LncRNA MCM3AP-AS1 promotes breast cancer progression via modulating miR-28-5p/CENPF axis

Chen, Qi; Xu, Huachao; Zhu, Jiang; Feng, Ke; Hu, Chang-Lu

doi:10.1016/j.biopha.2020.110289

Cited by 59 publications

(47 citation statements)

References 30 publications

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“…As a novel therapeutic target, CENPF has been found to be overexpressed in various cancers and related with aggressive tumor phenotype as well as poor prognosis in different cancers [16]. According to previous studies, MCM3AP-AS1 could hasten tumor growth in breast cancer by targeting CENPF via competitively binding to miR-28-5p [17]. Besides, overexpression of hnRNPR promoted the aggressiveness of gastric cancer by increasing the mRNA expression of CCNB1 and CENPF [18].…”

Section: Discussionmentioning

confidence: 98%

Overexpression of CENPF is associated with progression and poor prognosis of lung adenocarcinoma

Li¹,

Zhang²,

Dong³

et al. 2021

Int. J. Med. Sci.

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Background and aim: The molecular signatures of lung adenocarcinoma (LUAD) are not well understood. Centromere protein F (CENPF) has been shown to promote oncogenesis in many cancers; however, its role in LUAD has not been illustrated. We explored the role of CENPF in LUAD. Methods: CENPF expression level was investigated in public online database firstly, the prognosis of CENPF in LUAD were also assessed by Kaplan-Meier analysis. Then quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was performed using 13 matched pairs of clinical LUAD tissue samples. Subsequently, the impact of CENPF expression on cell proliferation, cell cycle, apoptosis, colony formation was investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), flow cytometric analysis and colony formation assay, respectively. Finally, experimental xenograft lung cancer model of nude mice armpit of right forelimb to determine the effect of CENPF on LUAD tumorigenesis. Results: CENPF mRNA expression was significantly elevated in LUAD tissues compared with adjacent non-tumor lung tissues in Gene Expression Profiling Interactive Analysis (GEPIA) ( P < 0.001). Up-regulated CENPF was remarkably positively associated with pathological stage, relapse free survival (RFS) as well as overall survival (OS) of LUAD patients. Besides, CENPF knockdown greatly suppressed A549 cell proliferation, induced S phase arrest, promoted apoptosis and decreased colony numbers of LUAD cells. Furthermore, knockdown of CENPF significantly inhibited the tumor growth of the LUAD cells in an experimental xenograft lung cancer model of nude mice armpit of right forelimb. Conclusion: Taken together, these results demonstrated that CENPF may serve as a potential biomarker of prognostic relevance and a potential therapeutic target for LUAD.

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Section: Discussionmentioning

confidence: 98%

Overexpression of CENPF is associated with progression and poor prognosis of lung adenocarcinoma

Li¹,

Zhang²,

Dong³

et al. 2021

Int. J. Med. Sci.

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“…CENPF encodes a protein that associates with the centromere-kinetochore complex and influences cell cycle, division, and differentiation [ 59 ]. It has been reported that CENPF is related to multiple kinds of malignancies such as prostate and breast cancer [ 60 , 61 ]. In particular, the research of Yang et al found that CENPF could promote the tumour growth of HCC [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of 5 Hub Genes Related to the Early Diagnosis, Tumour Stage, and Poor Outcomes of Hepatitis B Virus-Related Hepatocellular Carcinoma by Bioinformatics Analysis

