• glioma
• lncrna agap2-as1
• mirna-497-5p
• proliferation
• metastasis

• Competitive endogenous RNAs
• Human cancer
• LncRNA SNHG3,
• Long non-coding RNA
• Potential therapeutic target,
• Tumorigenesis biomarker,

• Guiweikejiaofa [2020]-15 Guangxi Training Program for Medical High-level Academic Leaders
• 2020-3-2 Bose Talent Highland
• 2024 Building Projects of Guangxi Bagui Scholars
• Guiweikejiaofa [2020]-17 Building Projects from the Key Laboratory of Molecular Pathology (Hepatobiliary Diseases) of Guangxi
• Guijiaokeyan [2022]-10 the Key Laboratory of Tumor Molecular Pathology of Guangxi Colleges & Universities
• Guiweiyifa [2022]-21 Clinical Key Specialty Building Project (For Pathology) of Guangxi
• the Key Laboratory of Tumor Molecular Pathology of Guangxi Colleges & Universities

• ITGA6
• cancer stem cells
• liver hepatocellular carcinoma
• long noncoding RNA SNHG3
• microRNA‐502‐3p

• Animals
• Female
• Humans
• Male
• Mice
• Middle Aged
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/pathology
• Carcinoma, Hepatocellular/metabolism
• Cell Line, Tumor
• Cell Proliferation/genetics
• Gene Expression Regulation, Neoplastic
• Integrin alpha6/metabolism
• Integrin alpha6/genetics
• Liver Neoplasms/genetics
• Liver Neoplasms/pathology
• Liver Neoplasms/metabolism
• Methyltransferases/metabolism
• Methyltransferases/genetics
• Mice, Nude
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Neoplastic Stem Cells/metabolism
• Neoplastic Stem Cells/pathology
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism

• ZDYF2022SHFZ117 Science and Technology Project of Hainan Province

• Breast cancer
• LncRNA
• NF-κB
• Notch
• TGF-β
• Wnt/β-catenin

• Humans
• Female
• Animals
• Breast Neoplasms/genetics
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• beta Catenin/metabolism
• Proto-Oncogene Proteins c-akt/metabolism
• NF-kappa B/metabolism
• Hedgehogs/genetics
• Hedgehogs/metabolism
• Signal Transduction
• TOR Serine-Threonine Kinases/metabolism
• Transforming Growth Factor beta/metabolism
• Phosphatidylinositol 3-Kinases/metabolism
• Gene Expression Regulation, Neoplastic/genetics

• CircRNA
• Cytokine
• HOXB6
• MiRNA
• Osteosarcoma

• anticancer
• exosomal processing
• exosome
• lncRNAs
• natural product
• sponging miRNAs

• MOST 111-2320-B-037-015-MY3 Ministry of Science and Technology
• KMU-DK(A)112008 Kaohsiung Medical University
• KMU-TC108A04 Kaohsiung Medical University Research Center

Osteosarcoma (OS) is a primary solid malignant tumor that occurs most frequently in the metaphysis of long bones. More likely to happen to children and adolescents. OS has high mortality and disability rate. However, the etiology and pathogenesis of OS have not been fully understood till now. Due to the lack of effective biomarkers, OS cannot be precisely detected in the early stage. With the application of next-generation and high-throughput sequencing, more and more abnormally expressed non-coding RNAs(ncRNAs) have been identified in OS. Growing evidences have suggested the ncRNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), have played an important role in the tumorigenesis and progression of OS. Thus, they can be served as novel biomarkers for diagnosis, treatment and prognosis. This review summarized the application of ncRNA as biomarkers in OS in detail, and discussed the limitation and future improvement of the potential biomarkers.

Cancer has become the most life-threatening disease in the world. Mutations in and aberrant expression of genes encoding proteins and mutations in noncoding RNAs, especially long noncoding RNAs (lncRNAs), have significant effects in human cancers. LncRNAs have no protein-coding ability but function extensively in numerous physiological and pathological processes. Small nucleolar RNA host gene 3 (SNHG3) is a novel lncRNA and has been reported to be differentially expressed in various tumors, such as liver cancer, gastric cancer, and glioma. However, the interaction mechanisms for the regulation between SNHG3 and tumor progression are poorly understood. In this review, we summarize the results of SNHG3 studies in humans, animal models, and cells to underline the expression and role of SNHG3 in cancer. SNHG3 expression is upregulated in most tumors and is detrimental to patient prognosis. SNHG3 expression in lung adenocarcinoma remains controversial. Concurrently, SNHG3 affects oncogenes and tumor suppressor genes through various mechanisms, including competing endogenous RNA effects. A deeper understanding of the contribution of SNHG3 in clinical applications and tumor development may provide a new target for cancer diagnosis and treatment.

