Identification of key pathways and genes in the progression of cervical cancer using bioinformatics analysis

Abstract Cervical cancer is the third leading cause of cancer death among women in less-developed regions. Because of the poor survivorship of patients with advanced disease, finding new biomarkers for prognostic prediction is of great importance. In the current study, mRNA datasets (GSE9750 and GSE63514) were retrieved from Gene Expression Omnibus and was used to identify differentially expressed genes. The underlying molecular mechanisms associated with high-mobility group box 1 protein (HMGB1) were investigated using bioinformatics analysis. Immunohistochemical analysis of HMGB1 was performed on 239 cases of cervical cancer samples to investigate its possible correlation with clinicopathological characteristics and outcomes. A preliminary validation has been made to explore the possible correlation factors with HMGB1 that promote migration of cervical cancer cells. Bioinformatics analysis showed that adherens junction was significant for both P-value and enrichment scores, which was consistent with the clinical study. The underlying molecular mechanisms might be the interaction among HMGB1, RAC1, and CDC42. HMGB1 expression was significantly associated with tumor size, parametrial infiltration, the depth of cervical stromal invasion, and FIGO stage (P=0.003, 0.019, 0.013, and 0.003, respectively). FIGO stage, lymph mode metastasis, and HMGB1 expression were independent predictors of a poorer prognosis of patients with cervical cancer. Knockdown of HMGB1 inhibits migration of Siha and C33A cells in vitro. Western blot and quantitative real-time PCR (qRT-PCR) showed that the expression of RAC1 and CDC42 was positively correlated with HMGB1. HMGB1 is a useful prognostic indicator and a potential biomarker of cervical cancer. RAC1 and CDC42 may be involved in the progression of cervical cancer migration induced by HMGB1.

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LncRNA PVT1 promotes proliferation and invasion through enhancing Smad3 expression by sponging miR-140-5p in cervical cancer

Radiology and Oncology ◽

10.2478/raon-2019-0048 ◽

2019 ◽

Vol 53 (4) ◽

pp. 443-452 ◽

Cited By ~ 11

Author(s):

Qing-Qing Chang ◽

Chun-Yan Chen ◽

Zhao Chen ◽

Shuai Chang

Keyword(s):

Cervical Cancer ◽

Cancer Cells ◽

Bioinformatics Analysis ◽

Downstream Target ◽

Cervical Cancer Cells ◽

Proliferation And Metastasis ◽

Underlying Mechanisms ◽

Smad3 Expression ◽

Proliferation And Invasion ◽

Variant Translocation

Abstract Background Cervical cancer is one of the most frequent malignancies among females worldwide. Increasing evidence have indicated the participation of long noncoding RNAs (lncRNAs) in the progression and metastasis of cervical cancer. Our present study was conducted to explore the effects of lncRNA plasmacytoma variant translocation 1 (PVT1) on the progression of cervical cancer and the underlying mechanisms. Materials and methods Expressions of PVT1, miR-140-5p and Smad3 in cervical cancer cell lines were detected by qRT-PCR and western blotting. Bioinformatics analysis and luciferase assays were used to elucidate the potential correlations between PVT1, miR-140-5p and Smad3. The roles of PVT1 on the progression of cervical cancer cells were determined by transfecting sh-RNA through series function assays such as colony formation assay, wound healing assay, transwell assay. Results PVT1 and Smad3 were upregulated, and miR-140-5p was downregulated in cervical cancer cells. PVT1 could bind directly with miR-140-5p, and Smad3 was a downstream target of miR-140-5p. Inhibition of PVT1 could enhance expression of miR-140-5p, inhibit the expression of Smad3, significantly inhibited the proliferation, migration, invasion in cervical cancer cells. While transfection of miR-140-5p inhibitor could partially reverse the above changes in cervical cancer cells. Conclusions The results revealed that PVT1 could promote the proliferation and metastasis via increasing the Smad3 expression by sponging miR-140-5p, which might be a promising prognostic and therapeutic target for cervical cancer.

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The E545 Mutation of PIK3CA in Cervical Cancer Promotes the Survival by Several Different Pathways

10.21203/rs.3.rs-644504/v1 ◽

2021 ◽

Author(s):

Yan Chen ◽

Ma-Chi Yuan ◽

Jia-Zhen Shi ◽

Xia Zhao ◽

Nan He ◽

...

