Evaluation of miR-21 Inhibition and its Impact on Cancer Susceptibility Candidate 2 Long Noncoding RNA in Colorectal Cancer Cell Line

Simonian, Miganoosh; Sharifi, Mohammadreza; Mosallaie, Meysam; Khosravi, Sharifeh; Avan, Amir; Bagheri, Hadi; Salehi, Roya

doi:10.4103/abr.abr_214_16

Cited by 12 publications

(9 citation statements)

References 42 publications

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“…22 In addition, CASC2 was downregulated in glioma tissues and cell lines to play a suppressor in a variety of human cancer cells. [22][23][24][25][26][27][28] Due to its wide arrange of functions of CASC2 in the tumorigenesis prompted us to ask whether CASC2 could be a tumor suppressor in PTC formation.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA cancer susceptibility candidate 2 suppresses papillary thyroid carcinoma growth by inactivating the AKT/ERK1/2 signaling pathway

Huang

Zhang

Chen

et al. 2019

J of Cellular Biochemistry

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Objectives: Cancer susceptibility candidate 2 (CASC2) and long noncoding RNA (lncRNA) have been identified as a tumor suppressor in colorectal, lung, renal, and stomach cancer as well as in patient gliomas, but the function of CASC2 in papillary thyroid carcinoma (PTC) is not yet clear. The present study aimed to explore the effects of CASC2 in PTC.Methods: The CASC2 expression was measured in PTC samples and normal tissues by using quantitative real-time polymerase chain reaction. The lentiviral vectors were used to establish CASC2 overexpression models in PTC cell lines to determine the effects of CASC2 on cell proliferation, apoptosis, migration, and invasion. A tumor xenograft animal model was used to examine the functions of overexpression CASC2. Results: CASC2 expression was significantly decreased in PTC tumor tissues than adjacent normal tissues. CASC2 downregulation in PTC tissues significantly correlated with the tumor size, the presence of multifocal lesions, and the advanced pathological stage. CASC2 overexpression suppressed the cell proliferation and promoted apoptosis in PTC cell lines and CASC2 overexpression resulted in the inactivation of protein kinase B (PKB/AKT) and extracellular signal-regulated kinases (ERK1/2). The regulatory effects of CASC2 on PTC cell biological behavior were further enhanced by mitogen-activated protein kinase kinase (MEK) inhibitor U0126 or AKT1/2/3 inhibitor MK-2206 2HCl. CASC2 overexpression suppressed tumor growth in PTC cells in xenograft mouse models. Conclusion: Our results indicated that CASC2 significantly suppressed tumorigenesis in PTC and CASC2 may serve as a novel prognostic marker or therapeutic target.

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Section: Introductionmentioning

confidence: 99%

Long noncoding RNA cancer susceptibility candidate 2 suppresses papillary thyroid carcinoma growth by inactivating the AKT/ERK1/2 signaling pathway

Huang

Zhang

Chen

et al. 2019

J of Cellular Biochemistry

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“…miRNAs are a kind of small non-coding RNAs, which regulate the expression of target genes through promoting the degradation of target mRNA, via incompletely binding with the 3′-UTR of target proteins or inducing translational repression 4,5. Substantial evidence demonstrates that dysregulation of miRNAs is associated with the development and metastasis of several cancers, and miRNAs might be the potential treatment targets in cancers 6–9.…”

Section: Introductionmentioning

confidence: 99%

<p>miRNA-101-5p inhibits the growth and aggressiveness of NSCLC cells through targeting CXCL6</p>

