Long intergenic non-protein coding RNA 00858 functions as a competing endogenous RNA for miR-422a to facilitate the cell growth in non-small cell lung cancer

Zhu, Shirley; Wang, Junyu; Wang, Xianguo; Zhao, Jinping

doi:10.18632/aging.101171

Cited by 51 publications

(38 citation statements)

References 36 publications

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“…6,[22][23][24][25] As we have mentioned that LOC100129148 promotes nasopharyngeal carcinoma progression by targeting miR-539-5p, 9 lncRNA EWSAT1 promotes nasopharyngeal cancer development by targeting miR-326/-330-5p 10 and LncRNA 00858 acts as an ceRNA of miR-422a in non-samll cell lung cancer. 11 In this study, we notified that the expression level of microRNA-26a was negatively correlated with the expression level of DLX6-AS1 in RCC tissue samples. This result suggested that DLX6-AS1 may work as a ceRNA to sponge miR-26a in RCC cells.…”

Section: Discussionmentioning

confidence: 83%

“…5 It has been wildly investigated that lncRNAs modulate many types of tumor progression. [6][7][8] For example, lncRNA LOC100129148 and EWSAT1 have been reported to act as oncogenic role in nasopharyngeal carcinoma, 9,10 lncRNA 00858 functions as a competing endogenous RNA for miR-422a to facilitate the cell growth in non-small cell lung cancer 11 and Increased expression of long-noncoding RNA ZFAS1 is associated with epithelial-mesenchymal transition of gastric cancer. 12 It also has been reported that high DLX6-AS1 expression levels were significantly associated with both histological differentiation and TNM stage of lung cancer.…”

Section: Introductionmentioning

confidence: 99%

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Long noncoding RNA DLX6-AS1 promotes renal cell carcinoma progression via miR-26a/PTEN axis

Zeng

et al. 2017

Cell Cycle

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Recently, long non-coding RNAs (lncRNAs) have emerged as new gene regulators and prognostic markers in several types of cancer, including renal cell carcinoma (RCC). In this study, we identified an upregulated lncRNA, DLX6-AS1, in RCC tumor tissues compared with normal kidney tissues. Our data suggested that DLX6-AS1 promoted RCC cell growth and tumorigenesis via targeting miR-26a. In addition, we observed that PTEN overexpression restored the renal cancer cell growth and also rescued the RCC tumorigenesis. In summary, we conclude that DLX6-AS1 promotes renal cell carcinoma development via regulation of miR-26a/PTEN axis.

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Section: Discussionmentioning

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA DLX6-AS1 promotes renal cell carcinoma progression via miR-26a/PTEN axis

Zeng

et al. 2017

Cell Cycle

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“…LncRNA LINC00858 (LINC00858), a newly identified lncRNA, is locates in 10q23.1. Recently, the dysregulation of LINC00858 has been reported in two tumours, including osteosarcoma and lung cancer [19,20]. In addition, in these two tumours, LINC00858 played a positive regulator.…”

Section: Introductionmentioning

confidence: 98%

Long non-coding RNA LINC00858 promotes cells proliferation, migration and invasion by acting as a ceRNA of miR-22-3p in colorectal cancer

Sha¹,

Chen²,

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Though long non-coding RNA LINC00858 (LINC00858) has been shown to be involved in tumours of other tissues, its involvement in colorectal cancer (CRC) is still unknown. We aimed to investigated expression and mechanism LINC00858 in human CRC. In this study, we firstly found that LINC00858 expression was significantly up-regulated in both CRC tissues and cell lines by both online data and RT-PCR assay. Then, clinical assay revealed that high LINC00858 expression was significantly associated with advanced clinical progression and poor prognosis. Multivariate analysis demonstrated that high LINC00858 expression was an independent poor prognostic factor for CRC patients. Moreover, lost-offunction assay indicated that knockdown of LINC00858 suppressed CRC cells proliferation, migration and invasion, and promoted apoptosis. Mechanistically, bioinformatics analysis, dual-luciferase reporter assays, and western blot assays showed that LINC00858 functioned as competing endogenous RNA to repress miR-22-3p, which controlled its downstream target YWHAZ. Then, we suggested that LINC00858 exerted its function through the miR-22-3p/YWHAZ axis. To our knowledge, this is the first report which showed the role of LINC00858 in the progression of CRC. Our findings indicated that LINC00858 played an important role in CRC, and may serve as a novel prognostic factor and therapeutic target.

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“…Increased LINC00858 expression was reported in non-small cell lung cancer, and its upregulation significantly enhanced non-small cell lung cancer cell proliferation, migration and invasion. Upregulated LINC00858 expression was identified to be closely linked to the progression of non-small cell lung cancer (21). Another study indicated that the expression level of LINC00858 in lung adenocarcinoma was 5.23 times that in normal lung tissues (22).…”

Section: Discussionmentioning

confidence: 99%

LINC00858 promotes retinoblastoma cell proliferation, migration and invasion by inhibiting miR‑3182

et al. 2019

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The aim of the present study was to determine the role of long intergenic non-protein coding RNA 858 (LINC00858) in retinoblastoma (RB) and investigate the underlying molecular mechanisms. RB tissues and paracancerous tissues of 27 RB cases were obtained. RB cell lines (SO-RB50, Y79, HXO-RB44 and WERI-Rb1) and a normal retinal epithelial cell line (ARPE-19) were cultured for in vitro experiments. Batches of SO-RB50 and Y79 cells were assigned to groups transfected with small interfering RNA targeting LINC00858 (si-LINC00858 group), microRNA (miR)-3182 mimics or inhibitor, or the respective controls. A Cell Counting Kit-8 and Transwell assays were performed to assess the effect of the transfections on the proliferation, migration and invasion of SO-RB50 and Y79 cells. A luciferase reporter assay was performed using SO-RB50 cells to demonstrate the direct binding of LINC00858 and miR-3182. Reverse transcription-quantitative PCR was employed to detect LINC00858 and miR-3182 expression. Pearson correlation analysis was used to assess the correlation between the expression of LINC00858 and miR-3182. The results indicated that RB tissues and cells exhibited aberrantly elevated LINC00858 expression (P<0.05). Compared with those in the control-transfected group, SO-RB50 and Y79 cells of the si-LINC00858 group had a lower cell proliferation, as well as a lower number of migrated and invaded cells (all P<0.05). miR-3182 was proven to be a target gene of LINC00858, to be abnormally downregulated in RB tissues and cells (P<0.05) and to be negatively correlated with LINC00858 expression. Compared with those in the si-LINC00858 + inhibitor-negative control group, SO-RB50 and Y79 cells of the si-LINC00858 + miR-3182 inhibitor group exhibited a significantly higher relative proliferation, migration and invasion (all P<0.05). In conclusion, LINC00858 promoted RB cell proliferation, migration and invasion, at least partially by inhibiting miR-3182.

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Long intergenic non-protein coding RNA 00858 functions as a competing endogenous RNA for miR-422a to facilitate the cell growth in non-small cell lung cancer

Cited by 51 publications

References 36 publications

Long noncoding RNA DLX6-AS1 promotes renal cell carcinoma progression via miR-26a/PTEN axis

Long noncoding RNA DLX6-AS1 promotes renal cell carcinoma progression via miR-26a/PTEN axis

Long non-coding RNA LINC00858 promotes cells proliferation, migration and invasion by acting as a ceRNA of miR-22-3p in colorectal cancer

LINC00858 promotes retinoblastoma cell proliferation, migration and invasion by inhibiting miR‑3182

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