In vivo, we found that in nude mice that received cells knocked down for MYBL2, tumor growth was inhibited in comparison to the group that received control cells (P<0.05).ConclusionMYBL2 overexpression induces tumor proliferation in ESCC cells by regulating cell-cycle at the S and G2/M phase. Therefore, MYBL2 may serve as a novel prognostic biomarker in ESCC patients.

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Section: Discussionsupporting

confidence: 59%

<p>Prognostic implications and oncogenic roles of MYBL2 protein expression in esophageal squamous-cell carcinoma</p>

Qin

Zhang

et al. 2019

OTT

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“…MYBL2 is overexpressed in various cancers, including leukaemia 43 , neuroblastoma 44 , breast cancer 45 , lung cancer 46 , colorectal cancer 47 and hepatocellular carcinoma 48 . It has also been reported that MYBL2 expression is correlated with poor prognosis in several cancers 47 , 49 . By analysing the R2 database, we found that glioma patients with higher MYBL2 expression levels showed poorer prognosis (Fig.…”

Section: Discussionmentioning

confidence: 88%

Demethylzeylasteral inhibits glioma growth by regulating the miR-30e-5p/MYBL2 axis

Zhang

Pan

et al. 2018

Cell Death Dis

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Glioma is the most common and malignant form of primary brain tumour, and is characterised by high proliferation and extensive invasion and neurological destruction. Demethylzeylasteral (T-96), which is extracted from Tripterygium wilfordii, is considered to have immunosuppressive, anti-inflammatory and anti-angiogenic effects. Here, the anti-tumour effect of T-96 on glioma was evaluated. Our results demonstrated that T-96 significantly inhibited glioma cell growth and induced cell cycle arrest in G1 phase but did not induce apoptosis. Cell invasion and migration were dramatically suppressed after treatment with T-96. Almost all genes related to cell cycle and DNA replication were downregulated after treatment with T-96. Our results showed that miR-30e-5p was noticeably upregulated after T-96 treatment, and MYBL2, which is involved in cell cycle progression and is a target gene of miR-30e-5p, was significantly reduced in synchrony. Overexpression of MYBL2 partially rescued the T-96-induced inhibition of cell growth and proliferation. Moreover, a miR-30e-5p antagomir significantly reduced the upregulation of miR-30e-5p expression induced by T-96, leading to recovery of MYBL2 expression, and partially rescued the T-96-induced inhibition of cell growth and proliferation. More important, T-96 effectively upregulated miR-30e-5p expression and downregulated MYBL2 expression, thus inhibiting LN-229 cell tumour growth in a mouse model. These results indicated that T-96 might inhibit glioma cell growth by regulating the miR-30e-5p/MYBL2 axis. Our study demonstrated that T-96 might act as a promising agent for malignant glioma therapy.

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“…Moreover, our results from exome-sequencing and their validation by Sanger sequencing revealed a novel mutation in the MYBL2 gene, which is a transcription factor of the MYB proto-oncogene family and a critical regulator of cell proliferation, cell survival and differentiation [58]. Recently, it has been reported that MYBL2 is a novel candidate biomarker gene for various cancer cells such as colorectal [59], gallbladder [60] and cervical cancer [61]. In meningioma, the alterations of the MYBL2 might be involved in cancer initiation and progression by affecting cell cycle progression, resistance to therapy and favoring metastatic spread [62].…”

Section: Discussionmentioning

confidence: 91%

Characterization and comparison of genomic profiles between primary cancer cell lines and parent atypical meningioma tumors

Kim

et al. 2020

Cancer Cell Int

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Background: Meningiomas are the second most common primary tumors of the central nervous system. However, there is a paucity of data on meningioma biology due to the lack of suitable preclinical in vitro and in vivo models. In this study, we report the establishment and characterization of patient-derived, spontaneously immortalized cancer cell lines derived from World Health Organization (WHO) grade I and atypical WHO grade II meningiomas. Methods: We evaluated high-resolution 3T MRI neuroimaging findings in meningioma patients which were followed by histological analysis. RT-qPCR and immunostaining analyses were performed to determine the expression levels of meningioma-related factors. Additionally, flow cytometry and sorting assays were conducted to investigate and isolate the CD133 and CD44 positive cells from primary atypical meningioma cells. Further, we compared the gene expression profiles of meningiomas and cell lines derived from them by performing whole-exome sequencing of the blood and tumor samples from the patients, and the primary cancer cell lines established from the meningioma tumor. Results: Our results were consistent with earlier studies that reported mutations in NF2, SMO, and AKT1 genes in atypical meningiomas, and we also observed mutations in MYBL2, a gene that was recently discovered. Significantly, the genomic signature was consistent between the atypical meningioma cancer cell lines and the tumor and blood samples from the patient. Conclusion: Our results lead us to conclude that established meningioma cell lines with a genomic signature identical to tumors might be a valuable tool for understanding meningioma tumor biology, and for screening therapeutic agents to treat recurrent meningiomas.

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MYBL2 is a Potential Prognostic Marker that Promotes Cell Proliferation in Gallbladder Cancer

Cited by 22 publications

References 35 publications

<p>Prognostic implications and oncogenic roles of MYBL2 protein expression in esophageal squamous-cell carcinoma</p>

<p>Prognostic implications and oncogenic roles of MYBL2 protein expression in esophageal squamous-cell carcinoma</p>

Demethylzeylasteral inhibits glioma growth by regulating the miR-30e-5p/MYBL2 axis

Characterization and comparison of genomic profiles between primary cancer cell lines and parent atypical meningioma tumors

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