Highly expressed circ_0000285 from serum and cervical exfoliated cells as a novel biomarker for the diagnosis of early stage-cervical cancer.

Circ_0000285 is reported to play an oncogenic role in the development of cervical cancer (CC). The aim of this research was to investigate the diagnostic power of circ_0000285 in CC. The expression of circ_0000285 in 116 healthy volunteers, 65 early-stage CC (ESCC) patients, and 87 locally advanced CC (LACC) patients was detected by qRT-PCR. The diagnostic values of circ_0000285 for CC and ESCC were evaluated by ROC curves analysis. The circ_0000285 expression was upregulated in serum and cervical exfoliated cells from preoperative CC patients compared to that of healthy volunteers. Increased circ_0000285 expression was found in preoperative LACC patients more than that in ESCC patients. The circ_0000285 expression was downregulated in serum from CC patients after surgery. The postoperative CC patients with high serum circ_0000285 expression was more prone to have a tumour relapse. High circ_0000285 expression was positively correlated with SCC-Ag level and HPV positive rate. The AUC of circ_0000285 for the diagnosis of CC and ESCC were 0.855 and 0.804, better than CA125 and SCC-Ag. When circ_0000285, CA125, SCC-Ag and HPV were combined, the AUC could reach 0.911 and 0.894. In summary, highly expressed circ_0000285 from serum and cervical exfoliated cells might be a promising diagnostic biomarker for ESCC.Impact statementWhat is already known on this subject? The CA125 and SCC-Ag have limitations in the diagnosis of ESCC. Recently, circRNAs have caused great attention and have been developing rapidly in clinical diagnosis of malignant tumours.What do the results of this study add? Highly expressed circ_0000285 from serum and cervical exfoliated cells might be used as a novel, non-invasive biomarker for the diagnosis of ESCC.What are the implications of these findings for clinical practice and/or further research? Circ_0000285 is superior to CA125 and SCC-Ag for the diagnosis of ESCC in clinical practice. The results help to supplement the shortcomings of traditional tumour markers and improve the diagnosis of ESCC.

Hsa_circ_0000285 contributes to gastric cancer progression by upregulating FN1 through the inhibition of miR-1278.

BACKGROUND: Gastric cancer (GC) is one of the most severe cancers worldwide, particularly in China. Circular RNA (circRNA) plays an essential role in GC. Hsa_circ_0000285 regulates the progression of several cancers. However, its role in GC has not been reported. This study elucidated the molecular mechanism and role of hsa_circ_0000285 in GC progression. METHODS: GC cells were transfected with silencers of hsa_circ_0000285 and fibronectin 1 (FN1), an inhibitor of miR-1278, and their negative controls (NC). Mice were injected with short hairpin (sh) RNAs targeting hsa_circ_0000285 or NC. The expression levels of hsa_circ_0000285, miR-1278, and FN1 were assessed using western blotting and reverse transcription quantitative real-time polymerase chain reaction (qRT-PCR). Several assays were used to evaluate cell proliferation, invasion, and apoptosis. Tumor burden was also analyzed. The interactions between miR-1278, hsa_circ_0000285, and FN1 were ascertained using dual-luciferase reporter assays. An RNA immunoprecipitation (RIP) assay was used to assess the enrichment of hsa_circ_0000285 and miR-1278 in GC. RESULTS: Hsa_circ_0000285 was significantly overexpressed in the GC tissues. Silencing hsa_circ_0000285 inhibited cell proliferation and invasion, promoted apoptosis, and inhibited tumor development. Hsa_circ_0000285 sponged miR-1278. Inhibition of miR-1278 in vitro reversed the effects of hsa_circ_0000285 silencing on GC progression. MiR-1278 targeted FN1, and silencing FN1 neutralized the effects of miR-1278 inhibitors on GC progression. CONCLUSIONS: The hsa_circ_0000285/miR-1278/FN1 axis regulated GC progression. In addition, it may serve as a potential therapeutic biomarker for GC.

hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR-127-5p/CDH2.

