Up-regulation of lncRNA SNHG1 indicates poor prognosis and promotes cell proliferation and metastasis of colorectal cancer by activation of the Wnt/β-catenin signaling pathway

Zhu, Yumeng; Li, Bo; Liu, Zhuo; Jiang, Lai; Wang, Gang; Lv, Min; Li, Dechuan

doi:10.18632/oncotarget.22903

Cited by 50 publications

(43 citation statements)

References 36 publications

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“…It is known that lncRNAs play functional roles in a series of steps during tumor development, and they may interact with DNA, RNA, protein and/or various combinations to act as important regulators of chromatin organization and transcriptional as well as posttranscriptional regulation . Recent studies indicate that the ncRNA SNHG1 plays important roles in tumor development, and have provided new insights into the biological activities of SNHG1 in tumors (including CRC) . However, the roles of lncRNAs in CRC tumorigenesis remain incompletely understood.…”

Section: Discussionmentioning

confidence: 99%

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Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR‐137

Yin

Peng

et al. 2019

Molecular Carcinogenesis

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Small nucleolar RNA host gene 1 (SNHG1) is critical in the progression of cancers. However, the mechanism by which SNHG1 regulates the progression of colorectal cancer (CRC) remains unclear. Expressions of SNHG1 and miR‐137 in CRC tissues and cell lines were evaluated by quantitative real‐time polymerase chain reaction. A luciferase reporter gene assay was conducted to investigate miR‐137 target. Additionally, RNA pull‐down assay was performed to explore the physical association between miR‐137, SNHG1, and RNA induced silencing complex (RISC). Cell cycling and invasion were examined by flow cytometry (FCM) and transwell assays. The in vivo carcinogenic activity of SNHG1 was examined using murine xenograft models. Expression of RICTOR, serine/threonine kinase 1 (AKT), serum and glucocorticoid‐inducible kinase 1 (SGK1), p70S6K1, and LC3II/LC3I ratio was examined by Western blot analysis. SNHG1 upregulation was observed in CRC tissues and cell lines, which was associated with the lymph node metastasis, advanced TNM stage and poorer prognosis. SNHG1 increased RICTOR level in CRC via sponging miR‐137. In addition, SNHG1 silencing inhibited CRC cell proliferation and migration in vitro and in vivo. SNHG1 regulated RICTOR expression by sponging miR‐137 and promoted tumorgenesis in CRC.

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Section: Discussionmentioning

confidence: 99%

“…21 Recent studies indicate that the ncRNA SNHG1 | 2111 CRC). 22 However, the roles of lncRNAs in CRC tumorigenesis remain incompletely understood. The current study demonstrates that the oncogenic activity of SNHG1 in CRC is mediated through regulation of the miR-137/RICTOR axis.…”

Section: Discussionmentioning

confidence: 99%

Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR‐137

Yin

Peng

et al. 2019

Molecular Carcinogenesis

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“…Furthermore, cyclin D1, c-Myc, MMP9, and MDR1 are several pivotal downstream targets of Wnt/β-catenin pathway which play important roles in tumor proliferation, migration, invasion, and chemoresistance. 27,28 Interestingly, our data revealed the positive correlations between GPC4 and above target genes (Supporting Information Figure S1). More importantly, our further investigations demonstrated that both the mRNA levels and the protein levels of these genes were downregulated upon knockdown of GPC4 ( Figure 7C,D).…”

Section: Regulation Genesmentioning

confidence: 59%

“…However, GPC4‐knockdown cells showed a reduced level of nuclear β‐catenin and an increased level of cytoplasmic β‐catenin when compared with control cells (Figure B). Furthermore, cyclin D1, c‐Myc, MMP9, and MDR1 are several pivotal downstream targets of Wnt/β‐catenin pathway which play important roles in tumor proliferation, migration, invasion, and chemoresistance . Interestingly, our data revealed the positive correlations between GPC4 and above target genes (Supporting Information Figure S1).…”

Section: Resultsmentioning

confidence: 99%

Targeting glypican‐4 overcomes 5‐FU resistance and attenuates stem cell–like properties via suppression of Wnt/β‐catenin pathway in pancreatic cancer cells

