Study on expression of lncRNA RGMB-AS1 and repulsive guidance molecule b in non-small cell lung cancer

Li, Ping; Li, Juan; Yang, Rui; Zhang, Furui; Wang, Huaqi; Chu, Heying; Lu, Yiming; Dun, Shaozhi; Wang, Yuanyuan; Zang, Wenqiao; Du, Yuwen; Chen, Xiaonan; Zhang, Guojun

doi:10.1186/s13000-015-0297-x

Cited by 23 publications

(14 citation statements)

References 38 publications

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“…The Kaplan-Meier analysis showed FENDRR was a prognostic biomarker of overall survival for NSCLC patients, which corresponded to Xu's et al report in gastric cancer [8]. Recent studies showed that several lncRNAs, including HMlincRNA717 and RGMB-AS1 [20,21], were associated with overall survival of NSCLC patients, and could be prognostic factors for patients with NSCLC. Further penetrating research might provide a diagnosis target and prognostic biomarker for NSCLC.…”

Section: Discussionsupporting

confidence: 72%

Long non-coding RNA FOXF1 adjacent non-coding developmental regulatory RNA inhibits growth and chemotherapy resistance in non-small cell lung cancer

Xu¹

2019

aoms

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Introduction: Lung cancer is one of the most common malignant neoplasms around the globe. Its most common type is non-small cell lung cancer (NSCLC). The FOXF1 adjacent non-coding developmental regulatory RNA (FENDRR) gene is an lncRNA which has been reported to show low expression and a tumor suppressor role in NSCLC. Material and methods: The expression of FENDRR in NSCLC patients' tissues and cell line was detected by quantitative real-time PCR. MTT assay was used to detect cell proliferation and chemotherapy resistance. Cell apoptosis was measured by flow cytometry. Results: The expression of FENDRR was low in NSCLC tissues and cells in contrast to control tissues and cells, and low FENDRR expression correlated with high TNM stages and poor differentiation of NSCLC, and could be a promising prognostic factor for NSCLC. FENDRR enhancement could inhibit the proliferation ability and advance cell apoptosis of A549 cells. The expression of FENDRR in NSCLC tissues and cells insensitive to cisplatin was much lower than that in NSCLC tissues and cells sensitive to cisplatin. The chemotherapy resistance to cisplatin of A549/DDP cells was depressed by FENDRR enhancement, and IC50 for cisplatin presented a conspicuous depression. FENDRR up-regulation inhibited cell viability of A549/DDP cells under treatment with 5 μg/ml DDP. TCGA Pan-Cancer (PANCAN) showed that the expression of FENDRR was negatively correlated with the expression of ABCC10 in lung cancer, and our western blot found that FENDRR up-regulation inhibited the expression of ABCC10 in A549/DDP cells. Conclusions: LncRNA FENDRR has low expression in NSCLC and functions as a potential tumor-suppressing gene to inhibit growth and chemotherapy resistance of NSCLC cells.

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Section: Discussionsupporting

confidence: 72%

Long non-coding RNA FOXF1 adjacent non-coding developmental regulatory RNA inhibits growth and chemotherapy resistance in non-small cell lung cancer

Xu¹

2019

aoms

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“…Our microarray data analysis revealed that the XLOC_008466 level was up-regulated in NSCLC tissues [13]. In this study, we further verified the expression of XLOC_008466 in 63 NSCLC patients and analyzed its expression features in the patient clinicopathological characteristics.…”

Section: Resultsmentioning

confidence: 91%

“…Based on our previous microarray data analysis of lncRNAs in NSCLC tissues [13], our present study was performed to confirm the expression of XLOC_008466 and explore the potential regulatory network of XLOC_008466-miRNA-mRNA using bioinformatics prediction and sequence analysis.…”

