Long noncoding RNA SNHG6 promotes proliferation and angiogenesis of cholangiocarcinoma cells through sponging miR-101-3p and activation of E2F8

Wang, Huishan; Wang, Li; Tang, Ling-Yu; Ji, Hao; Zhang, Wen; Zhou, Jian; Li, Quanpeng; Ma, Lin

doi:10.7150/jca.40592

Cited by 24 publications

(23 citation statements)

References 38 publications

(35 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous study also showed that SNHG6 promoted the proliferation and angiogenesis of cholangiocarcinoma cells by sponging miR-101-3p. 27 These results confirmed that SNHG6 affects apoptosis in ESCC cells by regulating miR-101-3p expression.…”

Section: Dovepresssupporting

confidence: 67%

“…MiR-101-3p serves as a tumor suppressor gene in a variety of tumors including colorectal cancer, 18 gastric cancer, 26 and cholangiocarcinoma. 27 In the current study, we showed that miR-101-3p function as a tumor suppressor gene in ESCC. To confirm that SNHG6 affected apoptosis in ESCC cells by inhibiting miR-101-3p expression, we co-transfection si-SNHG6 and a miR-101-3p inhibitor and found that downregulation of miR-101-3p reversed its effects on apoptosis in SNHG6 knockdown cells.…”

Section: Dovepressmentioning

confidence: 56%

See 1 more Smart Citation

<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

Wang

Yang

et al. 2020

OTT

View full text Add to dashboard Cite

Background: The long non-coding RNA (lncRNA) SNHG6 was significantly upregulated in esophageal squamous-cell carcinoma (ESCC), and it promoted ESCC cell proliferation, invasion, and migration. However, the effects of SNHG6 on cell apoptosis and the corresponding underlying mechanisms have not yet reported. Methods: Apoptosis was detected by flow cytometric analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were used for mRNA and protein quantification, respectively. A luciferase reporter assay was performed to verify downstream target genes for SNHG6 and miR-101-3p. Results: Dysregulation of SNHG6 inhibited apoptosis in ESCC cells and regulated the expression of apoptosis-related proteins such as Bcl-2, Mcl-1, Bax and Caspase-3. Functionally, miR-101-3p could compete binding with 3′-untranslated region of SNHG6 and downregulation of miR-101-3p reversed its effect on cell apoptosis in SNHG6 knockdown cells. EZH2 was confirmed as a downstream target gene of miR-101-3p, silencing EZH2 expression had the same effect on apoptosis and protein expression as knocking down SNHG6. Overexpression of EZH2 reversed the effects of miR-101-3p overexpression on cell apoptosis in ESCC cells. Conclusion: In this study, we found that upregulation of the lncRNA SNHG6 inhibited apoptosis via miR-101-3p/EZH2 axis in ESCC. These findings may contribute to the diagnosis and treatment of ESCC.

show abstract

Section: Dovepresssupporting

confidence: 67%

Section: Dovepressmentioning

confidence: 56%

<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

Wang

Yang

et al. 2020

OTT

View full text Add to dashboard Cite

show abstract

“…For example, SNHG6 acts as an oncogene to promote the tumorigenesis and development of colorectal cancer ( 10 ). Furthermore, SNHG6 promotes cholangiocarcinoma (CCA) cell progression, and its upregulation is associated with poor overall survival in patients with CCA ( 11 ). SNHG6 facilitates the proliferation and invasion of breast cancer cells by sponging microRNA (miRNA/miR)-26a and by upregulating vasodilator stimulated phosphoprotein expression ( 12 ).…”

Section: Introductionmentioning

confidence: 99%

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

Zhou

Wang

et al. 2020

Oncol Lett

View full text Add to dashboard Cite

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.

show abstract

“…Recently, lncRNA SNHG6 and DANCR were identified to accelerate angiogenesis in cholangiocarcinoma by competitively binding miRNAs, thus leading to an increased expression of transcriptional factors [ 135 , 137 ]. In detail, SNHG6 binds miR-101-3p to prevent the inhibition of the transcription of E2F Transcription Factor 8 (E2F8) [ 137 ], whereas the DANCR–miR-345-5p interaction upregulates Twist1. In osteosarcoma, proangiogenic lncRNA TUG1 functions via silencing miR-143-5p, increasing the miRNA target HIF-1α [ 139 ].…”

Section: Lncrnas Regulating Tumor Angiogenesis In Different Cancermentioning

confidence: 99%

Involvement of Long Non-Coding RNAs (lncRNAs) in Tumor Angiogenesis

Teppan

Barth

Prinz

et al. 2020

ncRNA

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) are defined as non-protein coding transcripts with a minimal length of 200 nucleotides. They are involved in various biological processes such as cell differentiation, apoptosis, as well as in pathophysiological processes. Numerous studies considered that frequently deregulated lncRNAs contribute to all hallmarks of cancer including metastasis, drug resistance, and angiogenesis. Angiogenesis, the formation of new blood vessels, is crucial for a tumor to receive sufficient amounts of nutrients and oxygen and therefore, to grow and exceed in its size over the diameter of 2 mm. In this review, the regulatory mechanisms of lncRNAs are described, which influence tumor angiogenesis by directly or indirectly regulating oncogenic pathways, interacting with other transcripts such as microRNAs (miRNAs) or modulating the tumor microenvironment. Further, angiogenic lncRNAs occurring in several cancer types such as liver, gastrointestinal cancer, or brain tumors are summarized. Growing evidence on the influence of lncRNAs on tumor angiogenesis verified these transcripts as potential predictive or diagnostic biomarkers or therapeutic targets of anti-angiogenesis treatment. However, there are many unsolved questions left which are pointed out in this review, hence driving comprehensive research in this area is necessary to enable an effective use of lncRNAs as either therapeutic molecules or diagnostic targets in cancer.

show abstract

Long noncoding RNA SNHG6 promotes proliferation and angiogenesis of cholangiocarcinoma cells through sponging miR-101-3p and activation of E2F8

Cited by 24 publications

References 38 publications

<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

<p>LncRNA SNHG6 Inhibits Apoptosis by Regulating EZH2 Expression via the Sponging of MiR-101-3p in Esophageal Squamous-Cell Carcinoma</p>

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

Involvement of Long Non-Coding RNAs (lncRNAs) in Tumor Angiogenesis

Contact Info

Product

Resources

About