MCM5 Expression Is Associated With the Grade of Malignancy and Ki-67 Antigen in LSCC

Nowińska, Katarzyna; Ciesielska, Urszula; Piotrowska, Aleksandra; Jabłońska, Karolina; Partyńska, Aleksandra; Paprocka, Maria; Zatoński, Tomasz; Podhorska-Okołów, Marzena; Dzięgiel, Piotr

doi:10.21873/anticanres.13349

Cited by 19 publications

(16 citation statements)

References 29 publications

(73 reference statements)

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“…The coexpressed genes of MCM2/3/4/5/6/7/8 (top 25 correlated genes) were screened, and the results of intersection analysis are shown in Table 2 . A total of 9 intersections and 16 key coexpressed genes ( MCM5 [ 33 ], CHAF1B , MCM2 , GINS2 , MCM6 , RFC5 , FANCC , TIMELESS , CLSPN , BRIP1 , RBL1 , CDT1 , RFC2 , CDC45 , ORC1 , and TOP2A ) were obtained for further study.…”

Section: Resultsmentioning

confidence: 99%

Bioinformatics analysis of the transcriptional expression of minichromosome maintenance proteins as potential indicators of survival in patients with cervical cancer

2021

BMC Cancer

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Background As major regulators of DNA replication in eukaryotes, minichromosome maintenance (MCM) proteins play an important role in the initiation and extension of DNA replication. MCMs and their related genes may be new markers of cell proliferation activity, which is of great significance for the diagnosis and prognosis of cervical cancer. Methods To explore the role of MCMs and their related genes in cervical cancer, various bioinformatics methods were performed. First, the ONCOMINE and UALCAN databases were used to analyze the mRNA expression of different MCMs. The Human Protein Atlas database was used to analyze the protein expression of MCMs in normal and tumor tissues. The potential clinical value of MCMs was evaluated using the UALCAN, Kaplan-Meier plotter and cBioPortal databases. Then, the related genes and key coexpressed genes of MCMs were screened using GEPIA2 and cBioPortal analysis. For these genes, we used Metascape and the DAVID database to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, construct the related molecular interaction network, and obtain the key subnetworks and related hub genes. The Kaplan-Meier plotter database was used for survival analysis of cervical cancer patients to evaluate and predict the potential clinical value of the hub genes. Moreover, multiple gene comparisons of the expression of MCMs and related genes in different cancer types also showed the clinical significance of these potential targets. Results The mRNA and protein expression of MCMs increased in tumor tissue. Overexpression of MCM2/3/4/5/6/7/8/10 was found to be significantly associated with clinical cancer stage. Higher mRNA expression levels of MCM3/5/6/7/8 were found to be significantly associated with longer overall survival, and higher mRNA expression of MCM2/3/4/5/6/7/8 was associated with favorable OS. In addition, a high mutation rate of MCMs (71%) was observed. MCM2, MCM4, MCM8, MCM3 and MCM7 were the five genes with the most genetic alterations. In addition, the coexpressed genes and related genes of MCMs were successfully screened for enrichment analysis. These genes were significantly enriched in important pathways, such as the DNA replication, cell cycle, mismatch repair, spliceosome, and Fanconi anemia pathways. A protein-protein interaction network was successfully constructed, and a total of 13 hub genes (CDC45, ORC1, RPA1, CDT1, TARDBP, RBMX, SRSF3, SRSF1, RFC5, RFC2, MSH6, DTL, and MSH2) from 4 key subnetworks were obtained. These genes and MCM2/3/4/5/6/7/8 might have potential clinical value for the survival and prognosis of cervical cancer patients. Conclusions These findings promoted the understanding of the MCM protein family and clinically related molecular targets for cervical epithelial neoplasia and cervical cancer. Our results were helpful to evaluate the potential clinical value of MCMs and related genes in patients with cervical cancer.

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Section: Resultsmentioning

confidence: 99%

Bioinformatics analysis of the transcriptional expression of minichromosome maintenance proteins as potential indicators of survival in patients with cervical cancer

2021

BMC Cancer

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“…qRT-PCR was used to validate the expressions of survival-associated lncRNAs and hub mRNAs resulting from WGCNA analysis, including 8 lncRNAs (CYTOR, MIR4435-2HG, RP1-137D17.2, RP11-247A12.2, RP11-646E18.4, RP11-661A12.4, RP11-661A12.5, and RP11-977B10.2) and 12 hub mRNAs (IFIT2, XAF1, UBE2L6, IFITM3, HLA-C, CTSL, ARHGDIB, LGALS3BP, IFITM1, MLKL, SERPING1, TRIM21) in cultured LC cells (Hep-2 and TU177) and one control cell (HaCaT keratinocytes) (Figure 9) [23]. The results indicated significant difference for five survival-associated lncRNAs (CYTOR, MIR4435-2HG, RP11-247A12.2, RP11-661A12.4, and RP11-661A12.5) (Figure 9A), and eight hub mRNAs (CTSL, XAF1, ARHGDIB, LGALS3BP, IFITM1, MLKL, SERPING1, and TRIM21) (Figure 9B) between LC cells and control cells.…”