Qiang

Zhao

Tang³

et al. 2021

Computational and Mathematical Methods in Medicine

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Background. The majority of primary liver cancers in adults worldwide are hepatocellular carcinomas (HCCs, or hepatomas). Thus, a deep understanding of the underlying mechanisms for the pathogenesis and carcinogenesis of HCC at the molecular level could facilitate the development of novel early diagnostic and therapeutic treatments to improve the approaches and prognosis for HCC patients. Our study elucidates the underlying molecular mechanisms of HBV-HCC development and progression and identifies important genes related to the early diagnosis, tumour stage, and poor outcomes of HCC. Methods. GSE55092 and GSE121248 gene expression profiling data were downloaded from the Gene Expression Omnibus (GEO) database. There were 119 HCC samples and 128 nontumour tissue samples. GEO2R was used to screen for differentially expressed genes (DEGs). Volcano plots and Venn diagrams were drawn by using the ggplot2 package in R. A heat map was generated by using Heatmapper. By using the clusterProfiler R package, KEGG and GO enrichment analyses of DEGs were conducted. Through PPI network construction using the STRING database, key hub genes were identified by cytoHubba. Finally, KM survival curves and ROC curves were generated to validate hub gene expression. Results. By GO enrichment analysis, 694 DEGs were enriched in the following GO terms: organic acid catabolic process, carboxylic acid catabolic process, carboxylic acid biosynthetic process, collagen-containing extracellular matrix, blood microparticle, condensed chromosome kinetochore, arachidonic acid epoxygenase activity, arachidonic acid monooxygenase activity, and monooxygenase activity. In the KEGG pathway enrichment analysis, DEGs were enriched in arachidonic acid epoxygenase activity, arachidonic acid monooxygenase activity, and monooxygenase activity. By PPI network construction and analysis of hub genes, we selected the top 10 genes, including CDK1, CCNB2, CDC20, BUB1, BUB1B, CCNB1, NDC80, CENPF, MAD2L1, and NUF2. By using TCGA and THPA databases, we found five genes, CDK1, CDC20, CCNB1, CENPF, and MAD2L1, that were related to the early diagnosis, tumour stage, and poor outcomes of HBV-HCC. Conclusions. Five abnormally expressed hub genes of HBV-HCC are informative for early diagnosis, tumour stage determination, and poor outcome prediction.

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“…Other studies have also investigated the coordinated roles of miR‐28 and its host gene LPP in cell migration and adhesion, proliferation and apoptosis (Almeida et al, 2012; Yang et al, 2011). The MCM3AP‐AS1/miR‐28‐5p/CENPF axis accelerates breast cancer progression (Chen et al, 2020), and the miR‐28‐5p/CAMTA2 axis plays a critical role in human colon cancer (Luan et al, 2019). miR‐28‐5p, which activates mesenchymal stem cells (MSCs) through the PI3K/Akt signalling pathway (Xu et al, 2020), may become a new target for the treatment of multiple myeloma (Gao & Ma, 2019).…”

Section: Discussionmentioning

confidence: 99%

A nontoxic dose of chrysotile can malignantly transform Met‐5A cells, in which microRNA‐28 has inhibitory effects

Zhang

Yuan

Sun

et al. 2021

J of Applied Toxicology

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Chrysotile, which is classified as a class I carcinogen by the International Agency for Research on Cancer (IARC), has extensive application in the industry and can lead to lung or other cancers. However, whether chrysotile causes malignant mesothelioma and its molecular mechanism remain debatable. Thus, this study aimed to demonstrate the mesothelioma‐inducing potential of chrysotile at the mesothelial cellular level and the function of microRNA‐28 in malignantly transformed mesothelial MeT‐5A cells. MeT‐5A cells malignantly transformed by a nontoxic dose of chrysotile were named Asb‐T, and miR‐28 expression was downregulated in Asb‐T cells. Restoration of miR‐28 expression inhibited the proliferation, migration and invasion of Asb‐T cells. We verified that IMPDH is a putative target of miR‐28. The expression of IMPDH was significantly higher in Asb‐T MeT‐5A cells than in control cells, whereas the opposite trend was observed with miR‐28 overexpression. Additionally, inhibition of IMPDH had similar effects as miR‐28 overexpression. After miR‐28 was elevated or IMPDH was inhibited, Ras activation was reduced, and its downstream pathways (the Erk and Akt signalling pathways) were inhibited. Surprisingly, the content of miR‐28 in the blood of mesothelioma patients was higher than that in control subjects. Overall, nontoxic doses of chrysotile can cause malignant transformation of MeT‐5A cells. Moreover, miR‐28 inhibits the proliferation, migration and invasion of Asb‐T MeT‐5A cells, negatively regulates the expression of IMPDH through the Ras signalling pathway and may be an important therapeutic target.

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LncRNA MCM3AP-AS1 promotes breast cancer progression via modulating miR-28-5p/CENPF axis

Cited by 59 publications

References 30 publications

Overexpression of CENPF is associated with progression and poor prognosis of lung adenocarcinoma

Overexpression of CENPF is associated with progression and poor prognosis of lung adenocarcinoma

Identification of 5 Hub Genes Related to the Early Diagnosis, Tumour Stage, and Poor Outcomes of Hepatitis B Virus-Related Hepatocellular Carcinoma by Bioinformatics Analysis

A nontoxic dose of chrysotile can malignantly transform Met‐5A cells, in which microRNA‐28 has inhibitory effects

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