• Colorectal cancer
• ELK4
• Immune escape
• MiR-324-3p
• PD-L1
• SNHG16

• 2022JJ30336 Hunan Provincial Natural Scientific Foundation

• Colon cancer
• Digestive system cancers
• Long non-coding RNAs
• Small nucleolar RNA host gene 16

• Colon adenocarcinoma
• Diagnostic biomarkers
• Immune cells infiltration
• Liver metastasis
• Machine learning
• Primary tumor

• biomarker
• ceRNA
• human digestive system cancer
• risk factors
• small nucleolar RNA host gene 16

• Humans
• RNA, Long Noncoding/genetics
• Digestive System Neoplasms/genetics
• Digestive System Neoplasms/pathology
• Gene Expression Regulation, Neoplastic
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Prognosis

• biomarker
• cancer therapy
• gastrointestinal tumours
• lncRNAs
• small nucleolar RNA host genes

• Humans
• RNA, Long Noncoding/genetics
• RNA, Small Nucleolar/genetics
• Gastrointestinal Neoplasms/genetics
• Carcinogenesis
• Cell Transformation, Neoplastic

• MR/X008517/1 Medical Research Council
• 11370 Ferdowsi University of Mashhad

• Biomarker discovery
• Colorectal cancer
• Deubiquitinase protein family
• Drug target discovery
• Ubiquitin-specific peptidases

• RB1
• breast cancer
• gene expression
• miRNA-132

• Apoptosis
• Invasion
• PCMT1
• Prognostic biomarker
• Proliferation

• Esophageal squamous cell carcinoma (ESCC)
• bioinformatics analysis
• exosome transcriptome
• microRNA (miRNA)
• neoadjuvant chemoradiotherapy (nCRT)

Long non-coding RNAs (lncRNAs) play an key role in the biological processes of various malignant tumors. SNHG16 has been confirmed to be associated with the progression of various cancers. However, function and molecular mechanism of SNHG16 in melanoma have not been studied by scholars.

The expression of SNHG16 in melanoma tissues were detected by using qRT-PCR. Melanoma cases from The Cancer Genome Atlas (TCGA) and GEO#GSE15605 were included in this study. CCK-8 assay, EdU assay, transwell and scratch wound assay were used to explore the role of SNHG16 in melanoma cells. Luciferase reporter assays and RNA pull-down assay were used to explore the molecular mechanism of SNHG16 in melanoma.

Here, we found that SNHG16 was up-regulated in melanoma. SNHG16 enhances the growth and metastasis of melanoma. SNHG16 can promote the expression of P21-activated kinases 2 (PAK2) by sponging miR-205-5p. PAK2 is the target gene of miR-205-5p. We demonstrated that SNHG16 promotes the metastasis and growth of melanoma through miR-205-5p/PAK2 axis.

This study firstly confirmed the role and mechanism of SNHG16 in the occurrence and development of melanoma. Therefore, SNHG16 may become a key point in the diagnosis, prognosis and treatment of melanoma patients in the future.

• PAK2
• SNHG16
• growth and metastasis
• melanoma
• miR-205-5p

Regulation of ubiquitination is involved in various processes in cancer occurrence and development, including cell cycle arrest, cell proliferation, apoptosis, invasion, metastasis, and immunity. Ubiquitination plays an important role not only at the transcriptional and post-translational levels but also at the protein level. When ubiquitination is in a pathological state, abnormally activated biological processes will not only induce cancer progression but also induce immune evasion. The main function of deubiquitinases (DUBs) is to remove ubiquitin chains from substrates, changing the biological activity of the substrates. It has great potential to improve the prognosis of cancer by targeting DUB to regulate proteome. Ubiquitin-specific peptidase 22 (USP22) belongs to the ubiquitin-specific protease (USP) family of DUBs and has been reported to be related to various physiological and pathological processes. USP22 is abnormally expressed in various malignant tumors such as prostate cancer, lung cancer, liver cancer, and colorectal cancer, which suggests that USP22 may play an important role in tumors. USP22 may stabilize programmed death ligand 1 (PD-L1) by deubiquitination while also regulating T-cell infiltration into tumors. Regulatory T cells (Tregs) are a unique class of immunosuppressive CD4⁺ T cells that primarily suppress the immune system by expressing the master transcription factor forkhead box protein 3 (FOXP3). USP22 was found to be a positive regulator of stable FOXP3 expression. Treg-specific ablation of USP22 leads to reduced tumor volume in multiple cancer models. This suggests that USP22 may regulate tumor resistance to immunotherapy. In this article, we review and summarize the biological functions of USP22 in multiple signal transduction pathways during tumorigenesis, immune evasion, and drug resistance. Furthermore, we propose a new possibility of combining USP22 with chemotherapeutic, targeted, and immunosuppressive drugs in the treatment of cancer.

