ArticleOncoTargets and therapy2020
Long Non-Coding RNA SNHG16 Activates USP22 Expression to Promote Colorectal Cancer Progression by Sponging miR-132-3p.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Mechanism of Lenvatinib Resistance via Exosomal miRNA-132/Nrf2 Axis in Hepatocellular Carcinoma.Annals of gastroenterological surgery · 2026Article
- Targeting ubiquitin-specific peptidase 22 in solid tumours: from ubiquitination to immunotherapy.Frontiers in cell and developmental biology · 2026Review
- LncRNA SNHG16 Drives PD-L1-Mediated Immune Escape in Colorectal Cancer through Regulating miR-324-3p/ELK4 Signaling.Biochemical genetics · 2025Article
- Molecular mechanisms underlying roles of long non-coding RNA small nucleolar RNA host gene 16 in digestive system cancers.World journal of gastrointestinal oncology · 2024Article
- Identification of novel diagnostic biomarkers associated with liver metastasis in colon adenocarcinoma by machine learning.Discover oncology · 2024Article
- Roles of long non‑coding RNA SNHG16 in human digestive system cancer (Review).Oncology reports · 2024Review
- Comprehensive analysis of the role of ubiquitin-specific peptidases in colorectal cancer: A systematic review.World journal of gastrointestinal oncology · 2024Article
- Use of exosome transcriptome-based analysis to identify novel biomarkers in patients with locally advanced esophageal squamous cell carcinoma undergoing neoadjuvant chemoradiotherapy.Annals of translational medicine · 2023Article
- Down-regulation ofInternational journal of molecular epidemiology and genetics · 2023Article
- Targeting kinesin family member 21B by miR-132-3p represses cell proliferation, migration and invasion in gastric cancer.Bioengineered · 2022Article
- Novel lncRNA SNHG16 Promotes the Growth and Metastasis of Malignant Melanoma by Regulating miR-205-5p/PAK2 Axis.Clinical, cosmetic and investigational dermatology · 2022Article
- Immune Evasion and Drug Resistance Mediated by USP22 in Cancer: Novel Targets and Mechanisms.Frontiers in immunology · 2022Review
- Article
- lncRNA-disease association prediction based on latent factor model and projection.Scientific reports · 2021Article
- Molecular mechanisms of the microRNA-132 during tumor progressions.Cancer cell international · 2021Review
- LncRNA SNHG16 contributes to tumor progression via the miR-302b-3p/SLC2A4 axis in pancreatic adenocarcinoma.Cancer cell international · 2021Article
- A Review on the Role of Small Nucleolar RNA Host Gene 6 Long Non-coding RNAs in the Carcinogenic Processes.Frontiers in cell and developmental biology · 2021Review
- Construction and Analysis of a Colorectal Cancer Prognostic Model Based on N6-Methyladenosine-Related lncRNAs.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is the most common cause of cancer-related mortality in the world. Long non-coding RNAs (lncRNAs) are involved in the development of many cancers. However, studies on the effect of lncRNA small nucleolar RNA host gene 16 (SNHG16) on the proliferation, metastasis and apoptosis of CRC are still few.
methodsQuantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the expression levels of SNHG16, microRNA-132-3p (miR-132-3p) and ubiquitin specific peptidase 22 (USP22). The proliferation, apoptosis, migration and invasion of CRC cells were evaluated by the 3-(4,5-dimethyl-2 thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, flow cytometry and transwell assay, respectively. Dual-luciferase reporter assay was used to verify the interactions among SNHG16, miR-132-3p and USP22. Also, Western blot analysis was used to assess the protein levels of USP22 and metastasis-related markers. Moreover, mice xenograft models were used to determine the effect of SNHG16 on CRC tumor growth in vivo.
resultsSNHG16 was highly expressed in CRC tissues and cells. Knockdown of SNHG16 reduced the proliferation, migration, invasion, and promoted the apoptosis of CRC cells. MiR-132-3p could interact with SNHG16, and its inhibitor recovered the suppression effect of silenced SNHG16 on CRC cell progression. Besides, USP22 was a target of miR-132-3p, and its overexpression restored the inhibition effect of miR-132-3p mimic on CRC cell progression. In addition, interference of SNHG16 reduced CRC tumor growth in vivo.
conclusionLncRNA SNHG16 might act as an oncogene in CRC. The discovery of the SNHG16/miR-132-3p/USP22 pathway provided new thinking for the treatment of CRC.
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