Cao

Sun

et al. 2018

J of Cellular Biochemistry

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The existences of cancer stem cells in patients with pancreatic cancer are considered as pivotal factors contributing to chemoresistance and disease relapse. Glypican-4 (GPC4) is one of the members of the glypicans family, which underlies human congenital malformations and multiple diseases. However, its potential biological function in pancreatic cancer still remains elusive. In this study, we are the first to demonstrate that GPC4 was involved in 5-fluorouracil (5-FU) resistance and pancreatic cancer stemness through comprehensive bioinformatical analysis. Functional experiments showed that knockdown of GPC4 sensitized pancreatic cancer cells to 5-FU and attenuated stem cell-like properties. In terms of mechanism research, knockdown of GPC4 suppressed the activation of Wnt/β-catenin pathway and its downstream targets. Furthermore, the expression of GPC4 was significantly upregulated in pancreatic cancer tissues compared with normal tissues and remarkably correlated with patients' overall survival according to the data derived from the Cancer Genome Atlas database. Taken together, our results suggest that GPC4 is a key regulator in chemoresistance and pancreatic cancer stemness. Thus, targeting GPC4 may serve as a promising strategy for pancreatic cancer therapy.

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“…Upon receiving the Wnt canonical ligand, β-catenin accumulates and is trans-localized to the nucleus where it binds to TCFs and triggers the expression of downstream target genes [20]. Numerous lncRNAs such as lncTCF7 and SNHG1 have been reported to regulate Wnt/β-catenin signaling [39,40], while none of these lncRNAs bind to β-catenin. Our data showed that LINC01197 sequesters β-catenin binding to TCF4 in PDAC cells and then inhibits Wnt/β-catenin signaling.…”

Section: Discussionmentioning

confidence: 99%

FOXO1-regulated lncRNA LINC01197 inhibits pancreatic adenocarcinoma cell proliferation by restraining Wnt/β-catenin signaling

Jing

Wang

Liu

et al. 2019

J Exp Clin Cancer Res

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Background Recent studies have revealed that numerous oncogenic long non-coding RNAs (lncRNAs) play pivotal roles in pancreatic ductal adenocarcinoma (PDAC) progression, but little is known about tumor-suppressive lncRNAs in PDAC. This study was conducted to evaluate the function of tumor-suppressive LINC01197 in PDAC progression and investigate the detailed mechanisms. Methods LncRNA microarray was used to identify differentially expressed lncRNAs in FOXO1-overexpressing PANC1 cells. LINC01197 expression was evaluated by quantitative PCR, Northern blotting, and fluorescence in situ hybridization. The Cancer Genome Atlas database was used to analyze the prognostic role of LNC01197 in PDAC. A luciferase reporter assay was performed to confirm the interaction between LNC01197 and FOXO1. The biological function of LINC01197 was evaluated by colony formation assay in vitro and in an animal subcutaneous tumorigenesis experiment and Ki67 staining in vivo. RNA-pulldown, western blotting, RNA immunoprecipitation assay, and co-immunoprecipitation were further performed to determine the molecular mechanism of LNC01197 and β-catenin in the Wnt pathway. Results We found that a FOXO1-related lncRNA, LINC01197, was significantly decreased in PDAC malignant tissues and that its low expression predicted poor prognosis. Moreover, LINC01197 was mainly localized in the nucleus and inhibited PDAC cell proliferation both in vitro and in vivo. Mechanistically, LINC01197 was found to bind to β-catenin and inhibit Wnt/β-catenin signaling activity by disrupting β-catenin binding to TCF4 in PDAC cells. Conclusions The novel FOXO1/LINC01197/β-catenin axis was dysregulated during PDAC progression. Our study provides insight into the mechanisms of LINC01197 in PDAC and reveal a potential target for PDAC clinical therapy and prognostic prediction.

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Up-regulation of lncRNA SNHG1 indicates poor prognosis and promotes cell proliferation and metastasis of colorectal cancer by activation of the Wnt/β-catenin signaling pathway

Cited by 50 publications

References 36 publications

Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR‐137

Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR‐137

Targeting glypican‐4 overcomes 5‐FU resistance and attenuates stem cell–like properties via suppression of Wnt/β‐catenin pathway in pancreatic cancer cells

FOXO1-regulated lncRNA LINC01197 inhibits pancreatic adenocarcinoma cell proliferation by restraining Wnt/β-catenin signaling

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