• Drug Resistance
• Forkhead Transcription Factors/metabolism
• Humans
• Immune Evasion
• Male
• Neoplasms
• Thiolester Hydrolases/metabolism
• Ubiquitin Thiolesterase/metabolism

Recently, kinesin family member 21B (KIF21B) has been reported to be an oncogene in non-small cell lung cancer and hepatocellular carcinoma. However, the functional role of KIF21B and related molecular mechanisms in gastric cancer (GC) remain largely uncovered. In this study, online bioinformatics analysis showed that KIF21B was overexpression in GC and predicted poor prognosis. Consistently, we found that the protein expression of KIF21B was upregulated in GC tissues compared with adjacent tissues by immunohistochemistry. Knockdown of KIF21B significantly suppressed cell proliferation, migration and invasion in GC cell lines (AGS and SNU-5) using Cell counting kit‑8 (CCK-8) assay, colony formation and transwell assay. KIF21B was confirmed as the target of miR-132-3p in GC cells by luciferase reporter assay. Moreover, miR-132-3p was down-regulated and KIF21B expression was upregulated in GC tissues. Overexpression of KIF21B reversed the miR-132-3p-mediated suppressive effects on GC cell proliferation, migration and invasion. Furthermore, miR-132-3p overexpression downregulated the protein levels of Wnt1, c-Myc, β-catenin, proliferating cell nuclear antigen (PCNA) and N-cadherin, and upregulated E-cadherin expression in GC cells, which were all alleviated after KIF21B overexpression. In conclusion, our findings indicate that down-regulation of KIF21B by miR-132-3p suppresses cellular functions in GC, which might be linked to reduced Wnt/β-catenin signaling.

• Gastric cancer
• KIF21B
• Wnt/β-catenin signaling
• epithelial–mesenchymal transition
• miR-132-3p

• LncRNA MBNL1-AS1
• SOX4
• acute myocardial infarction
• cell apoptosis
• miR-132-3p

• 3' Untranslated Regions
• Animals
• Apoptosis
• Cell Line
• Cell Movement
• Cell Proliferation
• Creatine Kinase, MB Form/metabolism
• Disease Models, Animal
• MicroRNAs/genetics
• Myocardial Infarction/genetics
• Myocardial Infarction/metabolism
• Myocytes, Cardiac/cytology
• RNA, Long Noncoding/genetics
• Random Allocation
• Rats
• Rats, Wistar
• SOXC Transcription Factors/genetics
• Troponin I
• Up-Regulation

Being located on 17q25.1, small nucleolar RNA host gene 6 (SNHG16) is a member of SNHG family of long non-coding RNAs (lncRNA) with 4 exons and 13 splice variants. This lncRNA serves as a sponge for a variety of miRNAs, namely miR-520a-3p, miR-4500, miR-146a miR-16–5p, miR-98, let-7a-5p, hsa-miR-93, miR-17-5p, miR-186, miR-302a-3p, miR-605-3p, miR-140-5p, miR-195, let-7b-5p, miR-16, miR-340, miR-1301, miR-205, miR-488, miR-1285-3p, miR-146a-5p, and miR-124-3p. This lncRNA can affect activity of TGF-β1/SMAD5, mTOR, NF-κB, Wnt, RAS/RAF/MEK/ERK and PI3K/AKT pathways. Almost all studies have reported oncogenic effect of SNHG16 in diverse cell types. Here, we explain the results of studies about the oncogenic role of SNHG16 according to three distinct sets of evidence, i.e., in vitro, animal, and clinical evidence.

• SNHG6
• biomarker
• cancer
• expression
• lncRNA

• computational biology and bioinformatics
• bioinformatics

• hepatocellular carcinoma
• long non-coding rna
• meta-analysis
• prognosis
• snhg16

• Biomarkers, Tumor/genetics
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/pathology
• Humans
• Liver Neoplasms/metabolism
• Liver Neoplasms/pathology
• Prognosis
• RNA, Long Noncoding/genetics

