Long Noncoding RNA LINC00265 Promotes Glycolysis and Lactate Production of Colorectal Cancer through Regulating of miR-216b-5p/TRIM44 Axis

Sun, Shangfeng; Li, Weiwei; Ma, Xiaomin; Luan, Hong

doi:10.1159/000500195

Cited by 36 publications

(30 citation statements)

References 21 publications

(21 reference statements)

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“…The luciferase reporter assay also demonstrated that TUG1 could directly bind to miR-216b-5p through a complementary sequence in HCC cells. Many studies have reported that miR-216b-5p was a tumor suppressor with low expression in many cancers [31]. For example, miR-216b-5p as a tumor-inhibiting factor to hinder proliferation by targeting TPT1 in pancreatic cancer cells [32].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

et al. 2020

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Background: Accumulating evidence indicates that the long noncoding RNA taurine upregulated gene 1(TUG1) plays a critical role in cancer progression and metastasis. However, the overall biological role and clinical significance of TUG1 in hepatocellular carcinoma (HCC) remain largely unknown. Methods:The expressions of TUG1, microRNA-216b-5p and distal-less homeobox 2 (DLX2) were detected by Quantitative real-time polymerase chain reaction (qRT-PCR). The target relationships were predicted by StarBase v.2.0 or TargetScan and confirmed by dual-luciferase reporter assay. The cell growth, apoptosis, migration and invasion were detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Flow cytometry and Transwell assays, respectively. All protein expression levels were detected by western blot. Tumor xenografts were implemented to explore the role of TUG1 in vivo. Results:We found that there was a marked rise in TUG1 expression in HCC tissues and cells, and knockdown of TUG1 repressed the growth and metastasis and promoted apoptosis of HCC cells. In particular, TUG1 could act as a ceRNA, effectively becoming a sink for miR-216b-5p to fortify the expression of DLX2. Additionally, repression of TUG1 impared the progression of HCC cells by inhibiting DLX2 expression via sponging miR-216b-5p in vitro. More importantly, TUG1 knockdown inhibited HCC tumor growth in vivo through upregulating miR-216b-5p via inactivation of the DLX2.Conclusion: TUG1 interacting with miR-216b-5p contributed to proliferation, metastasis, tumorigenesis and retarded apoptosis by activation of DLX2 in HCC.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

et al. 2020

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“…LINC00265 was upregulated in CRC both in vivo and in vitro, which intimately associated with poorer prognosis. LINC00265-de ciency resulted into decreases in cell viability, glucose uptake, pyruvate production, and lactate production through regulating of miR-216b-5p/TRIM44 Axis [16]. LINC00265 is upregulated and predicts poor clinical outcome in human patients with CRC.…”

Section: Discussionmentioning

confidence: 99%

“…AML patients with higher serum LINC00265 expression suffer poorer overall survival. LINC00265 contributes to AML migration and invasion via modulation of PI3K/AKT signaling [15,16].…”

mentioning

confidence: 99%

Long Noncoding RNA LINC00265 Promotes Proliferation of Gastric Cancer by Acting as A Competing Endogenous RNA on microRNA-144-3p Thereby Upregulating CBX4

Yang¹,

Ouyang²,

Zheng³

et al. 2020

Preprint

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Background:The expression levels and detailed functions of LINC00265 in gastric cancer (GC) have not yet been explored. This study aimed to measure LINC00265 expression in GC tissues and cell lines, investigate its specific roles in the aggressive characteristics of GC cells in vitro and in vivo, and elucidate the regulatory mechanisms of LINC00265 action.Materials and methods: The qRT-PCR was performed to test the RNA expression levels in GC tissues and cell lines. Cell proliferation was detected by CCK-8 and colony formation assays. Western blot assay was used to measure relevant protein expression. Luciferase reporter assays were performed to investigate the association between LINC00265 and microRNA-144-3p and CBX4.Results: LINC00265 expression was high in GC tissue samples and cell lines; LINC00265 overexpression correlated with shorter overall survival of the patients. A LINC00265 knockdown inhibited GC cell proliferation in vitro and slowed tumor growth in vivo. Mechanism investigation revealed that LINC00265 acts as a competing endogenous RNA on microRNA-144-3p (miR- 144) in GC cells. Chromobox 4 (CBX4) mRNA was identified as a direct target of miR-144-3p in GC cells. The knockdown of miR-144-3p counteracted the reduction in the malignant characteristics of GC cells by the downregulation of LINC00265.Conclusion: In conclusion, LINC00265 functions as a competing endogenous RNA targeting miR-144-3p and increases the malignancy of GC cells in vitro and in vivo by upregulating CBX4.

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“…miR-216b-5p is an anti-tumor miRNA found in several cancers. (He et al 2019;Ren et al 2019;Sun et al 2019b;You et al 2017) It is believed that miR-216b-5p inhibits HCV by suppressing host autophagy (Huang et al 2018). Paradoxically, miR-216b-5p represses the expression of UDP-glucuronosyltransferase 2B, a group of enzymes that detoxifies carcinogens by binding to their 3'UTRs.…”

Section: Discussionmentioning

confidence: 99%

Peer Review #1 of "Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma (v0.2)"

2019

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Background. Hepatocellular carcinoma (HCC) is one of the leading causes of cancerrelated deaths worldwide. Although multiple efforts have been made to understand the development of HCC, morbidity and mortality rates remain high. In this study, we aimed to discover the mRNAs and long non-coding RNAs (lncRNAs) that contribute to the progression of HCC. We constructed a lncRNA-related competitive endogenous RNA (ceRNA) network to elucidate the molecular regulatory mechanism underlying HCC. Methods. A microarray dataset (GSE54238) containing information about both mRNAs and lncRNAs was downloaded from the GEO database. Differentially expressed genes (DEGs) and lncRNAs (DElncRNAs) in tumor tissues and non-cancerous tissues were identified using the limma package of the R software. The miRNAs that are targeted by DElncRNAs were predicted using miRcode, while the target mRNAs of miRNAs were retrieved from miRDB, miRTarBas, and TargetScan. Functional annotation and pathway enrichment of DEGs were performed using the EnrichNet website. We constructed a protein-protein interaction (PPI) network of DEGs using STRING, and identified the hub genes using Cytoscape. Survival analysis of the hub genes and DElncRNAs was performed using the GEPIA database. The expression of molecules with prognostic values was validated on the UALCAN database. The hepatic expression of hub genes was examined using The Human Protein Atlas. The hub genes and DElncRNAs with prognostic values as well as the predictive miRNAs were selected to construct the ceRNA networks. Results. We found that 10 hub genes (KPNA2, MCM7, CKS2, KIF23, HMGB2, ZWINT, E2F1, MCM4, H2AFX, and EZH2) and four lncRNAs (FAM182B, SNHG6, SNHG1, and SNHG3) with prognostic values were overexpressed in the hepatic tumor samples. We also constructed a network containing 10 lncRNA-miRNA-mRNA pathways, which might be responsible for

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Long Noncoding RNA LINC00265 Promotes Glycolysis and Lactate Production of Colorectal Cancer through Regulating of miR-216b-5p/TRIM44 Axis

Cited by 36 publications

References 21 publications

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

Long non-coding RNA TUG1 promotes cell progression in hepatocellular carcinoma via regulating miR-216b-5p/DLX2 axis

Long Noncoding RNA LINC00265 Promotes Proliferation of Gastric Cancer by Acting as A Competing Endogenous RNA on microRNA-144-3p Thereby Upregulating CBX4

Peer Review #1 of "Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma (v0.2)"

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