Long noncoding RNA BDNF-AS is downregulated in cervical cancer and has anti-cancer functions by negatively associating with BDNF

Zhang, Huimin; Liu, Caihong; Yan, Ting; Wang, Jun; Liang, Wei

doi:10.1016/j.abb.2018.03.023

Cited by 16 publications

(15 citation statements)

References 17 publications

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“…BDNF has been reported to be upregulated and act as a predominant oncogenic factor in a variety human cancers 37,38 . Interestingly, BDNF-AS was demonstrated to be reversely associated with BDNF and downregulated expressed in RB, NSCLC, and CC 12,39,40 . Xiong et al found that mature BDNF induces glioma cells in vitro 41 .…”

Section: Discussionmentioning

confidence: 99%

“…Brain-derived neurotrophic factor antisense (BDNF-AS) is a natural noncoding antisense of BDNF, locates at chromosome region 11p14.1, plays important roles in neuronal system together with BDNF 11 . Besides, BDNF-AS was lowly expressed in retinoblastoma (RB), non-small cell lung cancer (NSCLC) and CC, and suppressed cells proliferation and migration in these cancers 12 . The relationship between BDNF-AS and glioblastoma has not been found yet.…”

Section: Introductionmentioning

confidence: 99%

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PABPC1-induced stabilization of BDNF-AS inhibits malignant progression of glioblastoma cells through STAU1-mediated decay

Zheng

et al. 2020

Cell Death Dis

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Glioblastoma is the most common and malignant form of primary central nervous tumor in adults. Long noncoding RNAs (lncRNAs) have been reported to play a pivotal role in modulating gene expression and regulating human tumor's malignant behaviors. In this study, we confirmed that lncRNA brain-derived neurotrophic factor antisense (BDNF-AS) was downregulated in glioblastoma tissues and cells, interacted and stabilized by polyadenylate-binding protein cytoplasmic 1 (PABPC1). Overexpression of BDNF-AS inhibited the proliferation, migration, and invasion, as well as induced the apoptosis of glioblastoma cells. In the in vivo study, PABPC1 overexpression combined with BDNF-AS overexpression produced the smallest tumor and the longest survival. Moreover, BDNF-AS could elicit retina and anterior neural fold homeobox 2 (RAX2) mRNA decay through STAU1-mediated decay (SMD), and thereby regulated the malignant behaviors glioblastoma cells. Knockdown of RAX2 produced tumor-suppressive function in glioblastoma cells and increased the expression of discs large homolog 5 (DLG5), leading to the activation of the Hippo pathway. In general, this study elucidated that the PABPC1-BDNF-AS-RAX2-DLG5 mechanism may contribute to the anticancer potential of glioma cells and may provide potential therapeutic targets for human glioma.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

PABPC1-induced stabilization of BDNF-AS inhibits malignant progression of glioblastoma cells through STAU1-mediated decay

Zheng

et al. 2020

Cell Death Dis

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“…For example, lncRNA Hox transcript antisense intergenic RNA (HOTAIR) was highly expressed in CRC tissues and induced genome‐wide retargeting of polycomb‐repressive complex 2 (PRC2) composed of enhancer of zeste 2 (EZH2), suppressor of zeste 12 homologue (SUZ12), and embryonic ectoderm development (EED), leading to trimethylation of histone H3 lysine 27 (H3K27me3), which in turn promoted the invasion of CRC cells . The brain‐derived neurotrophic factor antisense RNA (BDNF‐AS) is a naturally conserved noncoding antisense RNA transcript that negatively regulated the transcription of BDNF in various human and animal tissues . A recent study has declared that lncRNA BDNF‐AS, through its association with the epigenetic EZH2, guided the histone methyltransferase to the BDNF gene promoter, thereby repressing BDNF transcription .…”

Section: Introductionmentioning

confidence: 58%

“…7 The brain-derived neurotrophic factor antisense RNA (BDNF-AS) is a naturally conserved noncoding antisense RNA transcript that negatively regulated the transcription of BDNF in various human and animal tissues. 8,9 A recent study has declared that lncRNA BDNF-AS, through its association with the epigenetic EZH2, guided the histone methyltransferase to the BDNF gene promoter, thereby repressing BDNF transcription. 10 However, the functions and underlying mechanism of lncRNA BDNF-AS in CRC pathogenesis have not been reported yet.…”

mentioning

confidence: 99%

LncRNA BDNF‐AS suppresses colorectal cancer cell proliferation and migration by epigenetically repressing GSK‐3β expression

