CRNDE, a long-noncoding RNA, promotes glioma cell growth and invasion through mTOR signaling

Wang, Yunliang; Wang, Yutong; Li, Jinfeng; Zhang, Yuzhen; Yin, Honglei; Han, Bing

doi:10.1016/j.canlet.2015.03.027

Cited by 231 publications

(181 citation statements)

References 23 publications

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“…A transcript isoform (CRNDE-h) found in patient plasma may serve as a biomarker [23]. The CRNDE lncRNA is also strongly upregulated in glioma, and contributes to disease progression by promoting cell proliferation, migration and invasion by mTOR signaling [24]. CRNDE is also overexpressed in melanoma and lymphocytic leukemia cells.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: The colorectal neoplasia differentially expressed (CRNDE) gene is a long noncoding RNA (lncRNAs) that is upregulated in colorectal cancer and glioma. Here, we investigated the regulatory function of CRNDE in gastric cancer (GC). Methods: CRNDE and miR-145 expression were assayed by qRT-PCR, and E2F3 protein expression was measured by western blotting. A luciferase reporter assay was used to detect the direct regulation of miR-145 by CRNDE. Cell viability and colony formation of human GC cells were detected using MTT and colony formation assay, respectively. Results: CRNDE was highly expressed in GC cell lines and tissues; overexpression of CRNDE increased GC cell viability and promoted colony formation. Knockdown of CRNDE did not result in loss of expression-related effects on cell proliferation and colony formation. Further investigation revealed that the miR-145 target gene E2F3 was strongly expressed following CRNDE competitive molecular sponging of miR-145. Conclusion: CRNDE acted as a growth-promoting lncRNA in GC and maybe a potential target of GC treatment.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145

Zhang

et al. 2017

Cell Physiol Biochem

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“…Cell migration and invasion assay, luciferase reporter assay, and pull-down assay Cell migration and invasion assay, luciferase reporter assay, and pull-down assay were described previously [22,23].…”

Section: Apoptosis Detectionmentioning

confidence: 99%

Long noncoding RNA NEAT1 promotes glioma pathogenesis by regulating miR-449b-5p/c-Met axis

et al. 2015

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Growing evidence demonstrates that long noncoding RNAs (lncRNAs) are involved in the progression of various cancers including glioma. Nuclear enriched abundant transcript 1 (NEAT1), an essential lncRNA for the formation of nuclear body paraspeckles, was not fully explored in glioma. We aimed to determine the expression, roles, and functional mechanisms of NEAT1 in the progression of glioma. By real-time PCR, we suggested that NEAT1 was upregulated in glioma tissues than noncancerous brain tissues. Knockdown of NEAT1 reduced glioma cell proliferation, invasion, and migration. RNA immunoprecipitation assay combined with luciferase reporter assay confirmed miR-449b-5p-specific binding to NEAT1. Furthermore, we verified that c-Met was a directly target of miR-449b-5p. Rescue assays demonstrated NEAT1 functions a molecular sponge for miR-449b-5p and leads to the upregulation of c-Met. This regulation menchaism promotes glioma pathogenesis and may provide a potential target for the prognosis and treatment of glioma.

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“…Glioma is the most aggressive and common primary tumor that appears in the nervous system, accounting for about 80% of primary malignant brain tumors [1] . Glioma has a significant impact on human health due to its high invasiveness, high recurrence rate, poor prognosis and pessimistic survival status [2].…”

Section: Introductionmentioning

confidence: 99%

Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway

Ding

Wang²,

Wang³

et al. 2016

Pharmacology

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Objective: To test the effects of Tanshinone IIA (Tan IIA) on cell viability, cycle, apoptosis, and autophagy of human glioma cell U251 by regulating phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signal pathway. Methods: Tan IIA and PI3K agonist (740 Y-P) were used to treat glioma cells U251. MTT assay was used to assess cell viability and flow cytometry was used to detect cell apoptosis and cell cycle. The expressions of apoptosis-related proteins (Bcl-2 and Bax), autophagy-related proteins (LC3B and Beclin 1) and PI3K/Akt/mTOR signal pathway-associated proteins (p-PI3K, p-Akt and p-mTOR) were evaluated by Western blotting. Results: Tan IIA decreased the expression of p-PI3K and p-Akt proteins, inhibited cell viability and promoted apoptosis. Meanwhile, the expression of Bax increased, while the expression of Bcl-2 decreased. In addition, Tan IIA promoted autophagy in U251 glioma cells and raised the expression of LC3B and Beclin 1. However, 740 Y-P played a reversed role of Tan IIA in cell viability, cycle, apoptosis, and autophagy of U251 cells. Conclusion: Tan IIA could suppress the viability of U251 cells and induce cell apoptosis and autophagy, which might be related to the inhibition of the PI3K/Akt/mTOR signal pathway.

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CRNDE, a long-noncoding RNA, promotes glioma cell growth and invasion through mTOR signaling

Cited by 231 publications

References 23 publications

Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145

Long Noncoding RNA CRNDE Promotes Proliferation of Gastric Cancer Cells by Targeting miR-145

Long noncoding RNA NEAT1 promotes glioma pathogenesis by regulating miR-449b-5p/c-Met axis

Tanshinone IIA Affects Autophagy and Apoptosis of Glioma Cells by Inhibiting Phosphatidylinositol 3-Kinase/Akt/Mammalian Target of Rapamycin Signaling Pathway

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