SNHG17 promotes the proliferation and migration of colorectal adenocarcinoma cells by modulating CXCL12-mediated angiogenesis

Yang, Liu; Li, Qinshan; Tang, Dongdong; Li, Mengxing; Zhao, Peng; Yang, Wenxiu; Shu, Liping; Wang, Jishi; He, Zhixu; Li, Yanju; Wang, Feiqing

doi:10.1186/s12935-020-01621-0

Cited by 22 publications

(20 citation statements)

References 32 publications

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“…Recent studies have indicated the oncogenic role of SNHG17 in several cancer types, including CRC. For example, recent studies showed that SNHG17 promotes tumor cell proliferation and invasion in tongue squamous cell carcinoma and CRC by sponging miR-23a-3p and miR-876, respectively [ 25 , 27 ]. In addition, SNHG17 aggravates prostate cancer progression by positively regulating its homolog SNORA71B [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

“…As the host genes of snoRNAs, lncRNA small nucleolar RNA host genes (SNHGs) have been shown to be abnormally expressed in multiple cancers and regulate cell proliferation, metastasis, and chemoresistance [ 18 , 19 ]. Of them, SNHG17 has been reported to be aberrantly overexpressed in multiple human cancers [ 20 – 25 ], suggesting that SNHG17 has extensive functions and universal roles in tumorigenesis. However, the biological function and mechanism of SNHG17 in CRC remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

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SNHG17 promotes colorectal tumorigenesis and metastasis via regulating Trim23-PES1 axis and miR-339-5p-FOSL2-SNHG17 positive feedback loop

Bian

Zhou

Cui

et al. 2021

J Exp Clin Cancer Res

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Background Small nucleolar RNA host gene (SNHG) long noncoding RNAs (lncRNAs) are frequently dysregulated in human cancers and involved in tumorigenesis and progression. SNHG17 has been reported as a candidate oncogene in several cancer types, however, its regulatory role in colorectal cancer (CRC) is unclear. Methods SNHG17 expression in multiple CRC cohorts was assessed by RT-qPCR or bioinformatic analyses. Cell viability was evaluated using Cell Counting Kit-8 (CCK-8) and colony formation assays. Cell mobility and invasiveness were assessed by Transwell assays. Tumor xenograft and metastasis models were applied to confirm the effects of SNHG17 on CRC tumorigenesis and metastasis in vivo. Immunohistochemistry staining was used to measure protein expression in cancer tissues. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and dual luciferase assays were used to investigate the molecular mechanism of SNHG17 in CRC. Results Using multiple cohorts, we confirmed that SNHG17 is aberrantly upregulated in CRC and correlated with poor survival. In vitro and in vivo functional assays indicated that SNHG17 facilitates CRC proliferation and metastasis. SNHG17 impedes PES1 degradation by inhibiting Trim23-mediated ubiquitination of PES1. SNHG17 upregulates FOSL2 by sponging miR-339-5p, and FOSL2 transcription activates SNHG17 expression, uncovering a SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop. Conclusions We identified SNHG17 as an oncogenic lncRNA in CRC and identified abnormal upregulation of SNHG17 as a prognostic risk factor for CRC. Our mechanistic investigations demonstrated, for the first time, that SNHG17 promotes tumor growth and metastasis through two different regulatory mechanisms, SNHG17-Trim23-PES1 axis and SNHG17-miR-339-5p-FOSL2-SNHG17 positive feedback loop, which may be exploited for CRC therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

SNHG17 promotes colorectal tumorigenesis and metastasis via regulating Trim23-PES1 axis and miR-339-5p-FOSL2-SNHG17 positive feedback loop

Bian

Zhou

Cui

et al. 2021

J Exp Clin Cancer Res

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“…SNHG17 with high expression in colorectal adenocarcinoma can promote the proliferation and migration of colorectal adenocarcinoma cells. 31 Knockdown of SNHG17 decreases prostate cancer cell proliferation, invasion, migration, and epithelial-to-mesenchymal transition (EMT) but strengthened apoptosis, to promote prostate cancer progression. 32 Besides, SNHG17 also promotes the progression of breast cancer, 33 ovarian cancer, 34 and oral squamous cell carcinoma.…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG17 Contributes to the Progression of Cervical Cancer by Targeting microRNA-375-3p

