RETRACTED: Silencing Long Non-coding RNA LINC01224 Inhibits Hepatocellular Carcinoma Progression via MicroRNA-330-5p-Induced Inhibition of CHEK1

Gong, Dan; Feng, Pengcheng; Ke, Xing-Fei; Kuang, Hui-Lan; Pan, Lili; Ye, Qiang; Jianbing, WU

doi:10.1016/j.omtn.2019.10.007

Cited by 67 publications

(72 citation statements)

References 34 publications

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“… 11 LINC01224 could up-regulate the expression of CHEK1 by competitively binding to miR-330-5p, thus promoting hepatocellular carcinoma development. 10 In the present study, similar to the previous studies, we found that the expression of LINC01224 was significantly increased in CRC tissues and cell lines. Moreover, in vitro analysis demonstrated that LINC01224 silence suppressed cell proliferation and invasion.…”

Section: Discussionsupporting

confidence: 92%

“…It was reported that LINC01224 promoted hepatocellular carcinoma progression through microRNA-330-5p-induced inhibition of CHEK1. 10 Moreover, Xing et al reported that LINC01224 exhibited cancer-promoting activity in EOC (epithelial ovarian cancer) through microRNA-485-5p-mediated PAK4 upregulation. 11 However, the biological function and underlying mechanism of LINC01224 in the development of human cancer, including CRC are still elusive.…”

Section: Introductionmentioning

confidence: 99%

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LINC01224 Promotes Colorectal Cancer Progression by Sponging miR-2467

Chen

Zhao

et al. 2021

CMAR

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Introduction Colorectal cancer (CRC) is one of the most common human cancers and a leading cause of cancer-related death. Accumulating evidence has confirmed that long non-coding RNA (lncRNA) plays crucial roles in CRC development. Methods qRT-PCR was performed to examine the expressions of LINC01224 and miR-2467. CCK-8 assay, colony formation assay and transwell invasion assay were used to examine the progression of breast cancer cells. Luciferase and RNA-binding protein immunoprecipitation (RIP) assay were applied to verify the binding site. Correlation analysis of miR-2467 and LINC01224 expression in lung cancer tissues was shown. Pancreatic cancer cells growth in vivo was evaluated using xenograft tumor assay. Results LINC01224 expression was observed to be up-regulated in CRC tissues and cell lines. Functional studies suggested that LINC01224 silence inhibited CRC cells proliferation and invasion of CRC cells, while co-transfection with a miR-2467 inhibitor reversed these biological effects. Luciferase reporter assays illustrated that LINC01224 regulated miR-2467 directly, and RNA-binding protein immunoprecipitation (RIP) further confirmed that the suppression of LINC01224 by miR-2467 was in an RISC-dependent manner. Finally, LINC01224 silence inhibited the growth CRC cells in vivo. Conclusion In conclusion, our findings showed that LINC01224 promoted CRC progression through sponging miR-2467. LINC01224 may serve as a potential diagnostic biomarker and therapeutic target for CRC patients.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

LINC01224 Promotes Colorectal Cancer Progression by Sponging miR-2467

Chen

Zhao

et al. 2021

CMAR

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“…Checkpoint kinase1 (CHEK1), one of the DNA-damage checkpoint proteins, was reported reducing the stem cell population in ovarian cancer, triggered by its inhibitor (LY2603618) [46]. In hepatocellular carcinoma (HCC), downregulation of CHEK1 by silencing LINC01224 or elevating miR-330-5p could inhibit stemness, by reducing the expression of CSC biomarkers (OCT4, CD133 and SOX2) [47]. The genes of CDC45, ESPL1, CCNA2, MCM6, and ORC1 have not been reported on the CSC issues in our survey.…”

Section: Discussionmentioning

confidence: 99%

mRNAsi Index: Machine Learning in Mining Lung Adenocarcinoma Stem Cell Biomarkers

Zhang

Tseng

Lien

et al. 2020

Genes

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Cancer stem cells (CSCs), characterized by self-renewal and unlimited proliferation, lead to therapeutic resistance in lung cancer. In this study, we aimed to investigate the expressions of stem cell-related genes in lung adenocarcinoma (LUAD). The stemness index based on mRNA expression (mRNAsi) was utilized to analyze LUAD cases in the Cancer Genome Atlas (TCGA). First, mRNAsi was analyzed with differential expressions, survival analysis, clinical stages, and gender in LUADs. Then, the weighted gene co-expression network analysis was performed to discover modules of stemness and key genes. The interplay among the key genes was explored at the transcription and protein levels. The enrichment analysis was performed to annotate the function and pathways of the key genes. The expression levels of key genes were validated in a pan-cancer scale. The pathological stage associated gene expression level and survival probability were also validated. The Gene Expression Omnibus (GEO) database was additionally used for validation. The mRNAsi was significantly upregulated in cancer cases. In general, the mRNAsi score increases according to clinical stages and differs in gender significantly. Lower mRNAsi groups had a better overall survival in major LUADs, within five years. The distinguished modules and key genes were selected according to the correlations to the mRNAsi. Thirteen key genes (CCNB1, BUB1, BUB1B, CDC20, PLK1, TTK, CDC45, ESPL1, CCNA2, MCM6, ORC1, MCM2, and CHEK1) were enriched from the cell cycle Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, relating to cell proliferation Gene Ontology (GO) terms, as well. Eight of the thirteen genes have been reported to be associated with the CSC characteristics. However, all of them have been previously ignored in LUADs. Their expression increased according to the pathological stages of LUAD, and these genes were clearly upregulated in pan-cancers. In the GEO database, only the tumor necrosis factor receptor associated factor-interacting protein (TRAIP) from the blue module was matched with the stemness microarray data. These key genes were found to have strong correlations as a whole, and could be used as therapeutic targets in the treatment of LUAD, by inhibiting the stemness features.

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“… [33] Gong et al found that LINC01224 regulated the expression levels of CHEK1 by competitively binding to miR-330-5p, thus inhibiting hepatocellular carcinoma progression. [34] LINC00668 is overexpressed in BC tissues and contributes to the progression of BC by accelerating cell cycle progression and inhibiting cell apoptosis. [35] In view of the outstanding performance of prognostic prediction, the roles of these lncRNAs in cancers should be investigated in the future, especially for BC.…”

Section: Discussionmentioning

confidence: 99%