Section: Introductionmentioning

confidence: 99%

Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874

Yang

Zhang

et al. 2017

Cell Physiol Biochem

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Background: The therapy and prognosis of lung cancer are difficult because of multiple genetic and epigenetic alterations. Long non-coding RNAs (lncRNAs) have been verified as new mediators of cancer development and progression by virtue of their various functions. Here, we focused on the lncRNA XLOC_008466 based on previous microarray data. However, whether aberrant expression of XLOC_008466 in human non-small cell lung cancer (NSCLC) is correlated with malignancy, metastasis or prognosis has not been elucidated. Methods: We performed real-time PCR, CCK-8, flow cytometry, trans-well, western blotting, luciferase reporter assays, RNA immunoprecipitation (RIP) assay and surface plasmon resonance (SPR) assay to detect the function of XLOC_008466 in NSCLC. Results: Up-regulation of XLOC_008466 in NSCLC patients was related to lymph node metastasis and the TNM stage. In vitro, down-regulation of XLOC_008466 inhibited cell proliferation and invasion of A549 and H460 cells in vitro, but promoted cell apoptosis. Experiments on mechanisms revealed that XLOC_008466 functioned as a ceRNA, directly binding to miR-874, and could affect cell proliferation, apoptosis and invasion through regulation of miR-874 expression as well as by increasing matrix metalloproteinase 2 (MMP2) and X-linked inhibitor of apoptosis (XIAP) expression. Conclusions: XLOC_008466 functions as an oncogene in NSCLC by regulating the miR-874-MMP2/XIAP axis, which indicates that XLOC_008466 may be a useful marker and potential therapeutic target in NSCLC.

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“…1B, Supplementary Table S1). In addition to the selected lncRNAs, we chose 18 well characterized lncRNAs associated with the occurrence and development of NSCLC as positive controls [38][39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57] ( Supplementary Table S1).…”

Section: Repurposing Microarray Data For Lncrna Selection In Nsclcmentioning

confidence: 99%

Construction of a CRISPR‐based paired‐sgRNA library for chromosomal deletion of long non‐coding RNAs

Tao¹,

Mu²,

Zhang³

et al. 2020

Quant. Biol.

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Background: Derived from an adaptive bacterial immune system, the clustered regularly interspaced palindromic repeats (CRISPR)/CRISPR-associated 9 (Cas9) system has shown great potential in high-throughput functional genomic screening, especially for protein-coding genes. However, it is still challenging to apply the similar strategy to study non-coding genomic elements such as long non-coding RNAs (lncRNAs) or clusters of microRNAs, because short insertions or deletions may not be sufficient to generate loss-of-function phenotypes. Methods: Here, we presented a systematic strategy for designing a CRISPR-based paired-sgRNA library for highthroughput screening in non-coding regions. Due to the abundance of lncRNAs and their diverse regulatory roles in vivo, we repurposed microarray datasets to select 600 highly expressed lncRNAs in non-small-cell lung cancer and designed two schemes for lncRNA deletion with~20 paired-sgRNAs for each lncRNA. Through Golden-Gate assembly, we generated a pooled CRISPR-based library with a total of 12,878 sgRNA pairs. Results: Over 80% of paired-sgRNAs were recovered from final pooled library with a relatively even distribution. Cleavage efficiency of sgRNA pairs was validated through experiments of transient transfection and viral infection. Moreover, randomly selected paired-sgRNAs showed that efficient deletion of genomic DNA could be achieved with a deletion size within the range of 500 to 3000 bp. Conclusions: In summary, we have demonstrated a strategy to design and construct a pooled paired-sgRNA library to generate genomic deletion in the lncRNA regions, validated their deletion efficiency and explored the relationship of deletion efficiency with respect to deletion size. This method would be also suitable for investigation of other uncharacterized non-coding genomic regions in mammalian cells in an efficient and cost-effective manner.Author summary: The CRISPR/Cas9 system has shown great potential in functional genomic screening, especially for protein-coding genes. However, it is challenging to apply the similar strategy to study non-coding genomic elements, because short insertions or deletions may not be sufficient to generate loss-of-function phenotypes. In this paper, we proposed a strategy to design and construct a CRISPR-based paired-sgRNA library for chromosomal deletions of lncRNA loci in mammalian cells and confirm the cleavage efficiency through experiments. This approach demonstrates a simple and scalable tool for genome-wide functional study of non-coding elements in mammalian cells. # Present address: Zhejiang

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Study on expression of lncRNA RGMB-AS1 and repulsive guidance molecule b in non-small cell lung cancer

Cited by 23 publications

References 38 publications

Long non-coding RNA FOXF1 adjacent non-coding developmental regulatory RNA inhibits growth and chemotherapy resistance in non-small cell lung cancer

Long non-coding RNA FOXF1 adjacent non-coding developmental regulatory RNA inhibits growth and chemotherapy resistance in non-small cell lung cancer

Long Non-Coding RNA XLOC_008466 Functions as an Oncogene in Human Non-Small Cell Lung Cancer by Targeting miR-874

Construction of a CRISPR‐based paired‐sgRNA library for chromosomal deletion of long non‐coding RNAs

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