Section: Resultsmentioning

confidence: 99%

“…Hep-2 cells were cultured in EMEM medium, TU177 cells were cultured in 1640 medium, and HaCaT cells were in DMEM medium (Corning, NY, USA) supplemented with 10% fetal bovine serum (FBS, Gibco). All these cells were maintained with 5% CO2 atmosphere at 37°C [23].…”

Section: Methodsmentioning

confidence: 99%

Characterization of long non-coding RNA and messenger RNA profiles in laryngeal cancer by weighted gene co-expression network analysis

Liu

Sun

Tian

et al. 2019

Aging

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Laryngeal cancer (LC) is a malignant tumor in the head and neck region. It was recently elucidated that long noncoding RNAs (lncRNAs) participate in the pathogenesis of LC. However, the detailed mechanism of lncRNA in LC and whether long non-coding RNAs serve as effective biomarkers remains unclear. Ribonucleic acid (RNA) sequence data of LC and 11 patient clinical traits were extracted from The Cancer Genome Atlas (TCGA) database and analyzed by weighted gene co-expression network analysis (WGCNA). A total of 9 co-expression modules were identified. The co-expression Pink module significantly correlated with four clinical traits, including history of smoking, lymph node count, tumor status, and the success of follow-up treatment. Based on the co-expression Pink module, lncRNA-microRNA (miRNA)-messenger RNA (mRNA) and lncRNA-RNA binding protein-mRNA networks were constructed. We found that 8 lncRNAs significantly impacted overall survival (OS) in LC patients. These identified lncRNA and hub gene biomarkers were also validated in multiple LC cells in vitro via qPCR. Taken together, this study provided the framework of co-expression gene modules of LC and identified some important biomarkers in LC development and disease progression.

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“…LSCC cell lines TU-177 and AMC-HN-8 and the normal human keratinocyte cell line HaCaT were purchased from the American Type Culture Collection. HaCaT cells are immortalized human epidermal cells that has been previously used as the control cell line for laryngeal squamous cell carcinoma cells (18,19). The LSCC cell line TU686 was purchased from the Cell Center of Life Science of Chinese Academy of Science.…”

Section: Methodsmentioning

confidence: 99%

Long non‑coding RNA MIAT promotes the proliferation and invasion of laryngeal squamous cell carcinoma cells by sponging microRNA‑613

Song¹,

Yang²,

Liu³

2021

Exp Ther Med

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Accumulating evidence indicates that the long non-coding RNA myocardial infarction associated transcript (lncRNA MIAT) serves an important role in the progression of a number of cancer types. However, the precise molecular mechanism of MIAT in laryngeal squamous cell carcinoma (LSCC) progression remain elusive. The aim of the current study was to assess the effects and to clarify the molecular mechanism of MIAT on the proliferation and invasion of LSCC cells. The expression of MIAT was detected in LSCC tissues and cells using reverse transcription-quantitative PCR. MTT and colony formation assays were performed to examine the effects of MIAT on the proliferation of LSCC cells. Additionally, wound healing and Transwell experiments were employed to examine cellular migration and invasion. Luciferase reporter gene assay was also used to confirm the direct binding between MIAT and microRNA (miR)-613 in LSCC cells. An RNA immunoprecipitation assay was performed to verify the interaction between MIAT and miR-613. In the present study, it was found that the expression of MIAT in LSCC tissues was markedly higher compared with that in adjacent non-tumor tissues. In addition, MIAT expression was also increased in the human LSCC cell lines TU686, TU-177 and AMC-HN-8 compared with that in normal human keratinocytes (HaCaT). Knocking down MIAT expression significantly reduced LSCC cell proliferation and inhibited colony formation, a shown by MTT and colony formation assays, respectively. MIAT knockdown also substantially inhibited the migratory and invasive abilities of LSCC cells, as shown by wound healing and Transwell invasion assays, respectively. Subsequently, luciferase reporter assays verified that MIAT could bind to miR-613, where a negative correlation was observed between the expression of MIAT and miR-613 in LSCC tissues. Suppression of miR-613 partially reversed the inhibitory effects of MIAT knockdown on the proliferation, migration and invasion of LSCC cells. Taken together, the present study identified that MIAT may function as an oncogenic lncRNA to promote LSCC progression, which provides a potential therapeutic target or as a novel diagnostic biomarker for LSCC.

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MCM5 Expression Is Associated With the Grade of Malignancy and Ki-67 Antigen in LSCC

Cited by 19 publications

References 29 publications

Bioinformatics analysis of the transcriptional expression of minichromosome maintenance proteins as potential indicators of survival in patients with cervical cancer

Bioinformatics analysis of the transcriptional expression of minichromosome maintenance proteins as potential indicators of survival in patients with cervical cancer

Characterization of long non-coding RNA and messenger RNA profiles in laryngeal cancer by weighted gene co-expression network analysis

Long non‑coding RNA MIAT promotes the proliferation and invasion of laryngeal squamous cell carcinoma cells by sponging microRNA‑613

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