LINC00052 Promotes Gastric Cancer Cell Proliferation and Metastasis via Activating the Wnt/β-Catenin Signaling Pathway

Shan, Yuqiang; Ying, Rongchao; Zhong, Jia; Kong, Wencheng; Wu, Yi; Zheng, Shuier; Jin, Huicheng

doi:10.3727/096504017x14897896412027

Cited by 48 publications

(46 citation statements)

References 29 publications

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“…Previous studies have shown that LINC00052 suppressed the metastasis of HCC cells by upregulating EPB41L3 by means of binding miR-452-5p 9 and regulated NTRK3 expression to facilitated HCC cell metastasis via miR-485-3p and miR-128. 8 In breast cancer, LINC00052 promoted tumor growth by interplay with receptor tyrosine-protein kinase erbB-3 (HER3), 12 in gastric cancer, LINC00052 promoted cell proliferation and metastasis by activating the Wnt-β-catenin signaling pathway. 11 Nevertheless, what LINC00052 work in CRC had not been explored and what are the biological characteristic and mechanism of LINC00052 in CRC?…”

Section: Discussionmentioning

confidence: 99%

Retracted: Long noncoding RNA LINC00052 inhibits colorectal cancer metastasis by sponging microRNA‐574‐5p to modulate CALCOCO1 expression

Xiong

Liu

et al. 2019

J of Cellular Biochemistry

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The dysregulation of long‐chain noncoding ribonucleic acid (lncRNA) is a common phenomenon in many human cancers. Some studies on the biological function of long intergenic non‐protein‐coding RNA 52 (LINC00052) in cancer indicate that this gene can act as either oncogene or tumor suppressor in some kinds of cancers, such as breast cancer, gastric cancer, liver cancer, and lung cancer. However, the biological function of LINC00052 in colorectal cancer (CRC) has not been studied. Quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR) and Western blot (WB) techniques were applied to detect the expression levels of LINC00052, miR‐574‐5p, and calcium‐binding and coiled‐coil domain 1 (CALCOCO1) in CRC cells and tissues. We authenticated the biological function of LINC00052 and miR‐574‐5p in CRC, and find some target genes for LINC00052 and miR‐574‐5p via bioinformatics methods. Dual‐luciferase reporter gene assay was performed to identify the interaction between LINC00052 and miR‐574‐5p or CALCOCO1 and miR‐574‐5p. The results demonstrated that LINC00052 was downregulated in CRC tissues compared with their adjacent tissues. And LINC00052 could suppress CRC cells metastasis both in vivo and in vitro. Beyond that, miR‐574‐5p was upregulated in CRC tissues, and as an oncogene, it accelerated CRC cell migration and invasion. More importantly, the results of our research demonstrated that LINC00052 could regulate the expression of CALCOCO1 via sponging miR‐574‐5p in CRC. Overall, our study illuminated the lncRNA‐miRNA functional networks in CRC, and these results might provide a new research direction for the diagnosis and treatment of CRC.

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Section: Discussionmentioning

confidence: 99%

Retracted: Long noncoding RNA LINC00052 inhibits colorectal cancer metastasis by sponging microRNA‐574‐5p to modulate CALCOCO1 expression

Xiong

Liu

et al. 2019

J of Cellular Biochemistry

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“…It is well-documented that WNT/β-catenin pathway involves in a wide variety of cellular processes, such as cell growth, cell cycle, differentiation, tumorigenesis and chemoresistance (10,13,26,27). Recent evidence has showed that WNT/β-catenin pathway serves as a good biomolecular target for GC treatment (28).…”