• Small nucleolar RNA host gene 3
• Long noncoding RNAs, Biomarker
• Clinical characters
• Molecular mechanism
• Competing endogenous RNA
• Liver cancer

• Animals
• Biomarkers
• Cell Proliferation/genetics
• Gene Expression Regulation, Neoplastic
• Humans
• Liver Neoplasms/genetics
• RNA, Long Noncoding/genetics
• RNA, Small Nucleolar/genetics

• Long non-coding RNA
• SNHG3
• bioinformatics analysis
• diagnosis
• meta-analysis
• prognosis

• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Humans
• Neoplasms/diagnosis
• Neoplasms/genetics
• Neoplasms/metabolism
• Oncogenes
• Prognosis
• RNA, Long Noncoding/genetics

• HOXC8
• gastric cancer
• miR-4256
• migration
• network
• overall survival
• proliferation

Bone metastasis is closely related to tumor death in prostate cancer (PC). Long noncoding RNA small nucleolar RNA host gene 3 (SNHG3) has been implicated in the initiation and progression of multiple human cancers. Nevertheless, the biological function of SNHG3 in PC has not been elucidated. Our results indicated that SNHG3 was upregulated in bone metastasis-positive PC tissues compared to bone metastasis-negative PC tissues and adjacent normal tissues. High expression of SNHG3 indicates advanced clinicopathological features and predicts poor prognosis in patients with PC. Meanwhile, SNHG3 knockdown suppressed the proliferation, migration, and invasion abilities of PC cells and inhibited PC cell metastasis to the bone. Mechanistically, SNHG3 enhanced the expression of transforming growth factor beta receptor 1 (TGFBR1) and activated transforming growth factor-Beta (TGF-β) signaling by targeting miR-214-3p. Our study demonstrated the novel role of the SNHG3/miR-214-3p/TGF-β axis in tumor growth and bone metastasis in PC, indicating that SNHG3 may act as a biomarker and promising therapeutic target against PC.

• SNHG3
• miR-214-3p
• prostate cancer
• tgf-β signaling
• tgfbr1

• LMX1B
• SNHG3
• glioma
• miR-485-5p
• xenografts

Osteosarcoma is a frequent bone malignancy in children and young adults. Despite the availability of some prognostic biomarkers, most of them fail to accurately predict prognosis in osteosarcoma patients. In this study, we used bioinformatics tools and machine learning algorithms to establish an autophagy-related long non-coding RNA (lncRNA) signature to predict the prognosis of osteosarcoma patients.

We obtained expression and clinical data from osteosarcoma patients in the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) and Gene Expression Omnibus (GEO) databases. We acquired an autophagy gene list from the Human Autophagy Database (HADb) and identified autophagy-related lncRNAs by co-expression analyses. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the autophagy-related lncRNAs were conducted. Univariate and multivariate Cox regression analyses were performed to assess the prognostic value of the autophagy-related lncRNA signature and validate the relationship between the signature and osteosarcoma patient survival in an independent cohort. We also investigated the relationship between the signature and immune cell infiltration.

We initially identified 69 autophagy-related lncRNAs, 13 of which were significant predictors of overall survival in osteosarcoma patients. Kaplan-Meier analyses revealed that the 13 autophagy-related lncRNAs could stratify patients based on their outcomes. Receiver operating characteristic curve analyses confirmed the superior prognostic value of the lncRNA signature compared to clinically used prognostic biomarkers. Importantly, the autophagy-related lncRNA signature predicted patient prognosis independently of clinicopathological characteristics. Furthermore, we found that the expression levels of the autophagy-related lncRNA signature were significantly associated with the infiltration levels of different immune cell subsets, including T cells, NK cells, and dendritic cells.

The autophagy-related lncRNA signature established here is an independent and robust predictor of osteosarcoma patient survival. Our findings also suggest that the expression of these 13 autophagy-related lncRNAs may promote osteosarcoma progression by regulating immune cell infiltration in the tumor microenvironment.