Cao

2021

CMAR

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Purpose Cervical cancer is a great threat to women’s health all over the world. Non-coding RNAs performed a wide range of functions. This study aimed to clarify the clinical significance and biological function of lncRNA SNHG17 and miRNA-375-3p (miR-375-3p) in cervical cancer (CC). Patients and Methods Blood samples from 124 CC patients and 119 healthy volunteers were collected. The relative expression of SNHG17 and miR-375-3p in CC patient serums and cells was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The receiver operating curve (ROC) was plotted for diagnostic value estimation. The CCK-8 and transwell assay were conducted to explore the function of SNHG17 on CC cells. A luciferase reporter assay was carried out to confirm the interaction of SNHG17 and miR-375-3p. Rescue experiments were performed to verify the interaction. Results SNHG17 showed an ascending expression while miR-375-3p descended in the serum of CC patients. For SNHG17 and miR-375-3p, respectively, the AUC was 0.863 and 0.869, the sensitivity was 84.7% and 75.8%, and the specificity was 78.2% and 86.6%. Knockdown of SNHG17 inhibited proliferation, migration, and invasion of CC cells. Serum SNHG17 expression was negatively correlated with miR-375-3p expression, and miR-375-3p was the target miRNA of SNHG17. Rescue experiments verified the knockdown of SNHG17 inhibited cell growth through repressing miR-375-3p expression. Conclusion SNHG17 and miR-375-3p have the potential to be diagnostic markers for CC. Overexpression of SNHG17 in CC promoted the progression of CC partly via targeting miR-375-3p, implying a novel therapeutic target for CC emerging.

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“…In addition, lncRNA TBILA and AGAP2-AS1 expression levels are upregulated in patients with NSCLC, and thus may be potential diagnostic biomarkers for NSCLC ( 15 ). lncRNA SNHG17 has been reported to play a vital role in different types of cancer, including colorectal, pancreatic and breast cancers ( 16 – 18 ). However, the molecular basis of SNHG17 in LUAD remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA SNHG17 promotes lung adenocarcinoma progression by targeting the microRNA‑193a‑5p/NETO2 axis

et al. 2021

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Long non-coding RNAs (lncRNAs) play vital roles in human cancers. It has been reported that lncRNA SNHG17 expression is dysregulated in different types of cancer and involved in cancer progression. However, the role of SNHG17 in lung adenocarcinoma (LUAD) remains unclear. The present study aimed to investigate the role of SNHG17 in LUAD. Reverse transcription-quantitative (RT-q) PCR analysis was performed to detect SNHG17 expression in LUAD tissues and cells. The effects of SNHG17 on cancer cell migration, invasion, proliferation and epithelial-to-mesenchymal transition (EMT) were assessed via Transwell, MTT and western blot assays, respectively. The interactions between SNHG17 and microRNA (miRNA/miR)-193a-5p, miR-193a-5p and neuropilin and tolloid-like 2 (NETO2) were assessed via the dual-luciferase reporter assay. NETO2 expression and its potential role in LUAD were analyzed via RT-qPCR analysis and the UALCAN database. The results demonstrated that SNHG17 expression was significantly upregulated in LUAD tissues and cells, and high SNHG17 expression was associated with tumor-node-metastasis stage and poor prognosis of patients with LUAD. SNHG17 knockdown inhibited cell migration, invasion, proliferation and the EMT process. In addition, the results revealed that SNHG17 functions as a competing endogenous RNA of miR-193a-5p. The results of the dual-luciferase reporter assay confirmed that miR-193a-5p can directly target SNHG17. NETO2 was also predicted as a target protein of miR-193a-5p, which was confirmed via the dual-luciferase reporter assay. The roles of NETO2 knockdown in cancer cells were rescued following transfection with miR-193a-5p inhibitor or overexpression of SNHG17. Notably, high NETO2 expression was associated with poor prognosis of patients with LUAD. Bioinformatics analysis demonstrated that the promoter methylation level of NETO2 decreased in LUAD. Taken together, the results of the present study suggest that SNHG17 expression is upregulated in LUAD tissues and cells, and SNHG17 exerts tumor promoting effect by targeting the miR-193a-5p/NETO2 axis.

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SNHG17 promotes the proliferation and migration of colorectal adenocarcinoma cells by modulating CXCL12-mediated angiogenesis

Cited by 22 publications

References 32 publications

SNHG17 promotes colorectal tumorigenesis and metastasis via regulating Trim23-PES1 axis and miR-339-5p-FOSL2-SNHG17 positive feedback loop

SNHG17 promotes colorectal tumorigenesis and metastasis via regulating Trim23-PES1 axis and miR-339-5p-FOSL2-SNHG17 positive feedback loop

LncRNA SNHG17 Contributes to the Progression of Cervical Cancer by Targeting microRNA-375-3p

Long non‑coding RNA SNHG17 promotes lung adenocarcinoma progression by targeting the microRNA‑193a‑5p/NETO2 axis

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