LncRNA <i>TINCR</i>/microRNA-107/CD36 regulates cell proliferation and apoptosis in colorectal cancer via PPAR signaling pathway based on bioinformatics analysis

Zhang, Xuexiu; Yao, Jianning; Shi, Haoling; Gao, Bing; Zhang, Lianfeng

doi:10.1515/hsz-2018-0236

Cited by 86 publications

(60 citation statements)

References 38 publications

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“…Down-regulation of PPAR-α has been correlated with poor clinicopathological features of CRC that was remarkably higher in well to moderately differentiated adenocarcinoma than in mucinous adenocarcinoma [32]. In addition, lncRNA TINCR modulates PPAR signaling pathway through binding to miR-107 to up-regulate CD36 in CRC [33]. Recently, the PPAR aberration expression and its prime [34].…”

Section: Discussionmentioning

confidence: 99%

Integration analysis of long non-coding RNA (lncRNA) role in tumorigenesis of colon adenocarcinoma

et al. 2020

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Background: Colon adenocarcinoma (COAD) is one of the most common gastrointestinal cancers globally. Molecular aberrations of tumor suppressors and/or oncogenes are the main contributors to tumorigenesis. However, the exact underlying mechanisms of COAD pathogenesis are clearly not known yet. In this regard, there is an urgent need to indicate promising potential diagnostic and prognostic biomarkers in COAD patients. Methods: In the current study, level 3 RNA-Seq and miR-Seq data and corresponding clinical data of colon adenocarcinoma (COAD) were retrieved from the TCGA database. The "limma" package in R software was utilized to indicate the differentially expressed genes. For in silico functional analysis, GO and KEGG signaling pathways were conducted. PPI network was constructed based on the STRING online database by Cytoscape 3.7.2. A ceRNA network was also constructed by "GDCRNATools" package in R software. Kaplan-Meier survival analysis (log-rank test) and ROC curve analysis were used to indicate the diagnostic and prognostic values of the biomarkers. Results: The differential expression data demonstrated that 2995 mRNAs, 205 lncRNAs, and 345 miRNAs were differentially expressed in COAD. The GO and KEGG pathway analysis indicated that the differentially expressed mRNAs were primarily enriched in canonical processes in cancer. The PPI network showed that the CDKN2A, CCND1, MYC, E2F, CDK4, BRCA2, CDC25B, and CDKN1A proteins were the critical hubs. In addition, the Kaplan-Meier analysis revealed that 215 mRNAs, 14 lncRNAs, and 39 miRNAs were associated with overall survival time in the patients. Also, the ceRNA network data demonstrated that three lncRNAs including MIR17HG, H19, SNHG1, KCNQ1OT1, MALAT1, GAS5, SNHG20, OR2A1-AS1, and MAGI2-AS3 genes were involved in the development of COAD. Conclusions: Our data suggested several promising lncRNAs in the diagnosis and prognosis of patients with COAD.

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Section: Discussionmentioning

confidence: 99%

Integration analysis of long non-coding RNA (lncRNA) role in tumorigenesis of colon adenocarcinoma

et al. 2020

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“…Knockdown of ZFAS1 can block the cell cycle of colorectal cancer cells in the G1 phase, thereby inhibiting the proliferation of colon cancer cells [10,11]. LncRNA TINCR is downregulated in colorectal cancer, and overexpression of TINCR can inhibit the metastasis and proliferation of cancer cells [12]. LncRNA DQ786243 has been shown to regulate the proliferation and apoptosis of colon cancer cells in vitro and in vivo [13].…”

Section: Introductionmentioning

confidence: 99%

LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p

Zhang

Gao

2020

BioMed Research International

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Cervical cancer is one of the malignant tumors that seriously threaten women’s health. The mechanism of development needs to be deeply studied. In recent years, lncRNA has been identified as one of the important factors affecting the malignant progression of tumors. In this study, we illustrated the important mechanism of lncRNA CAR10 in the development of cervical cancer. We found that CAR10 is significantly increased in4 cervical cancer tissues and cells, which can promote the proliferation of cervical cancer cells in vitro and in vivo, indicating that CAR10 is involved in the progression of cervical cancer as an oncogene. Further studies showed that CAR10 is a target gene of miR-125b-5p, and miR-125b-5p can inhibit the effect of CAR10 on the proliferation of cervical cancer cells. In addition, we also found that 3-phosphoinositide-dependent protein kinase 1 (PDPK1) is also a target gene of miR-125b-5p, and CAR10 can upregulate the expression level of PDPK1. The results showed that CAR10 acts as a ceRNA to upregulate the expression of PDPK1 by sponging miR-125b-5p. Knockdown of PDPK1 can inhibit the effect of CAR10 on cervical cancer cells. Our study demonstrates that, based on ceRNA mechanism, CAR10/miR-125b-5p/PDPK1 network can regulate the proliferation of cervical cancer cells and play an important role in the development of cervical cancer. In addition, our study also suggests that intervention of CAR10/miR-125b-5p/PDPK1 network may be a new strategy for targeted therapy of cervical cancer.

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“…The PPAR signaling pathway has been reported to be involved in a variety of cancers, but its speci c function is unclear 19 . Some researchers believe that PPAR pathway activation could promote the initiation or development of tumors, while others hold the opposite opinion 20 . Arginine and proline are two important nonessential amino acids, and their synthesis could promote tumor growth 21 .…”

Section: Discussionmentioning

confidence: 99%

Identification of aberrantly methylated-differentially expressed genes and potential agents for Ewing’s sarcoma

Gao

et al. 2020

Preprint

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Background DNA methylation is a common epigenetic regulatory way, and it plays a critical role in various human diseases. However, the potential role of how DNA methylation impacts Ewing’s sarcoma (ES) is not clear. This study aimed to explore the regulatory role of DNA methylation in ES. Methods The microarray data of gene expression and methylation were downloaded from Gene Expression Omnibus (GEO) database, and analyzed via GEO2R. Venn analysis was then applied to identify aberrantly methylated differentially expressed genes (DEGs). Subsequently, Function and pathway enrichment analysis was conducted. Protein-protein interaction (PPI) network was constructed. Hub genes were determined. Besides, a connectivity map (CMap) analysis was performed to screen bioactive compounds for ES treatment. Results A total of 135 hypomethylated high expression genes and 523 hypermethylated low expression genes were identified. The hypomethylated high expression genes were enriched in signal transduction and the apoptosis process. Meanwhile, hypermethylated low expression genes were related to DNA replication and transcription regulation. We next determined 10 hub genes through PPI analysis, among them, C3, TF, and TCEB1 might serve as diagnostic and therapeutic targets. Furthermore, CMap analysis revealed 6 chemicals as potential options for ES treatment. Conclusions For the first time, we jointly analyzed gene profiling and methylation data about ES. The introduction of DNA methylation characteristics over DEGs is helpful to understand the pathogenesis of ES. The identified hub aberrantly methylated DEGs and chemicals might provide some novel insights on ES treatment.

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LncRNA TINCR/microRNA-107/CD36 regulates cell proliferation and apoptosis in colorectal cancer via PPAR signaling pathway based on bioinformatics analysis

Cited by 86 publications

References 38 publications

Integration analysis of long non-coding RNA (lncRNA) role in tumorigenesis of colon adenocarcinoma

Integration analysis of long non-coding RNA (lncRNA) role in tumorigenesis of colon adenocarcinoma

LncRNA CAR10 Upregulates PDPK1 to Promote Cervical Cancer Development by Sponging miR-125b-5p

Identification of aberrantly methylated-differentially expressed genes and potential agents for Ewing’s sarcoma

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