• autophagy-related lncRNA
• immune cell infiltration
• osteosarcoma
• prognostic signature
• survival

Long noncoding RNAs (lncRNAs) have been confirmed to play a crucial role in human disease, especially in tumor development and progression. Small nucleolar RNA host gene (SNHG3), a newly identified lncRNA, has been found dysregulated in various cancers. Nevertheless, the results remain controversial. Thus, we aim to analyze the comprehensive data to elaborate the association between SNHG3 expression and clinical outcomes in multiple cancers. We searched PubMed, Web of Science, Cochrane Library, Embase, and MEDLINE database to identify eligible articles. STATA software was applied to calculate the hazard ratio (HR) and odds ratio (OR) with 95% confidence interval (95% CI) for survival outcomes and clinical parameters, respectively. Besides, the data from The Cancer Genome Atlas (TCGA) dataset was extracted to verify the results in our meta-analysis. There were thirteen studies totaling 919 cancer patients involved in this meta-analysis. The results demonstrated that high SNHG3 expression was significantly associated with poor overall survival (OS) (HR = 2.53, 95% CI: 1.94-3.31) in cancers, disease-free survival (DFS) (HR = 3.89, 95% CI: 1.34-11.3), and recurrence-free survival (RFS) (HR = 2.42, 95% CI: 1.14-5.15) in hepatocellular carcinoma. Analysis stratified by analysis method, sample size, follow-up time, and cancer type further verified the prognostic value of SNHG3. Additionally, patients with high SNHG3 expression tended to have more advanced clinical stage, higher histological grade, earlier distant metastasis, and earlier lymph node metastasis. Excavation of TCGA dataset valuated that SNHG3 was upregulated in various cancers and predicted worse OS and DFS. Overexpressed SNHG3 was strongly associated with poor survival and clinical outcomes in human cancers and therefore can serve as a promising biomarker for predicting patients' prognosis.

Osteosarcoma (OS) is the most common malignant bone tumor in teens. Non-coding RNA activated by DNA damage (NORAD), a long non-coding RNA (lncRNA), has been reported to be involved in cancer biology, although its role in OS remains largely unknown. In the present study reverse transcription-quantitative PCR (RT-qPCR) was used to determine the expression levels of NORAD and miR-155-5p in samples from patients with OS. OS cell lines (Saos-2 and U2OS) were used as cell models. The biological influence of NORAD on OS cells was studied in vitro using Cell Counting Kit-8 and Transwell assays. The interaction between NORAD and miR-155-5p was clarified by bioinformatics analysis, RT-qPCR, luciferase reporter assay and RNA immunoprecipitation. NORAD was significantly increased in OS samples in comparison with controls, while miR-155-5p was reduced. Knockdown of NORAD and transfection of miR-155-5p mimics markedly inhibited the viability, migration and invasion of OS cells. There was a negative correlation between NORAD and miR-155-5p expression levels in OS samples. Taken together, the results of the present study indicated that the NORAD/miR-155-5p axis played a crucial role in regulating the proliferation, migration and invasion of OS cells. It is hypothesized that NORAD and miR-155-5p may serve as potential novel therapeutic targets for OS management.

• NORAD
• lncRNA
• miR-155-5p
• osteosarcoma

• Cancer stem cells
• anti-cancer targets
• long non-coding RNAs
• molecular mechanisms
• therapy resistance

Gastric cancer (GC) is ranked the fourth leading cause of cancer-related death, with an over 75% mortality rate worldwide. In recent years, miR-299-3p has been identified as a biomarker in multiple cancers, such as acute promyelocytic leukemia, thyroid cancer, and lung cancer. However, the regulatory mechanism of miR-299-3p in GC cell progression is still largely unclear. Cell viability and apoptosis tests were performed by CCK8 and flow cytometry assay, respectively. Transwell assay was recruited to examine cell invasion ability. The interaction between miR-299-3p and PAX3 was determined by the luciferase reporter system. PAX3 protein level was evaluated by western blot assay. The expression of miR-299-3p was downregulated in GC tissues and cell lines (MKN-45, AGS, and MGC-803) compared with the normal tissues and cells. Besides, overexpression of miR-299-3p significantly suppressed proliferation and invasion and promoted apoptosis in GC. Next, we clarified that PAX3 expression was regulated by miR-299-3p using a luciferase reporter system, qRT-PCR, and western blot assay. Additionally, downregulation of PAX3 repressed GC cell progression. The rescue experiments indicated that restoration of PAX3 inversed miR-299-3p-mediated inhibition on cell proliferation and invasion. miR-299-3p suppresses cell proliferation and invasion as well as induces apoptosis by regulating PAX3 expression in GC, representing desirable biomarkers for GC diagnosis and therapy.

