Metastasis-associated protein 3 in colorectal cancer determines tumor recurrence and prognosis

Huang, Yi; Li, Yunlong; He, Fenfei; Wang, Shi-qi; Li, Yaohui; Ji, Gang; Liu, Xiaonan; Zhao, Qingchuan; Li, Jipeng

doi:10.18632/oncotarget.16332

Cited by 13 publications

(15 citation statements)

References 29 publications

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“…MTA3 presented the highest fold change in normal and glioma tissues (Figure B). MTA3 has been reported to be a tumor inhibitor in several tumors, including glioma . Thus, we chose MTA3 for subsequent experiments.…”

Section: Resultsmentioning

confidence: 99%

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Long non‐coding RNA HCG11 suppresses the growth of glioma by cooperating with the miR‐4425/MTA3 axis

Zhang

Cao

Kou

et al. 2019

The Journal of Gene Medicine

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Background Glioma is a type of malignant tumor that occurs in the central nervous system of adults. Long non‐coding RNAs (lncRNAs) that potentially participate in the initiation and progression of glioma have been widely reported. As a now‐found lncRNA, HLA complex group 11 (HCG11) has not yet been studied in glioma. The present study aimed to determine the role of HCG11 in the tumorigenesis of glioma. Methods A quantitative real‐time polymerase chain reaction assay was performed to examine the expression pattern of HCG11 in 84 glioma tissues and cell lines. The overall survival rate of glioma patients with a high or low level of HCG11 or metastasis‐associated 1 family member 3 (MTA3) was analyzed by Kaplan–Meier analysis. The effect of HCG11 on glioma cell growth was determined by in vitro and in vivo experiments. MicroRNAs (miRNAs) that potentially interact with HCG11 were searched and determined by bioinformatics analysis and a luciferase reporter assay. Similarly, the target of miRNA‐4425 was identified. Finally, rescue assays were conducted to determine the bio‐function of the competing endogenous RNA pathway. Results HCG11 was downregulated in 84 pairs of glioma tissues and cell lines. Moreover, a low level of HCG11 indicted the lower overall survival rate of glioma patients. Regarding the mechanism, HCG11 was abundant in the cytoplasm of glioma cells and interacted with miR‐4425 to release the expression of MTA3. miR‐4425 and MTA3 participated in HCG11‐mediated glioma growth. Conclusions LncRNA HCG11 suppresses the growth of glioma by cooperating with the miR‐4425/MTA3 axis.

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Section: Resultsmentioning

confidence: 99%

“…MTA3 has been reported to be a tumor inhibitor in several tumors, including glioma. [21][22][23][24] Thus, we chose MTA3 for subsequent experiments.…”

Section: Mta3 Is a Target Of Mir-4425 In Gliomamentioning

confidence: 99%

Long non‐coding RNA HCG11 suppresses the growth of glioma by cooperating with the miR‐4425/MTA3 axis

Zhang

Cao

Kou

et al. 2019

The Journal of Gene Medicine

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“…The pathologic diagnosis of all tissue specimens was confirmed by the Department of Pathology, Tangdu Hospital. The disease‐free survival (DFS) and overall survival (OS) status was assigned by trained staff blinded to other clinicopathologic and ALKBH3 expression data …”

Section: Methodsmentioning

confidence: 99%

“…The disease-free survival (DFS) and overall survival (OS) status was assigned by trained staff blinded to other clinicopathologic and ALKBH3 expression data. 15 Immunohistochemistry. Immunohistochemistry assay on ALKBH3 was performed in all the 272 cases of liver cancer and adjacent non-tumorous specimens.…”

Section: Methodsmentioning

confidence: 99%

Association of AlkB homolog 3 expression with tumor recurrence and unfavorable prognosis in hepatocellular carcinoma

Wang

et al. 2018

J of Gastro and Hepatol

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“…In certain types of malignant tumors such as glioma, certain breast cancers, and adenocarcinomas, MTA3 is under-expressed and is implicated as a tumor suppressor [48–51]. In other carcinomas such as hepatocellular, lung, gastric, and colorectal cancers, MTA3 is reported to be overexpressed, with higher expression correlated with tumor progression and poorer prognosis [52–56]. In the Health ABC samples, the CpG (cg02162462) located in the first intron of MTA3 and overlapping a CpG island had lower methylation in the cancer-present group at Year 6.…”