Thyroid cancer (THCA) is a leading endocrine cancer and becomes the fifth most commonly diagnosed malignancy in females. It is confirmed that circular RNAs (circRNAs) perform regulatory potencies in the pathological progress of THCA. Our purpose was to certify the trait of hsa_circ_0000285 (circ_0000285) and investigate its modulatory mechanism in THCA progression. We identified the expression profile of hsa_circ_0000285 in THCA by conducting qRT-PCR assay. Therewith, the potential of hsa_circ_0000285 in THCA development was determined with a set of functional experiments, including CCK-8, wound healing assay, Western blot, and xenograft model. The molecular mechanism underlying hsa_circ_0000285 was investigated with bioinformatic analysis, RIP and dual-luciferase reporter experiments. As opposed to normal samples and cells, hsa_circ_0000285 level was overtly increased in THCA specimens and cells. The downregulation of hsa_circ_0000285 weakened the proliferative and migratory capacity of THCA cells and promoted cell apoptosis. In addition, hsa_circ_0000285 silence suppressed the tumor growth of xenograft model mice in vivo. Notably, we demonstrated that hsa_circ_0000285 might target miR-127-5p/CDH2 axis in THCA. Afterward, our findings manifested that miR-127-5p attenuation blocked the function of hsa_circ_0000285 depletion in THCA cells. In the final step, CDH2 was proven to mediate the repressive potency of miR-127-5p in the malignant behaviors of THCA. Mechanistically, hsa_circ_0000285 induced the development of THCA via functioning as a competing endogenous RNA (ceRNA) of miR-127-5p to enhance CDH2 expression, which provided a new perspective for THCA therapy.

Circular RNA hsa_circ_0000285 regulates the microRNA-599/G-protein subunit gamma 12 (miR-599/GNG12) axis to promote glioma progression.

OBJECTIVE: Glioma is the most common, rapidly progressing, lethal brain tumor. However, underlying mechanisms behind its abnormal progression remain largely unknown. This study aimed to investigate mechanism of action and effects of the hsa_circ_0000285 on glioma progression. METHODS: RT-qPCR was utilized to study RNA expression in glioma tissues and cell lines. The effects of hsa_circ_0000285 on glioma progression were studied by measuring cell proliferation and migration, apoptosis, tumor volume and weight in both glioma cells and xenograft glioma mice. The features of hsa_circ_0000285 were identified using chromatin fractionation and RNase digestion. Its mechanism of action was analyzed using bioinformatics, RNA-binding protein immunoprecipitation, and luciferase reporter assay. RESULTS: We found glioma tissues and cell lines were overexpressing hsa_circ_0000285. While hsa_circ_0000285 promoted cell proliferation and migration, it inhibited apoptosis in vitro. It also increased tumor volume and weight in vivo. Using bioinformatic analysis and verification experiments for studying its mechanisms, we confirmed that hsa_circ_0000285 sponged miR-599, which negatively regulated GNG12 by binding to its mRNA. CONCLUSION: Hsa_circ_0000285 is overexpressed in the glioma and promotes its progression by directly regulating the miR-599/GNG12 axis. This novel mechanism, therefore, shows that the hsa_circ_0000285/miR-599/GNG12 axis may be a promising therapeutic target for glioma treatment.

Circ_0000285 regulates proliferation, migration, invasion and apoptosis of osteosarcoma by miR-409-3p/IGFBP3 axis.

BACKGROUND: Circular RNAs (circRNAs) are important regulators in the pathogenesis of diseases and affects the occurrence and development of diseases. However, the role of circRNAs in osteosarcoma (OS) has not been fully elucidated. METHODS: The expression of circ_0000285, miR-409-3p and insulin-like growth factor binding protein 3 (IGFBP3) was detected using quantitative real-time PCR (qRT-PCR). The protein level of IGFBP3 was measured using western blot. CCK-8 and colony formation assays were used to determine cell proliferation. Flow cytometry was applied to measure cell cycle and cell apoptosis. Transwell assay was used to assess cell invasion and migration. Dual-luciferase reporter assay and RNA Binding Protein Immunoprecipitation (RIP) assay were performed to determine the relationship among circ_0000285, miR-409-3p and IGFBP3. The animal experiments were performed to determine the function of circ_0000285 in vivo. RESULTS: In this study, we found that the expression of circ_0000285 was significantly increased in OS tissues and cells and was enriched in the cytoplasm. Knockdown of circ_0000285 inhibited OS growth in vitro and in vivo. Moreover, miR-409-3p was a target miRNA of circ_0000285 and miR-409-3p targets to IGFBP3 in OS. Besides, circ_0000285 could promote proliferation, migration, invasion and inhibit apoptosis of osteosarcoma by miR-409-3p/IGFBP3 axis. CONCLUSION: In this study, circ_0000285 regulated proliferation, migration, invasion and apoptosis of OS cells by miR-409-3p/IGFBP3 axis, implying that circ_0000285 was a potential target for OS therapy.