Given the relatively poor understanding of the expression and functional effects of the N6-methyladenosine (m6A) RNA methylation on colorectal cancer (CRC), we attempted to measure its prognostic value and clinical significance. We comprehensively screened 37 m6A-related prognostic long non-coding RNAs (lncRNAs) with significant differences in expression based on 21 acknowledged regulators of m6A modification and data on 473 colorectal cancer tissues and 41 para-cancer tissues obtained from the TCGA database. Accordingly, we classified 473 CRC patients into two clusters by consensus clustering on the basis of significantly different survival outcomes. We also found a potential correlation between m6A-related prognostic lncRNAs and BRAF-KRAS expression, as well as immune cell infiltration. Then, we established a prognostic model by selecting 16 m6A-related prognostic lncRNAs via LASSO Cox analysis and grouped the CRC patients into low- and high-risk groups to calculate risk scores. Then, we performed stratified sampling to validate and confirm our model by categorising the 473 samples into a training group (N = 208) and a testing group (N = 205) in a 1:1 ratio. The survival curve showed a distinct clinical outcome in the low- and high-risk subgroups. We reconfirmed the reliability and independence of the prognostic model through various measures: risk curve, heat map and univariate and multivariate Cox analyses. To ensure that the outcomes were applicable to clinical settings, we performed stratified analyses on different clinical features, such as age, lymph node status and clinical stage. CRC patients with downregulated m6A-related gene expression, lower immune score, distant metastasis, lymph node metastasis or more advanced clinical staging had higher risk scores, indicating less-desirable outcomes. Moreover, we explored the immunology of colorectal cancer cells. The risk score showed positive correlations with eosinophils, M2 macrophages and neutrophils. In summary, our effort revealed the significance of m6A RNA methylation regulators in colorectal cancer, and the prognostic model we constructed may be used as an essential reference for predicting the outcome of CRC patients.

• N6-methylandenosine
• colorectal cancer
• long non-coding RNA
• prognostic model
• prognostic signature

Cancer as one of the leading causes of human deaths has always been one of the main health challenges in the world. Despite recent advances in therapeutic and diagnostic methods, there is still a high mortality rate among cancer patients. Late diagnosis is one of the main reasons for the high ratio of cancer related deaths. Therefore, it is required to introduce novel early detection methods. Various molecular mechanisms are associated with the tumor progression and metastasis. MicroRNAs (miRNAs) are a class of non-coding RNAs (ncRNAs) family that has important functions in regulation of the cellular processes such as cell proliferation, apoptosis, and tumor progression. Moreover, they have higher stability in body fluids compared with mRNAs which can be introduced as non-invasive diagnostic markers in cancer patients. MiR-132 has important functions as tumor suppressor or oncogene in different cancers. In the present review, we have summarized all of the studies which have been reported the role of miR-132 during tumor progressions. We categorized the miR-132 target genes based on their cell and molecular functions. Although, it has been reported that the miR-132 mainly functions as a tumor suppressor, it has also oncogenic functions especially in pancreatic tumors. MiR-132 mainly exerts its roles during tumor progressions by regulation of the transcription factors and signaling pathways. Present review clarifies the tumor specific molecular mechanisms of miR-132 to introduce that as an efficient non-invasive diagnostic marker in various cancers.

• Cancer
• Diagnosis
• Marker
• MiR-132
• Prognosis

• Cell cycle regulation
• Deubiquitination
• Immune microenvironment
• Neoplasms
• Stemness maintenance

It has been reported that the lncRNA SNHG16 has significantly increased expression in pancreatic adenocarcinoma (PC). However, the functions and mechanisms of SNHG16 are not clear. The aim of this study was to explore the effects of SNHG16 on PC.

qRT-PCR analysis was applied to detect the expression levels of SNHG16, miR-302b-3p and SLC2A4 in PC tissues and cells. CCK8 and EdU assays were used to evaluate the proliferation of PC cells. Transwell assays were used to assess PC cell migration and invasion. Apoptosis was evaluated by flow cytometry, and the expression of apoptosis-related proteins (including Bax, Bcl-2, cleaved caspase-3 and cleaved caspase-9) was tested by western blotting. The interactions between miR-302b-3p and SNHG16 or miR-302b-3p and the 3’UTR of SLC2A4 mRNA were clarified by a dual luciferase reporter assay and RNA immunoprecipitation.

SNHG16 expression was significantly elevated in PC tissues and cell lines and was associated with poor prognosis of PC patients. Knockdown of SNHG16 reduced PC cell proliferation, migration and invasion. SNHG16 acted as a sponge to regulate miR-302b-3p expression in PC cells. In addition, miR-302b-3p targeted SLC2A4 directly.

SNHG16 promoted the progression of PC via the miR-302b-3p/SLC2A4 axis and was expected to be a potential target for the early diagnosis and treatment of PC.

• Pancreatic adenocarcinoma
• SLC2A4
• SNHG16
• miR-302b-3p