Section: Discussionmentioning

confidence: 99%

Longitudinal Study of Leukocyte DNA Methylation and Biomarkers for Cancer Risk in Older Adults

Bartlett

Liang

Sandoval-Sierra

et al. 2019

Preprint

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19Background: Changes in DNA methylation over the course of life may provide 20 an indicator of risk for cancer. We explored longitudinal changes in CpG 21 methylation from blood leukocytes, and likelihood of a future cancer diagnosis. 22Methods: Peripheral blood samples were obtained at baseline and at follow-up 23 visit from 20 participants in the Health, Aging and Body Composition prospective 24 cohort study. Genome-wide CpG methylation was assayed using the Illumina 25 Infinium Human MethylationEPIC (HM850K) microarray. Results: Global 26 patterns in DNA methylation from CpG-based analyses showed extensive 27 changes in cell composition over time in participants who developed cancer. By 28 visit year 6, the proportion of CD8+ T-cells decreased (p-value = 0.02), while 29 granulocytes cell levels increased (p-value = 0.04) among participants diagnosed 30 with cancer compared to those who remained cancer-free (cancer-free vs. 31 cancer-present: 0.03 ± 0.02 vs. 0.003 ± 0.005 for CD8+ T-cells; 0.52 ± 0.14 vs. 32 0.66 ± 0.09 for granulocytes). Epigenome-wide analysis identified three CpGs 33 with suggestive p-values ≤ 10 -5 for differential methylation between cancer-free 34 and cancer-present groups, including a CpG located in MTA3, a gene linked with 35 metastasis. At a lenient statistical threshold (p-value ≤ 3 x 10 -5 ), the top 10 36 cancer-associated CpGs included a site near RPTOR that is involved in the 37 mTOR pathway, and the candidate tumor suppressor genes REC8, KCNQ1, and 38 ZSWIM5. However, only the CpG in RPTOR (cg08129331) was replicated in an 39 independent data set. Analysis of within-individual change from baseline to Year 40 6 found significant correlations between the rates of change in methylation in 41 RPTOR, REC8 and ZSWIM5, and time to cancer diagnosis. Conclusion: The 42 results show that changes in cellular composition explains much of the cross-43 sectional and longitudinal variation in CpG methylation. Additionally, differential 44 methylation and longitudinal dynamics at specific CpGs could provide powerful 45 indicators of cancer development and/or progression. In particular, we highlight 46CpG methylation in the RPTOR gene as a potential biomarker of cancer that 47 awaits further validation. 48 DNA methylation plays a central role in cell differentiation and in defining cellular 60 phenotypes. Differences in DNA methylation have been associated with a 61 growing list of morbidities, ranging from metabolic disorders and age-related 62 decline in health, to developmental and neuropsychiatric conditions. The 63 standard approach in an epigenome-wide association study (EWAS), which 64 attempts to link DNA methylation to disease, involves collection of a single 65 biospecimen from each participant (typically peripheral blood or saliva) and 66 performing cross-sectional analyses to compare methylation patterns in cases 67 against matched healthy controls [1, 2]. While differences in CpG methylation 68 between cases and controls may be directly related to disease, these case-69 control diff...

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Metastasis-associated protein 3 in colorectal cancer determines tumor recurrence and prognosis

Cited by 13 publications

References 29 publications

Long non‐coding RNA HCG11 suppresses the growth of glioma by cooperating with the miR‐4425/MTA3 axis

Long non‐coding RNA HCG11 suppresses the growth of glioma by cooperating with the miR‐4425/MTA3 axis

Association of AlkB homolog 3 expression with tumor recurrence and unfavorable prognosis in hepatocellular carcinoma

Longitudinal Study of Leukocyte DNA Methylation and Biomarkers for Cancer Risk in Older Adults

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