Circ_0000285 regulates nasopharyngeal carcinoma progression through miR-1278/FNDC3B axis.

BACKGROUND: Nasopharyngeal carcinoma (NPC) is cancer with high mortality and poor prognosis. Circular RNAs (circRNAs) have been identified in a wide variety of cancers. But the functional mechanism of circ_000285 in NPC remains unclear. PURPOSE: To decipher the biological function and molecular mechanism of circ_000285 in NPC. METHODS: Quantitative PCR (RT-qPCR) was applied for detecting the expression of circ_0000285, miR-1278, and FNDC3B. Western blot was used to measure the protein levels of Fibronectin type III domain containing 3B (FNDC3B), Bcl2 associated X (Bax), and B cell leukemia/lymphoma 2 (Bcl2). Cell proliferation, migration, and invasion were analyzed by colony formation, 5-ethynyl-2'-deoxyuridine (EdU), and transwell assays. Cell apoptosis was detected by flow cytometry assays. ELISA assay was used to analyze Caspase-3 activity. Bioinformatics was used to predict, and the target relationship between miR-1278 and circ_0000285 or FNDC3B was verified by luciferase reporter assay. Tumor xenograft models were established to examine how circ_0000285 functions during the mediation of NPC tumor growth in vivo. RESULTS: Increased circ_0000285 and FNDC3B expressions, and a decreased miR-1278 expression were observed in NPC tissues and cell lines. Knockdown of circ_0000285 inhibited NPC cell proliferation, migration, invasion, and while promoting NPC cell apoptosis in vitro. Circ_0000285 knockdown-mediated anti-tumor effects in NPC cells could be largely reversed by silencing of miR-1278 or overexpression of FNDC3B. Circ_0000285 could up-regulate FNDC3B expression by sponging miR-1278 in NPC cells. Knockdown of circ_0000285 could inhibit tumor growth in vivo. CONCLUSION: Circ_0000285 upregulates FNDC3B expression by adsorbing miR-1278 to promote NPC development.

Hsa_circ_0000285-Mediated miR-599/RGS17 Axis Participates in the Pathogenesis of Abdominal Aortic Aneurysm by Regulating the Functions of Vascular Smooth Muscle Cells.

OBJECTIVE: Abdominal aortic aneurysm (AAA) is characterized by vascular smooth muscle cell (VSMC) injury. Circ_0000285 has been declared to drive cancer development, but its role in AAA remains unclear. We thus intended to disclose circ_0000285's role and molecular mechanism in AAA. METHODS: VSMCs were exposed to hydrogen peroxide (H2O2) to induce cell injury. Circ_0000285, miR-599, and regulator of G protein signaling 17 (RGS17) mRNA expressions were ascertained by conducting RT-qPCR assay while the levels of RGS17 protein was ascertained via western blotting. MiR-599's predicted binding with circ_0000285 and RGS17 were validated by means of the dual-luciferase reporter experiment. Cell proliferation was evaluated through the CCK-8 and EdU assays. Cell apoptosis was assessed via the caspase-3 activity assay. RESULTS: The AAA samples and H2O2-treated VSMCs manifested high expressions of circ_0000285 and RGS17 as well as a poor miR-599 expression. H2O2 treatment impaired the proliferation of VSMCs while stimulating their apoptosis. Circ_0000285 overexpression further repressed cell proliferation and enhanced apoptosis in H2O2-treated VSMCs while miR-599 enrichment partly reversed these effects. Circ_0000285 directly bound to miR-599, and miR-599 interacted with RGS17 3'UTR. RGS17 overexpression also suppressed cell proliferation and stimulated apoptosis in H2O2-treated VSMCs. Nevertheless, these effects were offset by miR-599 enrichment. CONCLUSION: Circ_0000285 governed the miR-599/RGS17 network to regulate H2O2-induced VSMC injuries, thereby promoting the development of AAA.

hsa_circ_0000285 sponging miR-582-3p promotes neuroblastoma progression by regulating the Wnt/ß-catenin signaling pathway.

