Long noncoding RNA SNHG7 accelerates prostate cancer proliferation and cycle progression through cyclin D1 by sponging miR-503

Qi, Honggang; Wen, Bifeng; Wu, Qihang; Cheng, Wei; Lou, Jiangyong; Wei, Junjun; Huang, Jianjun; Yao, Xuping; Weng, Guobin

doi:10.1016/j.biopha.2018.03.011

Cited by 75 publications

(55 citation statements)

References 26 publications

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“…For example, HOT-TIP, MALAT1 and MEG3 are regarded as important regulators of tumor progression [7]. Small nucleolar RNA host gene 7 (SNHG7), a lncRNA located on chromosome 9q34.3 with a length of 2157 bp, is a novel identified oncogenic gene functioning in different types of human cancers, including breast cancer, bladder cancer, colorectal cancer and prostate cancer [8][9][10][11]. However, little is known about the role of SNHG7 in PC.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA SNHG7 promotes pancreatic cancer proliferation through ID4 by sponging miR-342-3p

Cheng

Fan²,

et al. 2019

Cell Biosci

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Background: Small nucleolar RNA host gene 7 (SNHG7) is a novel identified oncogenic gene in tumorigenesis. However, the role that SNHG7 plays in pancreatic cancer (PC) remains unclear. In this study, we aimed to investigate the functional effects of SNHG7 on PC and the possible mechanism. Methods: The expression levels of SNHG7 in tissues and cell lines were measured by RT-qPCR. Cell viability, apoptosis, migration and invasion were examined to explore the function of SNHG7 on PC. Bioinformatics methods were used to predict the target genes. The mechanism was further investigated by transfection with specific si-RNA, miRNA mimics or miRNA inhibitor. Tumor xenograft was carried out to verify the effects of SNHG7 in vivo. Results: We found that SNHG7 was overexpressed in both PC tissues and cell lines. High expression level of SNHG7 was correlated with the poor prognosis. SNHG7 knockdown inhibited the proliferation, migration and invasion of PC cells. Moreover, SNHG7 was found to regulate the expression of ID4 via sponging miR-342-3p. Additionally, this finding was supported by in vivo experiments. Conclusions: LncRNA SNHG7 was overexpressed in PC tissues, and knockdown of SNHG7 suppressed PC cell proliferation, migration and invasion via miR-342-3p/ID4 axis. The results indicated that SNHG7 as a potential target for clinical treatment of PC.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA SNHG7 promotes pancreatic cancer proliferation through ID4 by sponging miR-342-3p

Cheng

Fan²,

et al. 2019

Cell Biosci

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“…Various studies have pointed out that lncRNA-SNHG7 is highly expressed in various malignant tumors and is a potential molecular marker. Qi et al (27) indicated that through miR-503/cyclin D1 pathway, lncRNA-SNHG7 promoted the development of prostate cancer. Colorectal cancer patients with high expression of lncRNA-SNHG7 had a significantly poor prognosis (28).…”

Section: Univariate Analysis Multivariate Analysis ------------------mentioning

confidence: 99%

High expression of lncRNA-SNHG7 is associated with poor prognosis in hepatocellular carcinoma

Shen

et al. 2020

Oncol Lett

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Expression of long non-coding RNA SNHG7 (lncRNA-SNHG7) and its clinical significance in hepatocellular carcinoma (HCC) were explored. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression level of lncRNA-SNHG7 in cancer tissues. Kaplan-Meier curves and multivariate Cox proportional models were used to study the impact on clinical outcome. Expression of lncRNA-SNHG7 was much higher in cancer tissues than that in para-cancer tissues. The lncRNA-SNHG7 expression was correlated with tumor number, lymph node metastasis and clinical stage (P<0.05). In addition, HCC patients with higher lncRNA-SNHG7 expression had significantly poorer progression-free survival time and overall survival time (P<0.001). Both univariate analysis and multivariate analysis indicated that high expression of lncRNA-SNHG7 was an independent predictor of poor prognosis in HCC. LncRNA-SNHG7 might contribute to the development of HCC and serve as a clinical biomarker and a therapeutic target for HCC patients.

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“…Until now, SNHG7 has been recognized as an essential biomarker in different cancers. For instance, abundance of SNHG7 expression has been reported to expedite cell cycle and proliferation in prostate cancer via absorbing miR‐503 to enhance cyclin D1 . In addition, in the study by Sun et al .…”

Section: Discussionmentioning

confidence: 98%

Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis

et al. 2019

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Background: Non-small cell lung cancer (NSCLC) is an intractable malignant lung cancer with high rates of metastasis and mortality. Currently, long noncoding RNA nuclear RNA host gene 7 (SNHG7) is recognized as a biomarker of multiple cancers. However, the role of SNHG7 in NSCLC requires further understanding. Methods: The expression of SNHG7, miR-449a and TGIF2 in NSCLC tumors and cells was examined by quantitative real time polymerase chain reaction (qRT-PCR). Cell viability was measured by MTT assay. Cell migration and invasion was conducted using transwell assay. Protein expression of TGIF2, vimentin, N-cadherin and E-cadherin was detected by western blot. The interaction between miR-449a and SNHG7 or TGIF2 was determined by luciferase reporter system, RIP and RNA pull-down assay, respectively. Xenograft mice models were established by subcutaneously injecting A549 cells transfected with sh-SNHG7 and sh-control. Results: SNHG7 expression was upregulated in NSCLC tumors and cells compared with normal tissues and cells. SNHG7 silencing repressed cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) in NSCLC. Consistently, SNHG7 knockdown hindered tumor growth in vivo. The subsequent luciferase reporter system, RIP and RNA pull-down assay validated the interaction between miR-449a and SNHG7 or TGIF2. The rescue experiments displayed that miR-449a inhibitor counteracted SNHG7 silencing induced inhibition on proliferation, migration, invasion and EMT. Similarly, restoration of TGIF2 reversed miR-449a mediated inhibition on cell progression. In addition, the results indicated that SNHG7 could regulate cell progression by targeting miR-449a/TGIF2 axis. Conclusion: SNHG7 contributed to cell proliferation, migration, invasion and EMT in NSCLC by upregulating TGIF2 via sponging miR-449a, representing a novel targeted therapy method for NSCLC.

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Long noncoding RNA SNHG7 accelerates prostate cancer proliferation and cycle progression through cyclin D1 by sponging miR-503

Cited by 75 publications

References 26 publications

RETRACTED ARTICLE: LncRNA SNHG7 promotes pancreatic cancer proliferation through ID4 by sponging miR-342-3p

RETRACTED ARTICLE: LncRNA SNHG7 promotes pancreatic cancer proliferation through ID4 by sponging miR-342-3p

High expression of lncRNA-SNHG7 is associated with poor prognosis in hepatocellular carcinoma

Long noncoding RNA SNHG7 contributes to cell proliferation, migration, invasion and epithelial to mesenchymal transition in non‐small cell lung cancer by regulating miR‐449a/TGIF2 axis

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