Keyword(s):

Cervical Cancer ◽

Differential Expression ◽

Bioinformatics Analysis ◽

Cancer Tissue ◽

Ppi Network ◽

Tissue Samples ◽

Cervical Cancer Tissue ◽

Differential Expression Genes ◽

High Degree

Abstract Backgroud: The E545 mutation of PIK3CA in Cervical cancer is frequently happened. But the role of E545 mutation of PIK3CA in Cervical cancer is not clear.Methods: In this study, we analysised the molecular signatures of E545 mutation Cervical cancer by bioinformatics methods.Results: We collected transcriptome sequencing results of 227 no mutation cervical cancer tissue samples and 36 mutation cervical cancer tissue samples, then analyzed the data combining bioinformatics methods. A total of 5 differential expression miRNAs were obtained, including 3 up-regulated miRNAs, 1 down-rugulated miRNA. A total of 174 differential expression genes were obtained, including 132 up-regulated genes, 40 down-rugulated genes. GO analysis suggested that the up-regulated DEGs were mainly enriched in transcription factor activity, leukotriene signaling pathway and so on. Besides, we constructed a PPI network with DEGs to screen the top hub genes with a relatively high degree of connectivity. Among them CAV1, KRT20, FOS, had a degree of connectivity larger than 5 and functioned as hub module genes to promote the survival of E545 mutation cervical cancer. We also identified different miRNA-DEG axis, including hsa-mir-449a-AXL, hsa-mir-508-CGA, COL15A1, NNMT, hsa-mir-552-CHST6, NWD1. These axis regulated the survival of E545 mutation cervical cancer togetherly. Conclusions: In conclusion, this study identified DEGs and screened the key genes and pathways closely related to E545 mutation in Cervical cancer by bioinformatics analysis, These results might hold promise for finding potential therapeutic targets of cervical cancer harboring E545 mutation of PI3KCA.

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Bioinformatics analysis shows that TOP2A functions as a key candidate gene in the progression of cervical cancer

Biomedical Reports ◽

10.3892/br.2020.1328 ◽

2020 ◽

Cited By ~ 1

Author(s):

Qinfei Zhao ◽

Huaying Li ◽

Longyu Zhu ◽

Suping Hu ◽

Xuxiang Xi ◽

...

Keyword(s):

Cervical Cancer ◽

Candidate Gene ◽

Bioinformatics Analysis

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Identification of key pathways and genes in colorectal cancer using bioinformatics analysis

Medical Oncology ◽

10.1007/s12032-016-0829-6 ◽

2016 ◽

Vol 33 (10) ◽

Cited By ~ 55

Author(s):

Bin Liang ◽

Chunning Li ◽

Jianying Zhao

Keyword(s):

Colorectal Cancer ◽

Bioinformatics Analysis ◽

Key Pathways

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The Cytotoxicity Mechanism of 6-Shogaol-Treated HeLa Human Cervical Cancer Cells Revealed by Label-Free Shotgun Proteomics and Bioinformatics Analysis

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2012/278652 ◽

2012 ◽

Vol 2012 ◽

pp. 1-12 ◽

Cited By ~ 12

Author(s):

Qun Liu ◽

Yong-Bo Peng ◽

Lian-Wen Qi ◽

Xiao-Lan Cheng ◽

Xiao-Jun Xu ◽

...

Keyword(s):

Cervical Cancer ◽

Pathway Analysis ◽

Hela Cells ◽

Bioinformatics Analysis ◽

Zingiber Officinale ◽

Shotgun Proteomics ◽

Analysis Data ◽

Label Free ◽

M Cell ◽

Human Cervical Cancer

Cervical cancer is one of the most common cancers among women in the world. 6-Shogaol is a natural compound isolated from the rhizome of ginger (Zingiber officinale). In this paper, we demonstrated that 6-shogaol induced apoptosis and G2/M phase arrest in human cervical cancer HeLa cells. Endoplasmic reticulum stress and mitochondrial pathway were involved in 6-shogaol-mediated apoptosis. Proteomic analysis based on label-free strategy by liquid chromatography chip quadrupole time-of-flight mass spectrometry was subsequently proposed to identify, in a non-target-biased manner, the molecular changes in cellular proteins in response to 6-shogaol treatment. A total of 287 proteins were differentially expressed in response to 24 h treatment with 15μM 6-shogaol in HeLa cells. Significantly changed proteins were subjected to functional pathway analysis by multiple analyzing software. Ingenuity pathway analysis (IPA) suggested that 14-3-3 signaling is a predominant canonical pathway involved in networks which may be significantly associated with the process of apoptosis and G2/M cell cycle arrest induced by 6-shogaol. In conclusion, this work developed an unbiased protein analysis strategy by shotgun proteomics and bioinformatics analysis. Data observed provide a comprehensive analysis of the 6-shogaol-treated HeLa cell proteome and reveal protein alterations that are associated with its anticancer mechanism.

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