Section: Discussionmentioning

confidence: 99%

Caveolin-1 Promotes Chemoresistance of Gastric Cancer Cells to Cisplatin by Activating WNT/β-Catenin Pathway

et al. 2020

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Drug resistance is a major challenge for chemotherapy in treating human gastric cancer (GC), as the underlying molecular mechanism of chemoresistance in GC remains unknown. Caveolin-1 (Cav-1) is a scaffold protein of plasma membrane caveolae that acts as a tumor modulator by interacting with several cell signals. In this research, we showed that the survival rate of GC cells to cisplatin (CDDP) increased in the presence of Cav-1. Moreover, Cav-1 overexpression inhibited cisplatin-induced apoptosis and improved the survival rate of GC cells. Cav-1 overexpression and knock-down experiments indicated that Cav-1 expression stimulated wingless-type MMTV integration site (WNTs) pathway through the phosphorylation of LRP6 and dephosphorylation of β-catenin. Cav-1 was positively associated with the increase of WNT downstream target gene Met, which led to the activation of HER2 signaling. Moreover, our results demonstrated that the expression of Cav-1 and Met were positively associated with the resistance of GC cells to cisplatin. Collectively, Cav-1 enhances the cisplatin-resistance of GC cells by activating the WNT signaling pathway and Met-HER2 crosstalk. Understanding the role of Cav-1 in the chemoresistance of GC would help to develop novel therapies for a better treatment outcome of GC patients.

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“…The function of LINC00052 varies depending on the location of tumors. It acts as a tumor suppressor through inhibiting cell proliferation, invasion and migration in hepatocellular carcinoma (Xiong et al 2016;Yan et al 2018;Zhu et al 2017), whereas it could promote breast cancer growth (Salameh et al 2017) and gastric cell metastasis and proliferation (Shan et al 2017).…”

Section: Discussionmentioning

confidence: 99%

Peer Review #2 of "Comprehensive analysis of lncRNA-associated competing endogenous RNA network in tongue squamous cell carcinoma (v0.2)"

2019

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Background. Increasing evidence has demonstrated that long non-coding RNAs (lncRNAs) play an important role in the competitive endogenous RNA (ceRNA) networks in that they regulate protein-coding gene expression by sponging microRNAs (miRNAs). However, the understanding of the ceRNA network in tongue squamous cell carcinoma (TSCC) remains limited. Methods. Expression profile data regarding mRNAs, miRNAs and lncRNAs as well as clinical information on 122 TSCC tissues and 15 normal controls from The Cancer Genome Atlas (TCGA) database were collected. We used the edgR package to identify differentially expressed mRNAs (DEmRNAs), lncRNAs (DElncRNAs) and miRNAs (DEmiRNAs) between TSCC samples and normal samples. In order to explore the functions of DEmRNAs, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed. Subsequently, a ceRNA network was established based on the identified DElncRNAs-DEmiRNAs and DEmiRNAs-DEmRNAs interactions. The RNAs within the ceRNA network were analyzed for their correlation with overall disease survival. Finally, lncRNAs were specifically analyzed for their correlation with clinical features in the included TSCC patient samples. Results. A total of 1867 mRNAs, 828 lncRNAs and 81 miRNAs were identified as differentially expressed in TSCC tissues (|log 2 fold change| ≥ 2; adjusted P value < 0.01). The resulting ceRNA network included 16 mRNAs, 56 lncRNAs and 6 miRNAs. Six out of the 56 lncRNAs were found to be associated with the overall survival in TSCC patients (P < 0.05); 10 lncRNAs were correlated with TSCC progression (P < 0.05). Conclusion. Our study deepens the understanding of ceRNA network regulatory mechanisms in TSCC. Furthermore, we identified ten lncRNAs (PART1, LINC00261, AL163952.1, C2orf48, FAM87A, LINC00052, LINC00472, STEAP3-AS1, TSPEAR-AS1 and ERVH48-1) as novel, potential prognostic biomarkers and therapeutic targets for TSCC.

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LINC00052 Promotes Gastric Cancer Cell Proliferation and Metastasis via Activating the Wnt/β-Catenin Signaling Pathway

Cited by 48 publications

References 29 publications

Retracted: Long noncoding RNA LINC00052 inhibits colorectal cancer metastasis by sponging microRNA‐574‐5p to modulate CALCOCO1 expression

Retracted: Long noncoding RNA LINC00052 inhibits colorectal cancer metastasis by sponging microRNA‐574‐5p to modulate CALCOCO1 expression

Caveolin-1 Promotes Chemoresistance of Gastric Cancer Cells to Cisplatin by Activating WNT/β-Catenin Pathway

Peer Review #2 of "Comprehensive analysis of lncRNA-associated competing endogenous RNA network in tongue squamous cell carcinoma (v0.2)"

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