The long intergenic non-protein coding RNA 707 promotes proliferation and metastasis of gastric cancer by interacting with mRNA stabilizing protein HuR

Xie, Min; Ma, Tianshi; Xue, Jiangyang; Ma, Hongwei; Sun, Ming; Zhang, Zhihong; Liu, Minjuan; Liu, Yinghua; Ju, Shaoqing; Wang, Zhaoxia; De, Wei

doi:10.1016/j.canlet.2018.11.032

Cited by 82 publications

(100 citation statements)

References 46 publications

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“…The VAV family of guanine nucleotide exchange factors participates in numerous important pathological processes, including oncogenesis and cell transformation. Recent studies showed that VAV3 expression is increased in breast, prostate, and colorectal cancer [25][26][27], and VAV3 promoted cell metastasis in gastric cancer [28]. Consistent with this, we also found that VAV3 was upregulated in NSCLC, and its knockdown inhibited NSCLC cell invasion.…”

Section: Discussionsupporting

confidence: 90%

Up-regulated LINC01234 promotes non-small-cell lung cancer cell metastasis by activating VAV3 and repressing BTG2 expression

Chen

et al. 2020

J Hematol Oncol

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Background: Long noncoding RNAs (lncRNAs) are known to regulate tumorigenesis and cancer progression, but their contributions to non-small-cell lung cancer (NSCLC) metastasis remain poorly understood. Our previous and other studies have revealed the involvement of upregulated LINC01234 in regulating gastric cancer and colon cancer cells proliferation, and we aimed to investigate whether LINC01234 overexpression also contribute to cancer cells metastasis in this study. Methods:We collect the NSCLC tissues and adjacent non-tumor tissues and analyzed expression levels of LINC01234 by quantitative reverse-transcription PCR. LINC01234 were knocked down by using siRNAs or shRNAs, and overexpressed by transfection with overexpression vector; RNA levels of miRNA were downregulated or upregulated with inhibitors or mimics. Transwell assays were used to evaluate cell migration and invasive ability; in vivo metastasis experiments were performed to investigate the effect of LINC01234 on NSCLC cells metastasis. Luciferase reporter, RIP, and ChIP assays were used to determine the regulation of LINC01234 on its targets.Results: LINC01234 expression is increased in NSCLC tissues, and its upregulation is associated with metastasis and shorter survival in NSCLC. Downregulation of LINC01234 impairs cell migration and invasion in vitro, and inhibits cells metastasis in vivo by acting as a competing endogenous RNA for the miR-340-5p and miR-27b-3p. LINC01234 also interacts with the RNA-binding proteins LSD1 and EZH2, leading to histone modification and transcriptional repression of the anti-proliferative genes BTG2. Conclusions: Taken together, our findings identify two oncogenic regulatory axes in NSCLC centering on LINC01234: one involving miR-340-5p/miR-27b-3p in the cytoplasm and the second involving EZH2, LSD1, and BTG2 in the nucleus. Our study indicates that these genes may be targeted to reduce or prevent NSCLC metastasis.

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Section: Discussionsupporting

confidence: 90%

Up-regulated LINC01234 promotes non-small-cell lung cancer cell metastasis by activating VAV3 and repressing BTG2 expression

Chen

et al. 2020

J Hematol Oncol

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“…The procedures were shown as 95 °C for 10 min, 35 cycles of 95 °C for 15 s, 60 °C for 30 s and 72 °C for 45 s. The primers used were listed in Table 1. 2 −ΔΔCt method was used for the normalization of gene expression levels, where ΔΔCt = ΔCt (experiment) − ΔCt (control) , and ΔCt = Ct (target gene) − Ct (internal reference) [16].…”

