Long non‐coding RNA SNHG6 promotes the growth and invasion of non‐small cell lung cancer by downregulating miR‐101‐3p

Li, Ké; Jiang, Yongxin; Xiang, Xudong; Gong, Quan; Zhou, Chunyan; Zhang, Lijuan; Ma, Qianli; Li, Zhuang

doi:10.1111/1759-7714.13371

Cited by 18 publications

(22 citation statements)

References 24 publications

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“…Several studies have reported that SNHG6 sponges miR-101-3p-3p to modulate cancer progression. For example, Li et al ( 32 ) revealed that lncRNA SNHG6 contributed to the proliferation of non-small cell lung cancer cells by sponging miR-101-3p. Meng et al ( 33 ) also reported that SNHG6 accelerated glioma development via downregulating miR-101-3p, while Chang et al ( 34 ) indicated that SNHG6 modulated zinc finger E-box binding homeobox 1 expression by binding to miR-101-3p in hepatocellular carcinoma.…”

Section: Discussionmentioning

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

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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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Section: Discussionmentioning

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

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“…Meng et al found that SNHG6 also upregulates in glioma tissues and cells compared with normal brain tissues and cells [43]. In their research, SNHG6 promotes glioma cell Wang et al [10] Cancer Cell Inter Li et al [36] Thorac cancer…”

Section: Gliomamentioning

confidence: 99%

“…Silencing SNHG6 expression repressed cell growth and invasion in vitro and in vivo. Mechanically, SNHG6 was identified to regulate CDYL expression by acting as a sponge of miR-101-3p [36]. More than that, Liang et al found that SNHG6 expression is higher in lung adenocarcinoma (LAOD) tissues than in adjacent non-tumor tissues, and its overexpression is related to tumor development and poor survival in patients.…”

Section: Lung Cancer (Lc)mentioning

confidence: 99%

Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors

et al. 2020

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Increased expression of the small nucleolar RNA host gene 6 (SNHG6) has been reported in different cancers, such as hepatocellular carcinoma, colorectal cancer, and lung cancer. The high expression level of SNHG6 is associated with tumor progression and poor prognosis. This paper provides an overview of recent studies on the oncogenic role and potential clinical utilities of SNHG6. Upregulated SNHG6 arrests tumor cell cycle and reduces apoptosis but promotes migration, invasion, metastasis, epithelial-mesenchymal transition (EMT), and chemoresistance in tumors. Mechanically, SNHG6 primarily sponges tumor suppressor microRNA (miRNA), functioning as a competing endogenous RNA. Once sponged, miRNA is unable to degrade, silence, or hamper the translation of its downstream, mostly oncogenic genes, ultimately driving cancer-related processes. Thus, SNHG6 might serve as a biomarker for cancer diagnosis and prognosis.

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“…8 LncRNA SNHG6 overexpression facilitates lung cancer cell proliferation and metastasis. 9 MiR-340-5p dysregulation promotes tumorigenesis of esophageal squamous cell carcinoma. 10 In addition, miR-126 suppresses colon cancer cell survival and induces apoptosis.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

Du¹,

Liu²,

Tian³

et al. 2020

CMAR

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Background: Glioma is one of the leading causes of cancer-related deaths. This study aimed to investigate the function and mechanism of long noncoding RNA (lncRNA) LINC00173 in the regulation of glioma progression. Methods: LINC00173 expression was measured using qRT-PCR. Survival rate was analyzed through Kaplan-Meier method. CCK8, colony formation and EdU assays were performed to measure cell proliferation while transwell was used to determine cell migration and invasion. Luciferase reporter assay was conducted to test RNA interaction. Results: LINC00173 expression was elevated in glioma tissues and cells. LINC00173 high expression predicted poor prognosis. Loss of LINC00173 inhibited proliferation, migration and invasion. LINC00173 interacted with miR-765 to enhance NUTF2 expression. MiR-765 expression was negatively correlated with LINC00173 and NUTF2 in glioma tissues. NUTF2 level was increased in glioma tissues. NUTF2 overexpression rescued the potential of proliferation, migration and invasion in LINC00173-silenced cells. Conclusion: Our research demonstrated that LINC00173 promotes glioma progression through targeting miR-765/NUTF2 axis.

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Long non‐coding RNA SNHG6 promotes the growth and invasion of non‐small cell lung cancer by downregulating miR‐101‐3p

Cited by 18 publications

References 24 publications

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

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

Long noncoding RNA SNHG6 mainly functions as a competing endogenous RNA in human tumors

<p>Long Noncoding RNA LINC00173 Promotes NUTF2 Expression Through Sponging miR-765 and Facilitates Tumorigenesis in Glioma</p>

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