Schisandrin B down‐regulated lnc<scp>RNA BCYRN</scp>1 expression of airway smooth muscle cells by improving miR‐150 expression to inhibit the proliferation and migration of <scp>ASMC</scp> in asthmatic rats

Zhang, Xiaoyu; Tang, Xue-yi; Ma, Lijun; Guo, Yu; Li, Xiao-su; Zhao, Limin; Tian, Cui-jie; Cheng, Dongjun; Chen, Zhuochang; Zhang, Luo-xian

doi:10.1111/cpr.12382

Cited by 39 publications

(30 citation statements)

References 27 publications

(53 reference statements)

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“…Mechanistically, BcYrn1 may regulate gene expression by targeting mirnas. For example, BcYrn1 targeted mir-138 or mir-150 to alter the proliferation and metastasis of cervical cancer cells or airway smooth muscle cells, respectively (25,28).…”

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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“…Recently, it has been reported that abnormal expression of BCYRN1 has an impact on varieties of human cancers [19,24,25]. However, the regulatory mechanism of BCYRN1 is still unclear.…”

Section: Discussionmentioning

confidence: 99%

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

Lü

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long noncoding RNAs (lncRNAs) constitute a large proportion of noncoding transcripts that have recently emerged as a new class of important regulators in cancers. LncRNA BCYRN1, also known as BC200, has a potential function in tumorigenesis. However, the clinical significance of BCYRN1 and its effect on colorectal cancer (CRC) progression remains unclear. Methods: Quantitative reverse transcriptase PCR (qRT-PCR) was performed to investigate the expression of BCYRN1 in CRC tissues and cell lines. The biological function of BCYRN1 was also investigated through knockdown and overexpression of BCYRN1 in vitro. Microarray bioinformatics analysis was performed to analyze the putative targets of BCYRN1. Results: The results showed that BCYRN1 expression was significantly upregulated in 96 CRC tumor tissues compared with para-carcinoma control tissues. Additionally, BCYRN1 overexpression was associated with larger tumor size and advanced pathological stages in CRC patients. In vitro BCYRN1 knockdown significantly inhibited the proliferation and apoptosis of CRC cells. Furthermore, NPR3 was identified to be a target of BCYRN1 and was downregulated by BCYRN1 knockdown. Conclusion: Together, we provide the first evidence that BCYRN1 plays an oncogenic role in CRC cells. BCYRN1 may be a promising prognostic biomarker and a potential therapeutic target for CRC.

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“…It has been reported that BCYRN1 is highly expressed in various tumour tissues [16], such as hepatocellular carcinoma [17], gastric cancer [18], and lung cancer [15] but is expressed at lower levels in healthy control (HC) tissues. In addition, BCYRN1 plays an important role in inhibiting smooth muscle differentiation and vascular development in the cardiovascular system [19,20]. However, little is known about the role of BCYRN1 in CRC, which aroused our great interest.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA BCYRN1 exerts an oncogenic role in colorectal cancer by regulating the miR-204-3p/KRAS axis

et al. 2020

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Background It has been well documented that long non-coding RNAs (lncRNAs) regulate numerous characteristics of cancer, including proliferation, migration, metastasis, apoptosis, and even metabolism. LncRNA BCYRN1 (BCYRN1) is a newly identified brain cytoplasmic lncRNA with 200 nucleotides that was discovered to be highly expressed in tumour tissues, including those of hepatocellular carcinoma, gastric cancer and lung cancer. However, the roles of BCYRN1 in colorectal cancer (CRC) remain obscure. This study was designed to reveal the role of BCYRN1 in the occurrence and progression of CRC. Methods RT-PCR was used to detect the expression level of BCYRN1 in tumour tissues and CRC cell lines. BCYRN1 was knocked down in CRC cells, and cell proliferation changes were evaluated by cell counting kit-8 (CCK-8), 5-ethynyl-2′-deoxyuridine (EdU), and Ki-67 and proliferating cell nuclear antigen (PCNA) expression assays. Cell migration and invasion changes were evaluated by wound healing, Transwell and invasion-related protein expression assays. Flow cytometry analysis was used to assess whether BCYRN1 regulates the apoptosis of CRC cells. The dual luciferase reporter gene detects the competitive binding of BCYRN1 to miR-204-3p. In vivo experiments were performed to evaluate the effect of BCYRN1 on tumour development. TargetScan analysis and dual luciferase reporter gene assays were applied to detect the target gene of miR-204-3p. Rescue experiments verified that BCYRN1 affects CRC by regulating the effect of miR-204-3p on KRAS. Results We found that compared with normal tissues and human intestinal epithelial cells (HIECs), CRC tumour tissues and cell lines had significantly increased BCYRN1 levels. We further determined that knockdown of BCYRN1 inhibited the proliferation, migration, and invasion and promoted the apoptosis of CRC cells. In addition, bioinformatics analysis and dual luciferase reporter assay showed that BCYRN1 served as a competitive endogenous RNA (ceRNA) to regulate the development of CRC through competitively binding to miR-204-3p. Further studies proved that overexpression of miR-204-3p reversed the effects of BCYRN1 on CRC. Next, TargetScan analysis and dual luciferase reporter assay indicated that KRAS is a target gene of miR-204-3p and is negatively regulated by miR-204-3p. A series of rescue experiments showed that BCYRN1 affected the occurrence and development of CRC by regulating the effects of miR-204-3p on KRAS. In addition, tumorigenesis experiments in a CRC mouse model confirmed that BCYRN1 downregulation effectively inhibited tumour growth. Conclusions Our findings suggest that BCYRN1 plays a carcinogenic role in CRC by regulating the miR-204-3p/KRAS axis.

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Schisandrin B down‐regulated lncRNA BCYRN1 expression of airway smooth muscle cells by improving miR‐150 expression to inhibit the proliferation and migration of ASMC in asthmatic rats

Abstract: Schisandrin B increased miR-150 expression and decreased BCYRN1, and BCYRN1 expression was inhibited by miR-150, which indicated that Schisandrin B could regulate BCYRN1 through miR-150.

Cited by 39 publications

References 27 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 BCYRN1 Promotes the Proliferation of Colorectal Cancer Cells via Up-Regulating NPR3 Expression

Long non-coding RNA BCYRN1 exerts an oncogenic role in colorectal cancer by regulating the miR-204-3p/KRAS axis

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