The Effect and Mechanism of LINC00663 on the Biological Behavior of Glioma

Pan, Meichen; Shi, Jingren; Yin, Shangqi; Meng, Huan; He, Chaonan; Wang, Yajie

doi:10.1007/s11064-021-03311-3

Cited by 7 publications

(4 citation statements)

References 30 publications

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“…As expected, our data revelated that LINC00663 was overexpressed in activated LX-2 cells, and overexpression of LINC00663 accelerated the progression of HF through sponging miR-3916 to upregulate SF2-FN expression. In addition, previous studies confirmed that LINC00663 promoted the migration abilities of cells by regulating the AKT/mTOR pathway [38]. This is consistent with our study that LINC00663 overexpression can promote the migration of LX-2 cells.…”

Section: Discussionsupporting

confidence: 93%

The Fibrotic Effects of LINC00663 in Human Hepatic Stellate LX-2 Cells and in Bile Duct-Ligated Cholestasis Mice Are Mediated through the Splicing Factor 2-Fibronectin

Chu

Bao

Teng

et al. 2023

Cells

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Hepatic fibrosis can develop into cirrhosis or even cancer without active therapy at an early stage. Long non-coding RNAs (lncRNAs) have been shown to be involved in the regulation of a wide variety of important biological processes. However, lncRNA mechanism(s) involved in cholestatic liver fibrosis remain unclear. RNA sequence data of hepatic stellate cells from bile duct ligation (BDL) mice or controls were analyzed by weighted gene co-expression network analysis (WGCNA). Based on WGCNA analysis, a competing endogenous RNA network was constructed. We identified LINC00663 and evaluated its function using a panel of assays, including a wound healing assay, a dual-luciferase reporter assay, RNA binding protein immunoprecipitation and chromatin immunoprecipitation. Functional research showed that LINC00663 promoted the activation, migration and epithelial–mesenchymal transition (EMT) of LX-2 cells and liver fibrosis in BDL mice. Mechanistically, LINC00663 regulated splicing factor 2 (SF2)-fibronectin (FN) alternative splicing through the sponging of hsa-miR-3916. Moreover, forkhead box A1 (FOXA1) specifically interacted with the promoter of LINC00663. In summary, we elaborated the fibrotic effects of LINC00663 in human hepatic stellate LX-2 cells and in bile duct-ligated cholestasis mice. We established a FOXA1/LINC00663/hsa-miR-3916/SF2-FN axis that provided a potential target for the diagnosis and targeted therapy of cholestatic liver fibrosis.

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Section: Discussionsupporting

confidence: 93%

The Fibrotic Effects of LINC00663 in Human Hepatic Stellate LX-2 Cells and in Bile Duct-Ligated Cholestasis Mice Are Mediated through the Splicing Factor 2-Fibronectin

Chu

Bao

Teng

et al. 2023

Cells

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“…The mechanisms by which LINC00663 regulates tumorigenesis remain unclear. Although LINC00663 can suppress the expression of oncogene ENO1 in breast cancer 37 , it was upregulated in pancreatic cancer and glioma cells, promoting tumor progression 38 , 39 . The roles of ITGA9-AS1 and the interactions among the four lncRNAs have been relatively less studied.…”

Section: Discussionmentioning

confidence: 99%

The prognostic value of sialylation-related long non-coding RNAs in lung adenocarcinoma

Wang,

Hou,

et al. 2024

Sci Rep

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There has been increasing interest in the role of epigenetic modification in cancers recently. Among the various modifications, sialylation has emerged as a dominant subtype implicated in tumor progression, metastasis, immune evasion, and chemoresistance. The prognostic significance of sialylation-related molecules has been demonstrated in colorectal cancer. However, the potential roles and regulatory mechanisms of sialylation in lung adenocarcinoma (LUAD) have not been thoroughly investigated. Through Pearson correlation, univariate Cox hazards proportional regression, and random survival forest model analyses, we identified several prognostic long non-coding RNAs (lncRNAs) associated with aberrant sialylation and tumor progression, including LINC00857, LINC00968, LINC00663, and ITGA9-AS1. Based on the signatures of four lncRNAs, we classified patients into two clusters with different landscapes using a non-negative matrix factorization approach. Collectively, patients in Cluster 1 (C1) exhibited worse prognoses than those in Cluster 2 (C2), as well as heavier tumor mutation burden. Functional enrichment analysis showed the enrichment of several pro-tumor pathways in C1, differing from the upregulated Longevity and programmed cell death pathways in C2. Moreover, we profiled immune infiltration levels of important immune cell lineages in two subgroups using MCPcounter scores and single sample gene set enrichment analysis scores, revealing a relatively immunosuppressive microenvironment in C1. Risk analysis indicated that LINC00857 may serve as a pro-tumor regulator, while the other three lncRNAs may be protective contributors. Consistently, we observed upregulated LINC00857 in C1, whereas increased expressive levels of LINC00968, LINC00663, and ITGA9-AS1 were observed in C2. Finally, drug sensitivity analysis suggested that patients in the two groups may benefit from different therapeutic strategies, contributing to precise treatment in LUAD. By integrating multi-omics data, we identified four core sialylation-related lncRNAs and successfully established a prognostic model to distinguish patients with different characterizations. These findings may provide some insights into the underlying mechanism of sialylation, and offer a new stratification way as well as clinical guidance in LUAD.

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“…In pancreatic cancer samples, LINC00663 expression was measured to be higher as compared to normal pancreatic samples [ 14 ]. Also, LINC00663 was reported to be highly expressed in glioma, and LINC00663 knockdown could restrain cell viability by modulating AKT/mTOR pathway [ 34 ]. The above data suggested that LINC00663 may be an oncogene in the occurrence and development of cancers.…”

Section: Discussionmentioning

confidence: 99%

Silencing LINC00663 inhibits inflammation and angiogenesis through downregulation of NR2F1 via EBF1 in bladder cancer

Zhong,

Sun,

Liu

et al. 2024

RNA Biology

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The Effect and Mechanism of LINC00663 on the Biological Behavior of Glioma

Cited by 7 publications

References 30 publications

The Fibrotic Effects of LINC00663 in Human Hepatic Stellate LX-2 Cells and in Bile Duct-Ligated Cholestasis Mice Are Mediated through the Splicing Factor 2-Fibronectin

The Fibrotic Effects of LINC00663 in Human Hepatic Stellate LX-2 Cells and in Bile Duct-Ligated Cholestasis Mice Are Mediated through the Splicing Factor 2-Fibronectin

The prognostic value of sialylation-related long non-coding RNAs in lung adenocarcinoma

Silencing LINC00663 inhibits inflammation and angiogenesis through downregulation of NR2F1 via EBF1 in bladder cancer

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