c-Myc induced upregulation of long non-coding RNA SNHG16 enhances progression and carcinogenesis in oral squamous cell carcinoma

Li, Shangfeng; Zhang, Shengkai; Chen, Jie

doi:10.1038/s41417-018-0072-8

Cited by 43 publications

(42 citation statements)

References 34 publications

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“…Thus, these data supported the circUHRF1/ miR-526b-5p/c-Myc axis. It has been confirmed that c-Myc is a critical oncogene and transcription factor in the OSCC [24,34]. Furthermore, transcription factor c-Myc could promote the transcription level of TGF-β1 and ESRP1.…”

Section: Discussionmentioning

confidence: 86%

Splicing factor derived circular RNA circUHRF1 accelerates oral squamous cell carcinoma tumorigenesis via feedback loop

et al. 2019

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Emerging evidences have suggested the vital roles of circular RNA (circRNA) in the human cancers. However, the underlying biological functions and biogenesis of circRNA in the oral squamous cell carcinoma (OSCC) is still ambiguous. Here, we investigate the oncogenic roles and biogenesis of the novel identified circRNA, circUHRF1 (hsa_circ_0002185), in the OSCC tumorigenesis. Results showed that circUHRF1 was markedly upregulated in the OSCC cells and tissue, besides, the overexpression was closely correlated with the poor prognosis of OSCC patients. Functionally, circUHRF1 promoted the proliferation, migration, invasion, and epithelial mesenchymal transformation (EMT) in vitro and the tumor growth in vivo. Mechanically, circUHRF1 acted as the sponge of miR-526b-5p, thereby positively regulating c-Myc. Transcription factor c-Myc could accelerate the transcription of TGF-β1 and ESRP1. Moreover, splicing factor ESRP1 promoted the circularization and biogenesis of circUHRF1 by targeting the flanking introns, forming the circUHRF1/miR-526b-5p/c-Myc/ TGF-β1/ESRP1 feedback loop. In conclusion, our research identified the oncogenic roles of circUHRF1 in the OSCC tumorigenesis and EMT via circUHRF1/miR-526b-5p/c-Myc/TGF-β1/ESRP1 feedback loop, shedding light on the pathogenic mechanism of circUHRF1 for OSCC and providing the potential therapeutic target.

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Section: Discussionmentioning

confidence: 86%

Splicing factor derived circular RNA circUHRF1 accelerates oral squamous cell carcinoma tumorigenesis via feedback loop

et al. 2019

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“…Consistently, up‐regulated expression of SNHG16 was detected in DLBCL cells compared with normal B lymphocytes. SNHG16 is overexpressed in various types of human cancers . Moreover, increased expression of SNHG16 independently predicts a poor prognosis of patients with NSCLC and bladder cancer .…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA SNHG16 promotes proliferation and inhibits apoptosis of diffuse large B‐cell lymphoma cells by targeting miR‐497‐5p/PIM1 axis

Zhu

Guo

et al. 2019

J Cellular Molecular Medi

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The aberrant expression and dysfunction of long non‐coding RNAs (lncRNAs) have been identified as critical factors governing the initiation and progression of different human cancers, including diffuse large B‐cell lymphoma (DLBCL). LncRNA small nucleolar RNA host gene 16 (SNHG16) has been recognized as a tumour‐promoting factor in various types of cancer. However, the biological role of SNHG16 and its underlying mechanism are still unknown in DLBCL. Here we disclosed that SNHG16 was overexpressed in DLBCL tissues and the derived cell lines. SNHG16 knockdown significantly suppressed cell proliferation and cell cycle progression, and it induced apoptosis of DLBCL cells in vitro. Furthermore, silencing of SNHG16 markedly repressed in vivo growth of OCI‐LY7 cells. Mechanistically, SNHG16 directly interacted with miR‐497‐5p by acting as a competing endogenous RNA (ceRNA) and inversely regulated the abundance of miR‐497‐5p in DLBCL cells. Moreover, the proto‐oncogene proviral integration site for Moloney murine leukaemia virus 1 (PIM1) was identified as a novel direct target of miR‐497‐5p. SNHG16 overexpression rescued miR‐497‐5p‐induced down‐regulation of PIM1 in DLBCL cells. Importantly, restoration of PIM1 expression reversed SNHG16 knockdown‐induced inhibition of proliferation, G0/G1 phase arrest and apoptosis of OCI‐LY7 cells. Our study suggests that the SNHG16/miR‐497‐5p/PIM1 axis may provide promising therapeutic targets for DLBCL progression.

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“…International Publisher oral squamous cell carcinoma (OSCC) [7], osteosarcoma [8], non-small cell lung cancer (NSCLC) [9], bladder cancer [10], glioma [11], gastric cancer [12], pancreatic cancer [13], and so on [14]. Recently, Chen et al has reported that LncRNA SNHG16 promotes hepatocellular carcinoma proliferation, migration and invasion by regulating miR-186 expression [15].…”

Section: Ivyspringmentioning

confidence: 99%

Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

Guo²,

Liang

et al. 2020

J. Cancer

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Background: The lnc-SNHG16 serves as an oncogene and miR-128 acts as a tumor suppressor in various cancers. However, the functional role of lnc-SNHG16 and miR-128 in CC still remain unknown. This study aims to explore the expression level of lnc-SNHG16 and miR-128 and its biological roles in CC. Methods: lnc-SNHG16, miR-128, GSPT1 and WNT3A expression were analyzed using quantitative real-time PCR and bioinformatics in cervical cancer tissues and cells. Cell Counting Kit-8, EdU staining, colony formation assay, western blot, Transwell, immunofluorescence, immunohistochemical staining, luciferase reporter assay, electrophoretic mobility shift, tumor xenograft, and flow cytometry assays were employed to investigate the mechanisms underlying the effect of Lnc-SNHG16/miR-128 axis on cervical cancer. Results: lnc-SNHG16 was up-regulated in CC cell lines and tissues. lnc-SNHG16 knockdown inhibited proliferation, restrained the epithelial-mesenchymal transition (EMT) process by regulating cell apoptosis and cell cycle. The next study indicated that lnc-SNHG16 knockdown markedly increased miR-128 level which is down-regulated in CC. Moreover, miR-128 overexpression significantly inhibited proliferation, EMT process and tumor growth by directly targeting GSPT1 and WNT3A. Finally, lnc-SNHG16 activates but miR-128 inactivates the WNT/β-catenin pathways in CC cells. Conclusion: Our data suggest that lnc-SNHG16/miR-128 axis modulates malignant phenotype of CC cells through WNT/β-catenin pathway.

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c-Myc induced upregulation of long non-coding RNA SNHG16 enhances progression and carcinogenesis in oral squamous cell carcinoma

Cited by 43 publications

References 34 publications

Splicing factor derived circular RNA circUHRF1 accelerates oral squamous cell carcinoma tumorigenesis via feedback loop

Splicing factor derived circular RNA circUHRF1 accelerates oral squamous cell carcinoma tumorigenesis via feedback loop

Long non‐coding RNA SNHG16 promotes proliferation and inhibits apoptosis of diffuse large B‐cell lymphoma cells by targeting miR‐497‐5p/PIM1 axis

Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

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