Circular RNA has been reported to play a key role in neuroblastoma (NB); however, the role of circ_0000285 in NB remains unclear. The aim of this study was to elucidate the role of circ_0000285 in NB. We studied the expression patterns of miR-582-3p and circ_0000285 in NB tissues and cells using real-time quantitative polymerase chain reaction. The expression of proteins associated with apoptosis (Bax and Bcl-2) and the proteins associated with Wnt/ß-catenin (Wnt, p-Gsk-3ß, Gsk-3ß, ß-catenin, and C-myc) were quantified by western blotting. In vivo animal models were prepared for the functional verification of circ_0000285 on tumor growth. The potential binding of circ_0000285 to miR-582-3p was ascertained using dual-luciferase reporter and RNA-binding protein immunoprecipitation experiments. Noticeable upregulation of circ_0000285 expression was observed in NB tumor samples and cell lines. In vivo and in vitro experiments indicated that the absence of circ_0000285 repressed NB cell proliferation and migration, provoked apoptosis, and impaired the activity of Wnt/ß-catenin signaling. miR-582-3p is targeted by circ_0000285 and is poorly expressed in NB cells. The additional repression of miR-582-3p in NB cells after circ_0000285 silencing largely recovered circ_0000285 silencing-suppressed NB cell proliferation and migration and enhanced apoptosis. The absence of miR-582-3p restored Wnt/ß-catenin signaling activity impaired by the knockdown of circ_0000285. circ_0000285 functions as an miR-582-3p sponge to strengthen Wnt/ß-catenin signaling activity, thus exacerbating NB development.

Circular RNA_0000285: A novel double-edged sword circular RNA in human malignancies.

Circular RNAs (circRNAs) are a class of RNA molecules that are characterized by their covalently closed structure, which is formed through a process of back splicing of the precursor mRNA. Abnormal expression of circRNAs has been shown to indirectly affect their interaction with microRNAs (miRNAs), thereby modulating gene transcription. One such circRNA, circ_0000285, is known to be dysregulated in various cancers and human diseases. This circRNA is derived from the HIPK3 gene on chromosome 11 and acts as a competing endogenous RNA for several miRNAs, including miR-654-3p, miR-197-3p, miR-1278, miR-582-3p, and miR-599. Notably, circ_0000285 has been linked to poor overall survival and several clinicopathological features in multiple human cancers. In this review, we present a comprehensive summary of the oncogenic effect of circ_0000285 in various cancers, drawing on experiment performed on cell lines, animals, and human tissues. Furthermore, we predicted potential miRNAs and RNA-binding proteins that may interact with circ_0000285, thereby providing new insights for further studies.

circRNA_0000285 knockdown suppresses viability and promotes apoptosis of cervical cancer cells by sponging microRNA-654-3p.

Cervical cancer (CC) is one of the most common gynecological tumors worldwide. Several studies have reported that circular RNAs (circRNAs) play important roles in various types of diseases, including cancer. Thus, the present study aimed to investigate the role of circRNA_0000285 in CC development. Dual-luciferase reporter and RNA pull-down assays were performed to verify the binding region between circRNA_0000285 and miR-654-3p. The expression levels of circRNA_0000285 and miR-654-3p were analyzed in CC and the corresponding normal tissues, as well as in SiHa, HeLa, and NC104 cells using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In addition, the effect of circRNA_0000285 inhibition on cell viability, apoptosis, and the expression of apoptosis-related markers was assessed using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), flow cytometry, and Western blotting assays, respectively. The results verified that miR-654-3p directly targeted circRNA_0000285 expression. circRNA_0000285 was overexpressed and miR-654-3p expression was downregulated in CC tissues and cells compared to that in control. Moreover, circRNA_0000285 knockdown suppressed the viability and promoted the apoptosis of CC cells, which was accompanied by the downregulated and upregulated expressions B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X (Bax), respectively. The ratio of Bax/Bcl-2 levels also increased following circRNA_0000285 knockdown. However, these findings were abrogated after miR-654-3p inhibitor treatment. Hence, circRNA_0000285 knockdown suppressed cell viability and promoted apoptosis by targeting miR-654-3p in CC.

Hsa_circ_0000285 knockdown inhibits the progression of hepatocellular carcinoma by sponging miR-582-3p to regulate CCNB2 expression.