Chen¹,

Liú²,

Zhang³

et al. 2019

OTT

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BackgroundThe purpose of this study is to explore the potential biological roles of miR-101-5p in the progression of non-small-cell lung carcinoma (NSCLC).MethodsThe levels of miR-101-5p and chemokine (C-X-C motif) ligand 6 (CXCL6) in NSCLC tissues and cells were detected using the quantitative real-time PCR (qRT-PCR) assay. Proliferation, colony formation, migration and invasion assays were conducted using miR-101-5p-transfected NSCLC cells in vitro. The expression of CXCL6 was measured using immunofluorescence assay. Xenograft model and lung metastasis model were constructed to further reveal the precise roles of miR-101-5p in the lung metastasis and growth of NSCLC cells in vivo.ResultsmiR-101-5p was underregulated in NSCLC tissues when compared with that in the normal controls. The levels of miR-101-5p were lower in NSCLC cells (H1975, A549, HCC827 and H1650) than in non-tumorigenic human bronchial epithelial cells (BEAS-2B). Overregulation of miR-101-5p restrained the aggressiveness phenotypes of NSCLC cells in vitro. Furthermore, overregulation of miR-101-5p reduced the tumor growth and pulmonary metastasis of NSCLC cells in vivo. CXCL6 was the target gene of miR-101-5p in NSCLC. The mRNA levels of CXCL6 were negatively associated with the levels of miR-101-5p in NSCLC tissues. Finally, the rescue experiments suggested that the inhibitory role of miR-101-5p was mediated by regulating the expression of CXCL6 in NSCLC.ConclusionThese findings indicated that overregulation of miR-101-5p restrained the progression of NSCLC cells by targeting CXCL6 and might function as a potential therapeutic target for NSCLC.

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“…For the 5 identified lncRNA markers, CASC2 has been reported to be associated with colorectal cancer [33][34][35]. Studies have revealed that the deregulation of CASC2 by miRNA hsa-mir-21 and hsa-mir-18a increases the proliferation and migration of cancer cells in colorectal cancer [33][34][35].…”

Section: General Commentsmentioning

confidence: 99%

Integration analysis for novel lncRNA markers predicting tumor recurrence in human colon adenocarcinoma

Chen

Deng

et al. 2019

J Transl Med

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Background Numerous evidence has suggested that long non-coding RNA (lncRNA) acts an important role in tumor biology. This study focuses on the identification of novel prognostic lncRNA biomarkers predicting tumor recurrence in human colon adenocarcinoma. Methods We obtained the research data from The Cancer Genome Atlas (TCGA) database. The interaction among different expressed lncRNA, miRNA and mRNA markers between colon adenocarcinoma patients with and without tumor recurrence were verified with miRcode, starBase and miRTarBase databases. We established the lncRNA–miRNA–mRNA competing endogenous RNA (ceRNA) network based on the verified association between the selected markers. We performed the functional enrichment analysis to obtain better understanding of the selected lncRNAs. Then we use multivariate logistic regression to identify the prognostic lncRNA markers with covariates. We also generated a nomogram predicting tumor recurrence risk based on the identified lncRNA biomarkers and clinical covariates. Results We included 12,727 lncRNA, 1881 miRNA and 47,761 mRNA profiling and clinical features for 113 colon adenocarcinoma patients obtained from the TCGA database. After filtration, we used 37 specific lncRNAs, 60 miRNAs and 148 mRNAs in the ceRNA network analysis. We identified five lncRNAs as prognostic lncRNA markers predicting tumor recurrence in colon adenocarcinoma, in which four of them were identified for the first time. Finally, we generated a nomogram illustrating the association between the identified lncRNAs and the tumor recurrence risk in colon adenocarcinoma. Conclusions The four newly identified lncRNA biomarkers might be potential prognostic biomarkers predicting tumor recurrence in colon adenocarcinoma. We recommend that further clinical and fundamental researches be conducted on the identified lncRNA markers.

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Evaluation of miR-21 Inhibition and its Impact on Cancer Susceptibility Candidate 2 Long Noncoding RNA in Colorectal Cancer Cell Line

Cited by 12 publications

References 42 publications

Long noncoding RNA cancer susceptibility candidate 2 suppresses papillary thyroid carcinoma growth by inactivating the AKT/ERK1/2 signaling pathway

Long noncoding RNA cancer susceptibility candidate 2 suppresses papillary thyroid carcinoma growth by inactivating the AKT/ERK1/2 signaling pathway

<p>miRNA-101-5p inhibits the growth and aggressiveness of NSCLC cells through targeting CXCL6</p>

Integration analysis for novel lncRNA markers predicting tumor recurrence in human colon adenocarcinoma

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