RETRACTED ARTICLE: LncRNA SNHG7 promotes pancreatic cancer proliferation through ID4 by sponging miR-342-3p

Cheng, Dongfeng; Fan, Juanjuan; Ma, Yang; Zhou, Yiran; Qin, Kai; Shi, Minmin; Yang, Jian

doi:10.1186/s13578-019-0290-2

Cited by 76 publications

(52 citation statements)

References 32 publications

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“…Moreover, the present study revealed that miR-342-3p was a target miRNA of circSAMd4A. miR-342-3p has been demonstrated to be involved in cellular growth in cancers, including pancreatic cancer, hepatocellular carcinoma, prostate cancer and cervical cancer (35)(36)(37)(38). Zhang et al reported that miR-342-3p was downregulated in OS tissues and inhibited cell progression by targeting AEG-1 (39).…”

Section: Discussionmentioning

confidence: 64%

CircSAMD4A regulates cell progression and epithelial‑mesenchymal transition by sponging miR‑342‑3p via the regulation of FZD7 expression in osteosarcoma

Xie

Chen

et al. 2020

Int J Mol Med

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Osteosarcoma (OS) is a primary malignant tumor with a complex etiology. Therefore, research into the pathogenesis of osteosarcoma is considered a priority. circular RNAs play important roles in cell metabolism and in the immune response and are closely associated with cancer treatment. However, research into the association of circular RNAs with osteosarcoma is limited. In the present study, circSAMd4A was validated by RT-qPcR and agarose gel electrophoresis. circSAMd4A and miR-342-3p expression was detected by RT-qPcR. The relative protein expression levels were measured by western blot analysis. MTT assay and flow cytometry were used to detect cell cytotoxicity and apoptosis, respectively. Transwell assay was applied to assess cell migration and invasion. dual-luciferase reporter assay was used to determine the association among circSAMd4A, Frizzled-7 (FZd7) and miR-342-3p. In vivo, subcutaneous tumor formation assay was performed in an experiment with nude mice. The results revealed that the expression levels of circSAMd4A and FZd7 were upregulated, while those of miR-342-3p were downregulated in OS tissues and cells. The inhibition of circSAMd4A suppressed cell progression and epithelial-mesenchymal transition (EMT), and promoted cell apoptosis in OS. The reduction of miR-342-3p reversed the effects of circSAMd4A downregulation on cell cytotoxicity, migration, invasion, apoptosis and EMT in OS, while FZd7 overexpression blocked the effect of miR-342-3p upregulation on OS progression. The suppressive effect of sh-circSAMd4A on tumor growth was thus verified in OS. Overall, the present study demonstrated that circSAMd4A affected cell cytotox-icity, invasion, apoptosis, migration and EMT by regulating the miR-342-3p/FdZ7 axis in OS, thereby providing a novel regulatory mechanism and a potential therapeutic target for OS.

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Section: Discussionmentioning

confidence: 64%

CircSAMD4A regulates cell progression and epithelial‑mesenchymal transition by sponging miR‑342‑3p via the regulation of FZD7 expression in osteosarcoma

Xie

Chen

et al. 2020

Int J Mol Med

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“…Abnormal expression of snoRNA is a potential factor for carcinogenesis. It was reported that lncRNA-SNHG7 was able to affect the regulation of proliferation, metastasis and invasion and suppress apoptosis of malignant tumor cells including lung cancer (14), pancreatic cancer (15), esophageal cancer (16) and gastric cancer (17). However, its role in HCC has remained unclear.…”

Section: Introductionmentioning

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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“…SNHG7 was upregulated in hepatocellular carcinoma and promoted cell metastasis process through blocking RBM5 expression. SNHG7‐miR‐342‐3p‐ID4 feedback loop has also been reported to accelerate tumor growth in vitro and in vivo in pancreatic cancer . Similarly, in the report by Li et al .…”

Section: Discussionmentioning

confidence: 61%

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

Cited by 76 publications

References 32 publications

CircSAMD4A regulates cell progression and epithelial‑mesenchymal transition by sponging miR‑342‑3p via the regulation of FZD7 expression in osteosarcoma

CircSAMD4A regulates cell progression and epithelial‑mesenchymal transition by sponging miR‑342‑3p via the regulation of FZD7 expression in osteosarcoma

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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