Long non-coding RNA AFAP1-AS1 accelerates the progression of melanoma by targeting miR-653-5p/RAI14 axis

Liu, Fei; Hu, Lan-ting; Pei, Yi; Zheng, Ke; Wang, Wei; Li, Shenglong; Qiu, Enduo; Shang, Guanning; Zhang, Jiaming; Zhang, Xiaojing

doi:10.1186/s12885-020-6665-2

Cited by 37 publications

(30 citation statements)

References 33 publications

(37 reference statements)

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“…7 Accumulating evidence suggests that lncRNAs execute critical roles in regulating pathological and physiological behaviors of cancer cells. [8][9][10][11] During cancer genesis and progression, cancerinhibiting and cancer-promoting cellular pathways are regulated by lncRNAs via direct or indirect effects, including gene expression regulation, chromatin remodeling, posttranscriptional modulation, and translational regulation. 12 Recent evidence has revealed the dysregulation of lncRNAs in breast cancer and has shown that aberrantly expressed lncRNAs are implicated in breast cancer pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Long Intergenic Non-Coding RNA LINC00922 Aggravates the Malignant Phenotype of Breast Cancer by Regulating the microRNA-424-5p/BDNF Axis

Yue¹,

Wang²

2020

CMAR

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Long intergenic non-coding RNA 922 (LINC00922) plays a critical role in the progression of lung cancer. In this study, we aimed to quantify LINC00922 expression in breast cancer and determine its influence on the malignant behavior of breast cancer cells in vitro and in vivo. We also investigated the mechanism by which LINC00922 affects the progression of breast cancer. Materials and Methods: Reverse transcription-quantitative polymerase chain reaction was performed to quantify LINC00922 expression in breast cancer tissues and cell lines. The cell counting kit-8 assay, flow cytometry, Transwell migration and invasion assays, and tumor model assays were performed to determine the effects of LINC00922 deficiency on breast cancer cell proliferation, apoptosis, migration and invasion in vitro, and tumor growth in vivo, respectively. Furthermore, bioinformatics analysis was performed to predict the potential target microRNA of LINC00922. The prediction was further evaluated using luciferase reporter and RNA immunoprecipitation assays. Results: LINC00922 was clearly overexpressed in breast cancer tissues and cell lines. LINC00922 depletion restricted breast cancer cell proliferation, migration, and invasion but induced cell apoptosis in vitro. Additionally, its knockdown evidently repressed tumor growth of breast cancer cells in vivo. Mechanistically, LINC00922 was demonstrated to serve as a molecular sponge for miR-424-5p in breast cancer cells. Furthermore, brainderived neurotrophic factor (BDNF) was verified as a direct target of miR-424-5p in breast cancer cells, and BDNF expression was found to be positively regulated by LINC00922 through sponging miR-425-5p. Rescue experiments further revealed that the influences on breast cancer cell proliferation, apoptosis, migration, and invasion induced by LINC00922 silencing were abrogated by increasing the output of the miR-424-5p/BDNF axis. Conclusion: The LINC00922/miR-424-5p/BDNF pathway is implicated in the acceleration of the malignant behavior of breast cancer cells. These findings suggest that this pathway is a promising novel molecular target in breast cancer therapy.

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Section: Introductionmentioning

confidence: 99%

Long Intergenic Non-Coding RNA LINC00922 Aggravates the Malignant Phenotype of Breast Cancer by Regulating the microRNA-424-5p/BDNF Axis

Yue¹,

Wang²

2020

CMAR

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“…Previous studies have confirmed that lncRNAs can regulate various biological processes, such as proliferation, migration, invasion and apoptosis of melanoma cells ( 21 , 22 ). For instance, lncRNA lung adenocarcinoma associated transcript 1 expression is increased in melanoma via modulation of the miR-28-5p/RAP1B axis ( 23 ).…”

Section: Discussionmentioning

confidence: 84%

Long non‑coding RNA SNHG6 promotes tumorigenesis in melanoma cells via the microRNA‑101‑3p/RAP2B axis

