SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5

Cheng, Can; Huo, Qiang; Wang, Xiaolong; Chen, Bing; Yang, Qifeng

doi:10.1016/j.bbrc.2017.02.094

Cited by 149 publications

(123 citation statements)

References 21 publications

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“…Accumulating evidence has confirmed that lncRNAs may play a key role in biological and pathological processes by functioning as a competing endogenous RNA to sponge miRNAs. A previous study has reported that SNHG16 promotes breast cancer cell migration via competitively binding miR‐98 . Therefore, we also studied whether SNHG16 played a key role in bladder cancer by regulating miR‐98.…”

Section: Resultsmentioning

confidence: 95%

Retracted: Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR‐98/STAT3/Wnt/β‐catenin pathway axis

Feng

Chen

Huang

et al. 2018

J of Cellular Biochemistry

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This study aimed to investigate the role and the possible mechanism of the long noncoding small nucleolar RNA host gene 16 (SNHG16) in bladder cancer development. The expression of SNHG16 in the tumor tissues and plasma of patients with bladder cancer as well as bladder cancer cell lines was detected. T24 cells were then transfected with sh-SNHG16 to further investigate the effects of suppression of SNHG16 on T24 cell proliferation, apoptosis, migration, and invasion. In addition, the regulatory relationships between SNHG16 and miR-98 as well as the target of miR-98 were explored. Besides, the association between SNHG16 and the Wnt/β-catenin pathway was further elucidated. The SNHG16 expression was upregulated in the tumor tissues and plasma of patients with bladder cancer, as well as bladder cancer cells. Suppression of SNHG16 inhibited T24 cell proliferation, promoted apoptosis, and suppressed migration and invasion in vitro. In addition, SNHG16 negatively regulated miR-98 expression and regulated the malignant behaviors of T24 cells through sponging miR-98. Moreover, signal transducer and activator of transcription 3 (STAT3) was identified as a functional target of miR-98, and miR-98 regulated the malignant behaviors of bladder cancer cells by targeting STAT3. Besides, suppression of SNHG16 inhibited the activation of the Wnt/β-catenin pathway, which was further regulated by miR-98 and STAT3, indicating that the effects of SNHG16/miR-98/STAT3 on T24 cells were achieved through the Wnt/β-catenin pathway. Our findings reveal that long noncoding RNAs SNHG16 is upregulated in bladder cancer and contributes to the development of bladder cancer possibly via regulating the miR-98/STAT3/Wnt/β-catenin pathway axis. The SNHG16/miR-98/STAT3/Wnt/β-catenin pathway axis may provide a new strategy for bladder cancer treatment.

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Section: Resultsmentioning

confidence: 95%

Retracted: Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR‐98/STAT3/Wnt/β‐catenin pathway axis

Feng

Chen

Huang

et al. 2018

J of Cellular Biochemistry

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“…SNHG16 was highly expressed in osteosarcoma tissues and cell lines. Previous studies have shown that SNHG16 is upregulated and acts as a potential oncogene in malignant tumors [19][20][21]. Bioinformatics predicted that there are many miRNA-binding sites in the SNHG16 sequence, and the luciferase reporter assay confirmed the direct interaction between SNHG16 and miR-205.…”

Section: Cellular Physiology and Biochemistrymentioning

confidence: 70%

Long Noncoding RNA SNHG16 Promotes Cell Proliferation by Sponging MicroRNA-205 and Upregulating ZEB1 Expression in Osteosarcoma

Zhu¹,

Cheng²,

Qiu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long noncoding RNAs (lncRNAs) have been a research hotspot, as they play important roles in tumor development. However, their expression pattern and biological function in osteosarcoma have not yet been clarified. Methods: Differentially expressed lncRNAs in osteosarcoma and paracarcinoma tissues were identified by screening an lncRNA microarray, and candidate lncRNAs were verified by quantitative real-time PCR (qRT-PCR). A series of bioinformatics and molecular biological methods were adopted to investigate the interaction among lncRNA, microRNA (miRNA), and miRNA target genes during the development and occurrence of osteosarcoma. Cell viability was measured using a Cell Counting Kit-8 assay. Results: Chip microarray screening combined with the validation of differentially expressed candidate lncRNAs showed that the lncRNA small nucleolar RNA host gene 16 (SNHG16) had the largest fold change. SNHG16 was highly expressed in osteosarcoma tissues and cell lines, and its downregulation led to the suppressed proliferation of osteosarcoma cells. Further investigations revealed that SNHG16 could upregulate zinc finger E-box-binding homeobox 1 (ZEB1) expression by acting as an endogenous sponge of miR-205. Moreover, rescue assays proved that the effects of SNHG16 on the proliferation of osteosarcoma cells were dependent on miR-205. Conclusion: SNHG16 can significantly enhance the proliferation of osteosarcoma cells. In addition, SNHG16, miR-205, and ZEB1 interact in a common pathway during the development and occurrence of osteosarcoma, providing novel targets for intervention in the treatment of osteosarcoma.

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“…For instance, Cai et al . found that SNHG16 increases the mobility of breast cancer cells by competitively binding miR‐98 and E2F5, which may lead to a poor prognosis . Cao et al .…”

Section: Discussionmentioning

confidence: 99%

Circulating lncRNA SNHG11 as a novel biomarker for early diagnosis and prognosis of colorectal cancer

Zhou

Wang

et al. 2019

Intl Journal of Cancer

143

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Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer mortality worldwide. Emerging evidence indicates that tumour cells release substantial amounts of RNA into the bloodstream, in which RNA strongly resists RNases and is present at sufficient levels for quantitative analyses. Our study aimed to discover blood‐based markers for the early detection of CRC and to ascertain their efficiency in discriminating healthy controls, patients with polyps and adenomas and cancer patients. We first analysed and screened ZFAS1, SNHG11, LINC00909 and LINC00654 in a bioinformatics database and then collected clinical plasma samples for preliminary small‐scale analysis and further large‐scale verification. We then explored the mechanism of dominant lncRNA SNHG11 expression in CRC by in vitro and in vivo assays. The combination of ZFAS1, SNHG11, LINC00909 and LINC00654 showed high diagnostic performance for CRC (AUC: 0.937), especially early‐stage disease (AUC: 0.935). Plasma levels of the four candidate lncRNAs were significantly reduced in postoperative samples compared to preoperative samples. A panel including these four lncRNAs performed well in distinguishing patient groups with different stages of colon disease, and SNHG11 exhibited the greatest diagnostic ability to identify precancerous lesions and early‐stage tumour formation. Mechanistically, high SNHG11 expression promotes proliferation and metastasis by targeting the Hippo pathway. Taken together, the data indicate that SNHG11 may be a novel therapeutic target for the treatment of CRC and a potential biomarker for the early detection of CRC.

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SNHG16 contributes to breast cancer cell migration by competitively binding miR-98 with E2F5

Cited by 149 publications

References 21 publications

Retracted: Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR‐98/STAT3/Wnt/β‐catenin pathway axis

Retracted: Long noncoding RNA SNHG16 contributes to the development of bladder cancer via regulating miR‐98/STAT3/Wnt/β‐catenin pathway axis

Long Noncoding RNA SNHG16 Promotes Cell Proliferation by Sponging MicroRNA-205 and Upregulating ZEB1 Expression in Osteosarcoma

Circulating lncRNA SNHG11 as a novel biomarker for early diagnosis and prognosis of colorectal cancer

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