• GC biomarkers
• GC therapy
• PAX3
• gastric cancer
• miR-299-3p

Osteosarcoma (OS) is a musculoskeletal malignancy that originates from interstitial cells. An increasing number of studies have verified that long non-coding RNAs (lncRNAs) participate in the progression of numerous types of cancer. It has been reported that LINC00467 is a cancer-promoting gene in some types of cancer; however, the regulatory mechanism of LINC00467 in OS remains unknown. In the present study, reverse transcription-quantitative PCR was used to determine LINC00467 expression in OS tissues and cells. Additionally, the impact of LINC00467-knockdown on OS cell proliferation, migration and invasion was analyzed using Cell Counting Kit-8, colony formation and Transwell assays, as well as western blot analysis. RNA pulldown and luciferase reporter assays were conducted to investigate the regulatory mechanism of LINC00467 in OS. The results delineated that LINC00467 expression was elevated in OS tissues and cells, and that high LINC00467 expression was associated with a poor prognosis in patients with OS. LINC00467 inhibition suppressed OS progression by inhibiting cell proliferation, migration, invasion and epithelial-mesenchymal transition. LINC00467 served as a molecular sponge for microRNA (miR)-217, while karyopherin subunit α4 (KPNA4) was a downstream target gene of miR-217. Moreover, the overexpression of KPNA4 reversed the inhibitory effects of LINC00467 inhibition on OS progression. Therefore, the present study elucidated the potential mechanism of LINC00467 in OS and indicated that LINC00467 exerted its carcinogenic effects on OS through the miR-217/KPNA4 axis, implying that LINC00467 may be a novel potential therapeutic target for OS.

• LINC00467
• osteosarcoma
• microRNA‑217
• karyopherin subunit α4

Tumour growth and development are dependent on many factors including long noncoding RNAs (lncRNAs). However, limited information is available on the involvement of lncRNAs in non-small cell lung cancer (NSCLC) and the molecular mechanisms have not been defined. Here, we examined the expression of small nucleolar RNA host gene 3 (SNHG3) and its contribution to the development of NSCLC.

We detected SNHG3, miR-216a, and ZEB1 expression in tissues from NSCLC patients and lung adenocarcinoma cell lines using quantitative real-time polymerase chain reaction. Proliferation, migrations, invasion, and apoptosis of tumour cells were assessed using cell counting kit-8, transwell experiments, and flow cytometry after SNHG3 knockdown by small interfering RNAs. Bioinformatics and luciferase reporter assays were employed for analysing the interactions between SNHG3, miR-216a, and ZEB1.

We found highly upregulated SNHG3 in tissues and cells from NSCLC patients, which was linked to poor prognosis. SNHG3 silencing diminished the ability of NSCLC cells to proliferate, migrate, and invade and promoted apoptosis. Furthermore, SNHG3 competed with endogenous RNA and enhanced the expression of ZEB1 by interfering with miR-216a. ZEB1 overexpression or miR-216a blockade reversed SNHG3-induced tumour inhibition. Similar effects were observed in vivo where SNHG3 knockdown inhibited NSCLC tumour growth by reducing expression of miR-216a while increasing that of ZEB1.

Knockdown of SNHG3 inhibits NSCLC tumour development and progression by upregulation of ZEB1 and interference with miR-216a, revealing an attractive alternative target for patients with NSCLC.

• NSCLC
• competing endogenous RNA
• lncRNA SNHG3
• tumour apoptosis
• tumour invasion
• tumour migration
• tumour proliferation

Long noncoding RNAs (lncRNAs) are composed of > 200 nucleotides; they lack the ability to encode proteins but play important roles in a variety of human tumors. A large number of studies have shown that dysregulated expression of lncRNAs is related to tumor oncogenesis and progression. Emerging evidence shows that SNHG3 is a novel oncogenic lncRNA that is abnormally expressed in various tumors, including osteosarcoma, liver cancer, lung cancer, etc. SNHG3 primarily competes as a competitive endogenous RNA (ceRNA) that targets tumor suppressor microRNAs (miRNAs) and ceRNA mechanisms that regulate biological processes of tumors. In addition, abnormal expression of SNHG3 is significantly correlated with patient clinical features. Upregulation of SNHG3 contributes to biological functions, including tumor cell proliferation, migration, invasion and EMT. Therefore, SNHG3 may represent a potential diagnostic and prognostic biomarker, as well as a novel therapeutic target.

