Long Noncoding RNA BCYRN1 Promotes the Proliferation of Colorectal Cancer Cells via Up-Regulating NPR3 Expression

Gu, Lei; Lü, Lei; Zhou, Donglei; Liu, Zhongchen

doi:10.1159/000492649

Cited by 49 publications

(38 citation statements)

References 25 publications

(26 reference statements)

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“…consistent with these results, Hu and lu (12) also reported that BcYrn1 acted as an oncogene in nSclc as evidenced by the high cell proliferation and metastasis induced by BcYrn1. BcYrn1 has been reported to function as an oncogene in colorectal and cervical cancer, as well as in gastric carcinoma (25)(26)(27). Mechanistically, BcYrn1 may regulate gene expression by targeting mirnas.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA BCYRN1 promotes glycolysis and tumor progression by regulating the miR‑149/PKM2 axis in non‑small‑cell lung cancer

et al. 2020

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cancer cells use aerobic glycolysis to sustain their proliferation. long non-coding rna brain cytoplasmic rna 1 (BcYrn1) has been reported to act as an oncogene in non-small-cell lung cancer (nSclc). The present study investigated the role of BcYrn1 in nSclc glycolysis. BcYrn1 expression was detected in nSclc cells and tissues using reverse transcription-quantitative Pcr. The effect of BcYrn1 on aerobic glycolysis was examined by measuring nSclc cell glucose catabolism and lactate synthesis. The relationships between BcYrn1 and microrna (mir)-149, and between mir-149 and pyruvate kinase M1/2 (PKM2) were measured using a dual-luciferase reporter assay. cell proliferation and invasion were analyzed by the cell counting kit-8 assay and the Matrigel invasion assay, respectively. High BcYrn1 expression was observed in nSclc tissues and cells compared with the corresponding controls. BcYrn1 induced glycolysis and upregulated the expression levels of PKM2 in nSclc cells. in addition, BcYrn1 regulated mir-149 expression levels, and mir-149 inhibitor rescued the effects of si-BcYrn1 on glucose consumption and lactate production. miR-149 knockdown significantly enhanced the expression of PKM2. Furthermore, PKM2 inhibition significantly reversed the effects of mir-149 inhibitor on glucose catabolism and lactate synthesis. Furthermore, PKM2 was involved in nSclc cell proliferation and invasion, and BcYrn1 knockdown and mir-149 overexpression inhibited both processes. The present study suggested that BcYrn1 was involved in cell glycolysis, proliferation and invasion during nSclc via regulating mir-149 and PKM2.

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Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA BCYRN1 promotes glycolysis and tumor progression by regulating the miR‑149/PKM2 axis in non‑small‑cell lung cancer

et al. 2020

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“…The regulation of Bcl-xS by BC200 is of great significance for the pathogenesis of breast cancer. Gu et al (34) showed that BC200 can affect the expression of Bax and Bcl-2, suggesting that BC200 is involved in the apoptosis of colorectal cancer (CRC) cells. It has been previously reported that the ratio of Bax/Bcl-xL can be used to measure the level of apoptosis (35).…”

Section: Discussionmentioning

confidence: 99%

Effect of lncRNA‑BC200 on proliferation and migration of liver cancer cells in�vitro and in�vivo

et al. 2019

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In recent years, the important role of long noncoding RNAs (lncRNAs) in the development of liver cancer has received increasing attention. The abnormal expression level of long non-coding RNAs has been associated with the occurrence and development of liver cancer. However, the role and molecular mechanisms of lncRNAs in the development and progression of liver cancer are not fully understood. The present study aimed to clarify the function and molecular mechanism of lncRNA brain cytoplasmic 200 (BC200) in liver cancer. In the present study, it was found that BC200 expression level was higher in hepatocellular carcinoma (HCC) tissues than that in adjacent tissues. Cell function was examined by constructing BC200 knockout (KO) and BC200-overexpression in vitro models. It was found that BC200 affected the proliferation and migration of HepG2 cells. Interestingly, it was found that BC200 affected the expression of c-Myc protein but did not affect the mRNA expression level of c-MYC. BC200 KO cells exhibited a reduced protein expression level of Bax protein and an increased protein expression level of Bcl-xL. Conversely, BC200 overexpression reduced the expression of Bcl-xL protein and increased the expression of Bax protein. Importantly, it was found that BC200 affected the formation of subcutaneous tumors in nude mice. In conclusion, the present results suggested that lncRNA BC200 may play an important role in liver cancer.

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“…Long non-coding RNAs (lncRNAs) are a series of transcripts longer than 200 bp without coding potential [10][11][12]. An increasing number of studies have demonstrated that lncRNAs serve significant functions in biological and pathological processes, including heart disease [13], myocardial infarction [14], stroke [11], obesity [15], and tumour development [16][17][18][19]. The mechanisms underlying the actions of lncRNAs are also diverse, including regulation of the neighbouring gene [20], microRNA (miRNA)-sponge action [21], binding to a target protein, and DNA repair [22].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of the long non-coding RNA Oprm1 alleviates apoptosis from cerebral ischemia-reperfusion injury through the Oprm1/miR-155/GATA3 axis

Jing

Liu

Jia

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Numerous differentially expressed long non-coding RNAs (lncRNAs) have been identified in cerebral ischemia-reperfusion (I/R) injury using RNA-Seq analysis. However, little is known about whether and how lncRNAs are involved in cerebral I/R injury. In this study, we investigated the function of the lncRNA Oprm1 in cerebral I/R injury and explored the underlying mechanism. An oxygen-glucose deprivation model in N2a cells was utilized to mimic cerebral I/R injury in vitro. Trypan blue staining, terminal deoxytransferase-mediated dUTP-biotin nick end labelling and caspase-3 were measured to evaluate apoptosis. Middle cerebral artery occlusion was performed in mice to evaluate the function of lncRNA Oprm1 in vivo. Real-time PCR and western blotting were used to measure the expression levels of lncRNA Opmr1, caspase-3, miR-155, GATA binding protein 3 (GATA3) and nuclear factor (NF)-jB. lncRNA Oprm1 was mainly located in the cytoplasm. Overexpression of lncRNA Oprm1 alleviated the apoptosis induced by oxygen-glucose deprivation and significantly reduced cleaved caspase-3 levels. Infarct size was distinctly decreased in the lncRNA Oprm1-overexpression group. The neurological score was also improved. Our findings showed that the lncRNA Oprm1/miR-155/GATA3 axis plays an important role in cerebral I/R injury. lncRNA Oprm1 may attenuate cerebral injury through the NF-jB pathway. lncRNA Oprm1 may serve as a potential target for new therapeutic interventions in patients with ischemic stroke. ARTICLE HISTORY

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Long Noncoding RNA BCYRN1 Promotes the Proliferation of Colorectal Cancer Cells via Up-Regulating NPR3 Expression

Cited by 49 publications

References 25 publications

Long non‑coding RNA BCYRN1 promotes glycolysis and tumor progression by regulating the miR‑149/PKM2 axis in non‑small‑cell lung cancer

Long non‑coding RNA BCYRN1 promotes glycolysis and tumor progression by regulating the miR‑149/PKM2 axis in non‑small‑cell lung cancer

Effect of lncRNA‑BC200 on proliferation and migration of liver cancer cells in�vitro and in�vivo

Overexpression of the long non-coding RNA Oprm1 alleviates apoptosis from cerebral ischemia-reperfusion injury through the Oprm1/miR-155/GATA3 axis

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