Zhou

Wang

et al. 2020

Oncol Lett

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Numerous studies have reported that the long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6; ENSG00000245910) participates in the development of malignant tumors. However, the underlying mechanism of SNHG6 in the development of melanoma remains unknown. Thus, the present study aimed to investigate the biological role of SNHG6 in the progression of melanoma. SNHG6 expression in melanoma tissues and cells was assessed using a bioinformatics approach and reverse transcription-quantitative PCR analysis. Cell viability was determined using the Cell Counting Kit-8 and colony formation assays. The correlation between microRNA (miR)-101-3p, SNHG6 and RAP2B expression levels was assessed using Pearson's correlation analysis. Bioinformatic analysis and luciferase reporter assay were utilized to confirm the interaction between miR-101-3p and SNHG6 or RAP2B. The Transwell assay was conducted to examine the migratory and invasive activities of melanoma cells. In the present study, SNHG6 expression was upregulated in melanoma tissues and cell lines, and SNHG6 silencing suppressed melanoma cell viability, migration and invasion. SNHG6 was directly bound to miR-101-3p, which interacted with RAP2B. In addition, miR-101-3p expression was negatively correlated with SNHG6 or RAP2B expression. miR-101-3p silencing partially abrogated the suppressive effect of SNHG6-knockdown on RAP2B expression. Moreover, the data demonstrated that RAP2B overexpression reversed the inhibitory effects on melanoma cell proliferation, migration and invasion induced by SNHG6 silencing. In conclusion, the present study identified that SNHG6 accelerated melanoma progression via regulating the miR-101-3p/RAP2B axis. Thus, the SNHG6/miR-101-3p/RAP2B signaling pathway may be a novel therapeutic target for melanoma.

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“…4,5 Previous studies reported that lncRNAs are dysregulated in different types of cancers and have critical effects related to cancer biology. [6][7][8][9] Some lncRNAs have been reported to be closely related to liver cancer pathology, progression, prognosis, and the maintenance of cancer stem celllike properties. 10,11 For example, LINC00668 up-regulation accelerates cell proliferation, migration, and invasion of HCC via targeting miR-532-5p/YY1 axis; 12 HAGLROS is highexpressed in HCC and its high expression is correlated with the progression of HCC by affecting cell proliferation, apoptosis, and autophagy via regulating miR-5095/ATG12 axis; 13 HCC patients with high-expressed lncRNA PDZD7 tend to show a poorer prognosis; PDZD7 promotes stemness properties and inhibits chemosensitivity of HCC via regulating the miR-101/EZH2/ATOH8 pathway.…”

Section: Introductionmentioning

confidence: 99%

LncRNA CDKN2B-AS1 Promotes Cell Viability, Migration, and Invasion of Hepatocellular Carcinoma via Sponging miR-424-5p

Shen¹,

Yong²,

He³

et al. 2020

CMAR

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Objective: Hepatocellular carcinoma (HCC) results in high mortality and metastasis. In this study, the effects of long non-coding RNA (lncRNA) CDKN2B-AS1 on the progression of HCC were investigated. Materials and Methods: LncRNA CDKN2B-AS1 expression of HCC cancer and adjacent tissues, and HCC cells were detected. Subsequently, CDKN2B-AS1 was overexpressed and silenced in HCC cells to observe the effects of CDKN2B-AS1 on the cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT) of HCC cells by performing cell counting kit-8 (CCK-8), wound-healing, Transwell, and Western blot. The target gene of CDKN2B-AS1 was predicted and verified to be miR-424-5p, whose expression in HCC cells with up-or down-regulation of CDKN2B-AS1 expression was determined. Moreover, the effects of miR-424-5p on cell viability, migration, and invasion and EMT of HCC cells were investigated with miR-424-5p up-regulation or down-regulation, together with overexpression or silencing of CDKN2B-AS1. Results: CDKN2B-AS1 expression was increased in HCC tissues and cells. Silencing of CDKN2B-AS1 suppressed cell viability, migration, invasion, and EMT, while overexpression of CDKN2B-AS1 produced the opposite results. Furthermore, CDKN2B-AS1 was predicted and verified to target miR-424-5p and was confirmed to negatively modulate miR-424-5p expression. Moreover, overexpression of miR-424-5p partially suppressed the previously high cell viability, migration, and invasion, and activated EMT resulted from upregulation of CDKN2B-AS1, while silencing of miR-424-5p elevated the cellular processes inhibited by silencing the expression of CDKN2B-AS1. Conclusion: The present study revealed that high-expressed CDKN2B-AS1 may associate with the progression of HCC by affecting the cell viability, migration, invasion, and EMT of HCC cells by negatively regulating miR-424-5p.

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Long non-coding RNA AFAP1-AS1 accelerates the progression of melanoma by targeting miR-653-5p/RAI14 axis

Cited by 37 publications

References 33 publications

<p>Long Intergenic Non-Coding RNA LINC00922 Aggravates the Malignant Phenotype of Breast Cancer by Regulating the microRNA-424-5p/BDNF Axis</p>

<p>Long Intergenic Non-Coding RNA LINC00922 Aggravates the Malignant Phenotype of Breast Cancer by Regulating the microRNA-424-5p/BDNF Axis</p>

Long non‑coding RNA SNHG6 promotes tumorigenesis in melanoma cells via the microRNA‑101‑3p/RAP2B axis

<p>LncRNA CDKN2B-AS1 Promotes Cell Viability, Migration, and Invasion of Hepatocellular Carcinoma via Sponging miR-424-5p</p>

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