Upregulation of LncRNA BCYRN1 promotes tumor progression and enhances EpCAM expression in gastric carcinoma

Ren, Hao; Yang, Xingsheng; Yang, Yongmei; Zhang, Xiaoyu; Zhao, Rui; Wei, Ran; Zhang, Xin; Zhang, Yi

doi:10.18632/oncotarget.23585

Cited by 24 publications

(29 citation statements)

References 36 publications

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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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“…Recent studies have shown that specific lncRNA is closely related to neural cell differentiation, synapses, elevated neuronal excitability, and neural network connection and remodeling, suggesting that it may be involved in the occurrence and development of epilepsy. It is found that in the rat model of epilepsy, the over autophagy and apoptosis of hippocampal neurons can be antagonism by downregulation of lncRNA MALAT1, thus protecting the hippocampus of rats . LncRNA H19 has been reported to promote the apoptosis of hippocampal neurons by inhibiting let‐7b .…”

Section: Discussionmentioning

confidence: 99%

“…It is found that in the rat model of epilepsy, the over autophagy and apoptosis of hippocampal neurons can be antagonism by downregulation of lncRNA MALAT1, thus protecting the hippocampus of rats. 23 LncRNA H19 has been reported to promote the apoptosis of hippocampal neurons by inhibiting let-7b. 24 LncRNA UCA1 inhibits seizures and brain damage caused by epilepsy by modulating the miR-495/Nrf2-ARE signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA GAS5 silencing inhibits the expression of KCNQ3 by sponging miR‐135a‐5p to prevent the progression of epilepsy

Zheng

et al. 2019

The Kaohsiung J of Med Scie

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Epilepsy is one of the most common neurological disorders in humans. Recently, long noncoding RNAs (lncRNAs) have been reported to be important players in neurological diseases. Herein, this study aimed to examine the effect of lncRNA GAS5 on the occurrence of epilepsy in rat and cell models of epileptic seizure. The expression of lncRNA GAS5 was measured in the established rat and cell models. The binding sites between lncRNA GAS5 and miR‐135a‐5p, as well as those between miR‐135a‐5p and 3′ untranslated region of KCNQ3 were predicted by miRDB and Targetscan, separately, followed by verification using dual‐luciferase reporter gene assay. The expression of miR‐135a‐5p was measured in response to the overexpression of lncRNA GAS5. The mRNA and protein levels of KCNQ3 were examined in response to overexpression of miR‐135a‐5p. Next, the latency of epilepsy and frequency of epileptic seizures were assessed in rats injected with Lv‐shGAS5 and Lv‐miR‐135a‐5p in epileptic seizure model. In the rat and cell models, lncRNA GAS5 was highly expressed when epileptic seizure was induced. The expression of miR‐135a‐5p was decreased by overexpression of lncRNA GAS5. Meanwhile, the mRNA and protein levels of KCNQ3 were decreased in response to knockdown of miR‐135a‐5p. After the treatment of Lv‐shGAS5 and Lv‐miR‐135a‐5p, the average latent period of epilepsy was prolonged and the frequency of seizures was decreased. The key findings of the present study provide evidence emphasizing that lncRNA GAS5 functions as a competitive endogenous RNA of miR‐135a‐5p to increase expression of KCNQ3, and lncRNA GAS5 silencing inhibited the occurrence and progression of epilepsy.

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“…Meanwhile, recent research indicated that BCYRN1 accelerated the proliferation and metastasis of cervical cancer through regulating miR-138 in vitro and in vivo [9]. And research from Ren et al found that overexpression of BCYRN1 facilitated tumor progression and up-regulated EpCAM expression in gastric carcinoma [10]. Furthermore, BCYRN1 has been illustrated to be greatly expressed in HCC and its expression was actively connected with tumor-node-metastasis and unfavorable prognosis in HCC patients [11].…”

Section: Introductionmentioning

confidence: 99%

LncRNA BCYRN1/miR-490-3p/POU3F2, served as a ceRNA network, is connected with worse survival rate of hepatocellular carcinoma patients and promotes tumor cell growth and metastasis

et al. 2020

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LncRNA Brain Cytoplasmic RNA 1 (BCYRN1) has been certified to modulate cancer cells growth and aggressiveness in several tumors. However, research about function of BCYRN1 in hepatocellular carcinoma (HCC) is limited. Therefore, our research intends to explore the function of BCYRN1 in HCC. Methods: HepG2 and BEL-7402 cell lines were employed for later function experiments. Differently expression levels of BCYRN1, miR-490-3p, and POU class 3 homeobox 2 (POU3F2) were determined on the base of TCGA dataset including 375 HCC patients and 50 normal. 370 cases of patients, which have fairly complete clinical data, were utilized for survival analysis of BCYRN1, miR-490-3p, or POU3F2 by Kaplan-Meier method. Relative expression pattern of BCYRN1 was examined by quantitative real time polymerase chain reaction (qRT-PCR), and relative expression level of POU3F2 was assessed by qRT-PCR and western blot. Cell biological behaviors were analyzed by cell counting kit-8, cloning formation, and transwell assays. Bioinformatics software and dual luciferase assay were applied to predict and confirm the targeted relationship between BCYRN1 and miR-490-3p, as well as miR-490-3p and POU3F2. Further associations among BCYRN1, miR-490-3p, and POU3F2 were analyzed by rescue assays. Results: Our results exhibited that BCYRN1 was over expressed in HCC samples, which was connected with unfavorable prognosis in HCC patients. In addition, a series of experiments exhibited that overexpression of BCYRN1 significantly expedited HCC cells growth, clone formation, and movement abilities, and vice versa. Moreover, targeted relationships between BCYRN1 and miR-490-3p, as well as miR-490-3p and POU3F2 were affirmed by dual luciferase assay. Furthermore, POU3F2 expression was negatively connected with the expression of miR-490-3p and positively associated with BCYRN1 expression. Whilst, either overexpression of miR-490-3p or knockdown of POU3F2 could remarkably inhibit the increasing trends of proliferation, clone formation, invasion, and migration abilities induced by BCYRN1 in HCC cells.

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Upregulation of LncRNA BCYRN1 promotes tumor progression and enhances EpCAM expression in gastric carcinoma

Cited by 24 publications

References 36 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

Long noncoding RNA GAS5 silencing inhibits the expression of KCNQ3 by sponging miR‐135a‐5p to prevent the progression of epilepsy

LncRNA BCYRN1/miR-490-3p/POU3F2, served as a ceRNA network, is connected with worse survival rate of hepatocellular carcinoma patients and promotes tumor cell growth and metastasis

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