• Biomarker
• Cancer
• LncRNA
• SNHG3

• Biomarker
• Colorectal cancer (CRC)
• MicroRNA-196
• Therapy

Long-chain non-coding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) is reportedly overexpressed in malignant tumors, but its regulatory role in human ovarian cancer (OC) is not fully understood.

A qRT-PCR assay was carried out to detect the level of SNHG3 in OC tissues, serum and cells, a CCK-8 assay to measure the proliferation of OC cells, a transwell assay to measure the invasion and migration of OC cells, and a flow cytometry to detect the cell cycle distribution and apoptosis rate of OC cells. In addition, in vivo experiment was also conducted to determine the effect of SNHG3 on the growth of OC cells.

SNHG3 was overexpressed in OC tissues, serum, and cells, and the overexpression in serum indicated a poor prognosis of patients. It was also found that knockdown of SNHG3 could inhibit the malignant phenotypes of OC cells, cause G1/G0 cell cycle arrest, and intensify apoptosis. Furthermore, in in vitro experiments, the growth ability of OC cells was inhibited under knockdown of SNHG3. Assays for relationship verification showed that SNHG3 regulated the expression of miR-339-5p and the canonical transient receptor potential 3 (TRPC3), and the rescue experiment revealed that co-transfection of si-SNHG3+miR-339-5p-inhibitor or si-SNHG3+pcDNA3.1-TRPC3 could reverse the effects of knockdown of SNHG3 on the biological behavior of OC cells.

SNHG3 can be adopted as a marker for diagnosis and prognosis evaluation of OC and it plays a role in the progression of OC by enabling the miR-339-5p sponge to regulate TRPC3 expression.

• biological behavior
• long-chain non-coding RNA
• miR-339-5p
• ovarian cancer
• small nucleolar RNA host gene 3

• Biomarker
• DNA methylation
• LncRNA
• Osteosarcoma
• Prognosis

• SNHG3
• cisplatin resistance
• gastric cancer
• miR-3619-5p
• stem cell

• Base Sequence
• Cell Line, Tumor
• Cisplatin/pharmacology
• Drug Resistance, Neoplasm/drug effects
• Drug Resistance, Neoplasm/genetics
• GTP-Binding Proteins/metabolism
• Gene Expression Regulation, Neoplastic/drug effects
• Gene Knockdown Techniques
• Humans
• Interleukin-6/metabolism
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Models, Biological
• Neoplastic Stem Cells/metabolism
• Neoplastic Stem Cells/pathology
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• STAT3 Transcription Factor/metabolism
• Stomach Neoplasms/genetics
• Stomach Neoplasms/pathology
• Transcriptional Activation/drug effects
• Transcriptional Activation/genetics

Glioma is a malignant primary brain tumor that occurs in the central nervous system and has threatened the well-being of millions of patients. It is well acknowledged that long non-coding RNA (lncRNA) SNHG3 participates in the regulation of proliferation, inflation, differentiation, and metastasis in many cancers. However, the regulatory effect of SNHG3 on glioma progression is still controversial. The expression of SNHG3 and HDGF was upregulated, whereas miR-384 was downregulated in glioma tissues, compared with the normal tissues. Interestingly, high SNHG3 contributed to low survival rate while low SNHG3 showed the opposite result. Moreover, SNHG3 or HDGF knockdown significantly suppressed proliferation, migration, and invasion and induced apoptosis in glioma. Meanwhile, restoration of HDGF abrogated the inhibition of SNHG3 silencing on glioma cell progression. Besides, miR-384 inhibitor attenuated SNHG3 silencing induced inhibition on HDGF mRNA and protein expression in A172 and SHG44 cells. LncRNA SNHG3 promotes cell proliferation, migration, and invasion in glioma by enhancing HDGF expression via miR-384 sponging, representing the promising targets for the development of novel therapeutic strategies.