Section: Qrt-pcrmentioning

confidence: 99%

A long non-coding RNA LINC00461-dependent mechanism underlying breast cancer invasion and migration via the miR-144-3p/KPNA2 axis

et al. 2020

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Background: The purpose of this study was to explore the regulatory mechanism of the long non-coding RNA (lncRNA) LINC00461 underlying the breast cancer invasion and migration via the miR-144-3p/KPNA2 axis. Methods: Bioinformatics methods were applied to screen differentially expressed mRNAs, miRNAs and lncRNAs for construction of a competing endogenous RNA (ceRNA) network. LINC00461, KPNA2 and miR-144-3p were identified, and KPNA2 was predicted to be a target of miR-144-3p and significantly correlated with breast cancer prognosis. To make the findings more convincible, we used qRT-PCR to detect the expression levels of LINC00461 and miR-144-3p in breast cancer cells, and conducted western blot to determine KPNA2 protein level. Then, RIP was performed to assess the combination between miR-144-3p and LINC00461 or KPNA2, and dual-luciferase reporter assay was used to validate the targeted relationship between miR-144-3p and KPNA2. Furthermore, Transwell was employed for the examination of cell invasion and migration in breast cancer. Results: LINC00461 was predicted to regulate KPNA2 through sponging miR-144-3p as revealed by the ceRNA network. Besides, LINC00461 and KPNA2 were found to be remarkably highly-expressed in breast cancer cells, while miR-144-3p was poorly-expressed. Silencing LINC00461 could promote miR-144-3p expression, thus inhibiting cell invasion and migration. In addition, KPNA2 was confirmed to be a direct target of miR-144-3p. Silencing miR-144-3p or overexpressing KPNA2 could reverse the inhibitory effect of LINC00461 silencing on cell invasion and migration in breast cancer. Conclusion: LINC00461 promoted the expression of KPNA2 by competitively binding to miR-144-3p, thereby promoting the invasion and migration of breast cancer cells.

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“…The PCR program was designed as follows: 95 ℃ for 2 min, followed by 40 cycles at 94 ℃ for 20 s, 60 ℃ for 20 s, and 72 ℃ for 30 s. The primer sequences are shown in Table 1. The relative transcription level of each target gene was calculated by the relative quantitative method (2 -△△CT method) [28].…”

Section: Qrt-pcr Analysismentioning

confidence: 99%

Transcription Factor FOXK1 Regulates the lncRNA NEAT1 to Promote Glioma Development Through Mediating KDM3A

Liu¹,

Wu²,

Wu³

et al. 2020

Preprint

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Background: Long noncoding RNAs are widely studied in glioma. However, the role of the lncRNA NEAT1 and KDM3A in glioma has not yet been reported. We aimed to reveal the role of these two lncRNAs in the development of glioma through this study.Methods: Samples from glioma patients and normal brain tissues were collected, and the expression of NEAT1 was detected by qRT-PCR. A dual-luciferase reporter gene assay, chromatin immunoprecipitation (ChIP), RNA-binding protein immunoprecipitation (RIP), and RNA pulldown experiments were used to identify the relationship between FOXK1, NEAT1, miR-128, and KDM3A. The CCK8 assay, Transwell assay and flow cytometry were used to detect cell viability, invasion and migration ability, and the cell cycle and apoptosis, respectively. Tumor formation experiments verified the effect of NEAT1 on gliomas in vivo.Results: FOXK1 and NEAT1 were significantly overexpressed in glioma tissues and cells, and NEAT1 was significantly related to WHO classification. FOXK1 bound the NEAT1 gene promoter region in glioma cells, and interference with FOXK1 inhibited NEAT1 expression. NEAT1 inhibited miR-128 expression by binding miR-128; significantly improved cell viability and invasion and migration capabilities; increased the expression of KDM3A and activated the Wnt signaling pathway. Interference with KDM3A reversed the above results. In addition, interference with NEAT1 decreased KDM3A expression and inhibited tumor growth.Conclusion: Interference with NEAT1 promoted the expression of miR-128, thereby suppressing the expression of KDM3A and inhibiting the occurrence and development of glioma, while the expression of NEAT1 was shown to be regulated by the upstream transcription factor FOXK1.

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The long intergenic non-protein coding RNA 707 promotes proliferation and metastasis of gastric cancer by interacting with mRNA stabilizing protein HuR

Cited by 82 publications

References 46 publications

Up-regulated LINC01234 promotes non-small-cell lung cancer cell metastasis by activating VAV3 and repressing BTG2 expression

Up-regulated LINC01234 promotes non-small-cell lung cancer cell metastasis by activating VAV3 and repressing BTG2 expression

A long non-coding RNA LINC00461-dependent mechanism underlying breast cancer invasion and migration via the miR-144-3p/KPNA2 axis

Transcription Factor FOXK1 Regulates the lncRNA NEAT1 to Promote Glioma Development Through Mediating KDM3A

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