Zhi

Lian

2019

Cell Biochemistry & Function

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This study was designed to investigate the molecular mechanism and biological roles of long non‐coding RNA (lncRNA) brain‐derived neurotrophic factor antisense (BDNF‐AS) in colorectal cancer (CRC). The quantitative real‐time PCR (qRT‐PCR) and western blotting were performed to detect the expressions of lncRNA BDNF‐AS and glycogen synthase kinase‐3β (GSK‐3β) in human CRC tissues and cell lines. The cell proliferation, transwell migration, and invasion assays were carried out to evaluate the effect of lncRNA BDNF‐AS on the growth of CRC cells. RNA pull‐down and RNA immunoprecipitation (RIP) assays were conducted to confirm the interaction between lncRNA BDNF‐AS and enhancer of Zeste Homologue 2 (EZH2). Chromatin immunoprecipitation (ChIP) assay was used to verify the enrichment of EZH2 and histone H3 lysine 27 trimethylation (H3K27me3) in the promoter region of GSK‐3β in CRC cells. LncRNA BDNF‐AS expression was significantly decreased, while GSK‐3β was highly expressed in human CRC tissues and cell lines. Moreover, lncRNA BDNF‐AS induced inhibition of proliferation, migration, and invasion of CRC cells via inhibiting GSK‐3β expression. Mechanistically, BDNF‐AS led to GSK‐3β promoter silencing in CRC cells through recruitment of EZH2. In conclusion, lncRNA BDNF‐AS functioned as an oncogene in CRC and shed new light on lncRNA‐directed therapeutics in CRC. Significance of the study LncRNA BDNF‐AS is recently reported to be remarkably downregulated in a variety of tumours and served as a tumour suppressor. However, the functions and underlying mechanism of lncRNA BDNF‐AS in CRC pathogenesis have not been reported yet. Our study is the first to demonstrate the effect of lncRNA BDNF‐AS in CRC and revealed that lncRNA BDNF‐AS expression is negatively correlated with the aggressive biological behaviour of CRC. Further investigation demonstrated that lncRNA BDNF‐AS functioned as a tumour suppressor in CRC progression by suppressing GSK‐3β expression through binding to EZH2 and H3K27me3 with the GSK‐3β promoter, shedding light on the diagnosis and therapy for CRC.

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“…For example, the lncRNA LOC105374902 promotes the malignancy of CC cells by acting as a sponge of miR-1285-3p, a process enhanced by TNF-α (25). Furthermore, the lncRNA SBF2-AS1 promotes the progression of CC by regulating the miR-361-5p/FOXM1 axis (26), while the lncRNA BDNF-Anti-Sense is downregulated in CC and possesses anti-tumor functions by negatively associating with brain-derived neurotrophic factor (27). RP11-480I12.5 is a newly identified lncRNA and, to the best of our knowledge, has not yet been extensively studied.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA RP11‑480I12.5 promotes cervical carcinoma progression by regulating the Wnt/β‑catenin signaling pathway

Zhang¹,

Sona³

2019

Oncol Lett

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T he long non-coding R NA (lncR NA), RP11-480I12.5 is one of the most dysregulated lncRNAs, which is believed to contribute to the progression of cervical carcinoma (CC); however, the exact function of RP11-480I12.5 in human CC remains unknown. The present study aimed to investigate the function and underlying molecular mechanism of RP11-480I12.5 in CC. First, reverse transcription-quantitative PCR was implemented in order to detect differences in the expression of RP11-480I12.5 between normal and CC tissues. The present study used in vitro analysis to establish RP11-480I12.5 stable knockdown and overexpressing cell lines, in order to investigate the function and potential molecular mechanism of RP11-480I12.5 in the progression of CC. RP11-480I12.5 was upregulated in CC tissue compared with normal tissue. Furthermore, RP11-480I12.5 was associated with clinical stage, tumor size and lymph node metastasis. RP11-480I12.5 promoted the proliferation, migration and invasion of CC cell lines. Subsequently, the present study investigated the association between RP11-480I12.5 and the epithelial-to-mesenchymal transition (EMT) and Wnt/β-catenin pathways. RP11-480I12.5 promoted EMT through the Wnt/β-catenin pathway. Overall, the results of the present study demonstrate that RP11-480I12.5 promotes cercical cancer cell migration, invasion and EMT through the Wnt/β-catenin pathway.

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Long noncoding RNA BDNF-AS is downregulated in cervical cancer and has anti-cancer functions by negatively associating with BDNF

Cited by 16 publications

References 17 publications

PABPC1-induced stabilization of BDNF-AS inhibits malignant progression of glioblastoma cells through STAU1-mediated decay

PABPC1-induced stabilization of BDNF-AS inhibits malignant progression of glioblastoma cells through STAU1-mediated decay

LncRNA BDNF‐AS suppresses colorectal cancer cell proliferation and migration by epigenetically repressing GSK‐3β expression

Long non‑coding RNA RP11‑480I12.5 promotes cervical carcinoma progression by regulating the Wnt/β‑catenin signaling pathway

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