AIM: Hsa_circ_0000285, a novel circular RNA, has been proven to extensively take part in the pathogenesis of numerous tumors. In hepatocellular carcinoma (HCC), very little is known about hsa_circ_0000285 until now. Hence, this research aims to determine hsa_circ_0000285's functional role and underlying mechanisms in HCC. METHODS: The expressions of miR-582-3p, hsa_circ_000028, and cyclin B2 (CCNB2) among the HCC cells and tumor samples were determined by performing western blotting and qRT-PCR analyses. The impacts of hsa_circ_000028 on the proliferative and migratory abilities of HCC cells were examined through the execution of CCK-8 and wound-healing assays. Meanwhile, the expressions of the proteins Bcl-2 and Bax were detected via western blotting. Tumor xenograft models were established to examine how hsa_circ_000028 functions during the mediation of HCC tumor growth in vivo. RNA immunoprecipitation and luciferase reporter experiments were performed for the validation of the interactions of miR-582-3p, hsa_circ_000028, and CCNB2 with each other. RESULTS: Elevated hsa_circ_0000285 and CCNB2 expressions, and a decreased miR-582-3p expression were observed among the HCC cell lines and tumors. Hsa_circ_0000285 bound to miR-582-3p competitively to improve CCNB2 levels. Silencing of hsa_circ_0000285 promoted apoptosis and repressed proliferation and migration among HCC cells. Moreover, silencing hsa_circ_0000285 also impeded the growth of HCC tumors in vivo. Inhibiting hsa_circ_0000285 or CCNB2 reversed the miR-582-3p-knockdown-mediated promotion of malignant HCC cell phenotypes. CONCLUSION: Our study has demonstrated that hsa_circ_0000285 fosters the development of malignant HCC cells phenotypes through the modulation of the miR-582-3p/CCNB2 axis. Thus, these results suggest that hsa_circ_0000285 is a prospective target for HCC treatment.

Inhibition of circular RNA_0000285 prevents cell proliferation and induces apoptosis in thyroid cancer by sponging microRNA-654-3p.

Thyroid cancer is derived from follicular or thyroid cells and has become the most prevalent malignant tumor of endocrine organs, with increased morbidity and mortality. Circular RNAs (circRNAs) are used as prognostic and predictive markers for different types of cancer. However, the role of circRNA_0000285 in thyroid cancer and its potential molecular mechanism remain unclear. The present study aimed to investigate the roles and underlying molecular mechanism of circRNA_0000285 in thyroid cancer to identify novel treatments for this disease. The target binding site of circRNA_0000285 and microRNA-654-3p (miR-654-3p) were predicted and confirmed via the dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Thyroid cancer cell viability and apoptosis were determined via the MTT assay and flow cytometric analysis, respectively, whereas the expression levels of circRNA_0000285 and miR-654-3p were determined via reverse transcription-quantitative PCR analysis. In addition, the protein expression levels of the apoptosis-associated proteins, Bax and B-cell lymphoma 2 (Bcl-2), were detected via western blotting. The results of the dual-luciferase reporter and RIP assays demonstrated that miR-654-3p directly targeted circRNA_0000285. The expression levels of circRNA_0000285 and miR-654-3p in thyroid cancer cells (TPC-1 and FTC133) were upregulated and downregulated, respectively. Knockdown of circRNA_0000285 via small interfering (si)RNA inhibited circRNA_0000285 levels and increased miR-654-3p levels. In addition, miR-654-3p expression decreased following transfection with miR-654-3p inhibitor. Functional experiments demonstrated that circRNA_0000285-siRNA decreased thyroid cancer cell proliferation, promoted cell apoptosis, enhanced Bax expression and suppressed Bcl-2 expression. All these effects were reversed following transfection with miR-654-3p inhibitor. Taken together, the results of the present study suggest that circRNA_0000285 plays a vital role in thyroid cancer progression by regulating miR-654-3p, which provides a potential therapeutic target for this disease.

Circ_0000285 promotes podocyte injury through sponging miR-654-3p and activating MAPK6 in diabetic nephropathy.