• HDGF
• SNHG3
• glioma
• miR-384
• progression

• Breast cancer
• Competing endogenous RNA
• Long non-coding RNA SNHG3
• Notch signaling pathway
• microRNA-154-3p

• Animals
• Breast Neoplasms/metabolism
• Breast Neoplasms/pathology
• Cell Movement/genetics
• Cell Proliferation/genetics
• Female
• Gene Expression Regulation, Neoplastic
• Gene Silencing
• Humans
• MCF-7 Cells
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• MicroRNAs/metabolism
• Neoplasm Invasiveness/genetics
• Neoplasm Metastasis/genetics
• RNA, Long Noncoding/genetics
• RNA, Long Noncoding/metabolism
• RNA, Small Interfering/genetics
• Receptor, Notch2/metabolism
• Signal Transduction/genetics
• Tumor Burden/genetics
• Xenograft Model Antitumor Assays

• Breast cancer
• Cancer-associated
• Fibroblasts
• Metabolism reprogram
• SNHG3
• miR-330

• Animals
• Breast Neoplasms/genetics
• Breast Neoplasms/metabolism
• Cell Line, Tumor
• Cell Survival
• Disease Progression
• Exosomes/metabolism
• Female
• Fibroblasts/metabolism
• Gene Expression Regulation, Neoplastic
• Humans
• Inflammation
• MCF-7 Cells
• Mice
• Mice, Nude
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Microscopy, Electron, Transmission
• Mitochondria/metabolism
• Neoplasm Transplantation
• Oxygen Consumption
• Protein Binding
• Pyruvate Kinase/genetics
• Pyruvate Kinase/metabolism
• RNA, Long Noncoding/genetics

• 2019D01C258 The Natural Science Foundation of Xinjiang Uygur Autonomous Region

• Colorectal cancer
• RUNX2
• SNHG3
• miR-539

• Animals
• Cell Line, Tumor
• Cell Proliferation/genetics
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/pathology
• Core Binding Factor Alpha 1 Subunit/genetics
• Female
• Gene Expression Regulation, Neoplastic
• Gene Knockdown Techniques
• Humans
• Male
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• MicroRNAs/genetics
• Middle Aged
• Neoplasm Metastasis/genetics
• RNA, Long Noncoding/genetics
• Survival Rate
• Up-Regulation
• Xenograft Model Antitumor Assays

• SNHG
• cancer
• invasion
• lncRNAs
• malignant disease
• proliferation
• snoRNA

• SMURF1
• SNHG3
• miR-577
• prostate cancer

• ASB16-AS1
• hepatoma-derived growth factor
• microRNA-760
• osteosarcoma therapy

Previous genome-wide association study showed that GLDC/IL33 loci were associated with overall survival in patients with osteosarcoma (OS). We performed a replication study to explore whether variants of GLDC/IL33 are associated with the survival of OS patients and to further verify their functional role in the gene expression.

A total of 216 patients with OS were enrolled. The overall survival time was calculated from the date of diagnosis till the date of last follow-up or mortality. Two SNPs were genotyped, including rs55933544 and rs74438701. OS specimens were obtained from 72 patients during surgery. The gene expression level of IL33 and GLDC was evaluated by qPCR. Patients were classified into two groups according to the 5-year overall survival (death/survival). The chi-square test was used to analyze difference of genotype frequency. The Student t-test was used to compare the gene expression level between different genotypes. Cumulative survival time was calculated by the Kaplan–Meier method and analyzed by the log-rank test.

Genotype TT of rs55933544 was significantly associated with the event of death (0.176 vs. 0.061, p < 0.001). Patients with no risk allele T of rs55933544 showed a 5-year overall survival of 81.4% (110/141), which was significantly higher than an overall survival of 55.0% (29/54) for patients with one risk allele and 44.8% (12/21) for patients with two risk alleles (p < 0.01). Genotype TT of rs55933544 were indicative of remarkably lower expression of IL33 than genotype CC (0.00041 ± 0.00025 vs. 0.00065 ± 0.00031, p = 0.04). Patients with low IL33 expression presented remarkably worse survival as compared with the patients with high IL33 expression (p < .01)

Variant rs55933544 was associated with the survival time of OS patients. IL33 may contribute to a poor prognosis of OS. Further investigation into the biological mechanisms by which IL33 influences the overall survival can shed light on the improvement of clinical outcome for OS patients.

• IL33
• Osteosarcoma
• Overall survival
• Prognosis
• Variant

• Competitive endogenous RNAs
• GEO database
• Hepatocellular carcinoma
• Molecular biological mechanisms
• Prognostic values

• TTN antisense RNA 1
• dickkopf-1
• microRNA-376a
• therapeutic target

• Intrahepatic cholangiocarcinoma
• SNHG3
• long non-coding RNA
• prognosis

• EZH2
• NLRP6
• OIP5-AS1
• gastric cancer