Recently, increasing evidence has reported that circRNAs are non-coding RNAs and they bind with the corresponding miRNAs to modulate the target genes. However, the detailed role of circRNAs in the pathogenesis of DN still remains poorly known. Currently, we aimed to study how circ_0000285 functions in DN development. We found that circ_0000285 was significantly increased in DN mice models and mouse podocytes incubated with HG. Then, circ_0000285 was overexpressed in mouse podocytes and we observed that overexpression of circ_0000285 promoted podocytes injury. Moreover, miR-654-3p was precited as a target of circ_0000285. It was shown that circ_0000285 was strongly pulled down by circ_0000285 specific probe and circ_0000285 specific probe was used to successfully enrich miR-654-3p. In addition, we reported that miR-654-3p was obviously down-regulated in DN. Inhibitors of miR-654-3p greatly reversed the effects of circ_0000285 siRNA on podocytes injury. Moreover, the inflammation release was restrained by loss of circ_0000285, while induced by miR-654-3p inhibitors. IL-6, L-1ß and TNF-α level was remarkably depressed by the knockdown of circ_0000285 and miR-654-3p inhibitors induced that. Furthermore, MAPK6 was confirmed as a direct downstream target of miR-654-3p. As shown, MAPK6 was markedly suppressed by circ_0000285 siRNA, which was rescued by the decrease of miR-654-3p. These findings revealed that circ_0000285 promoted podocyte injury via sponging miR-654-3p and activating MAPK6 in DN.

Downregulation of circRNA_0000285 Suppresses Cervical Cancer Development by Regulating miR197-3p-ELK1 Axis.

BACKGROUND: Circular RNAs (circRNAs) are involved in the development of human cancers, including cervical cancer (CC). However, the role and mechanism of the circRNA hsa_circ_0000285 (circ_0000285) in CC development remain largely unknown. METHODS: Thirty paired CC and adjacent normal tissue samples were harvested. CC cell lines SiHa and HeLa were cultured in this study. The expression of circ_0000285, miR197-3p and ELK1 was detected via qRT-PCR or Western blot. CC development was assessed via cell viability, colony formation, apoptosis, cell cycle, and autophagy using MTT, colony-formation assays, flow cytometry and Western blot. The target association was analyzed via dual luciferase-reporter assay, RNA immunoprecipitation, and RNA pull-down. The role of circ_0000285 in CC in vivo was analyzed using a xenograft model. RESULTS: circ_0000285 abundance was enhanced in CC tissue and cells and mainly located in cytoplasm. Silence of circ_0000285 suppressed cell viability and colony formation, arrested the cell cycle at the G0/G1 phase, and induced apoptosis and autophagy in CC cells. miR197-3p was targeted by circ_0000285, and miR197-3p knockdown reversed the effect of circ_0000285 silence on CC development. miR197-3p directly targeted ELK1 to inhibit CC development. circ_0000285 regulated ELK1 by modulating miR197-3p. Knockdown of circ_0000285 reduced xenograft tumor growth in vivo. CONCLUSION: Knockdown of circ_0000285 repressed CC development by increasing miR197-3p and decreasing ELK1.

Upregulation of circRNA_0000285 serves as a prognostic biomarker for nasopharyngeal carcinoma and is involved in radiosensitivity.

Despite significant medical advancement, nasopharyngeal carcinoma (NPC) remains one of the most difficult types of cancer to detect and treat. Circular RNA (circRNA) signatures may be used as prognostic and predictive factors for cancer. Previous studies indicated that the biological role of circular homeodomain interacting protein kinase 3 (HIPK3) has cancer type-specificity. The HIPK3 gene locus formats three circRNA isoforms: circRNA_100783, circRNA_0000285 and circRNA_100782. However, their roles in NPC remain unknown. In the present study, whether these circRNAs could be used as a biomarker for NPC diagnosis and predicting treatment response was investigated. Reverse transcription-quantitative polymerase chain reaction was performed to measure the levels of circRNA_100783, circRNA_0000285 and circRNA_100782 in NPC and adjacent tissues. In addition, the circRNA_0000285 levels were further confirmed in serum samples from patients with NPC and healthy controls. The results demonstrated that circRNA_0000285, but not circRNA_100782 and circRNA_100783, was significantly increased in NPC tissues and serum samples from patients with NPC, compared with adjacent tissues and serum samples from healthy controls, respectively. Furthermore, circRNA_0000285 expression was increased in patients with radioresistant NPC, compared with patients with radiosensitive NPC. Further analysis demonstrated that circRNA_0000285 was significantly associated with tumor size (P<0.001), differentiation (P=0.022), lymph node metastasis (P=0.035), distant metastasis (P=0.022) and Tumor-Node-Metastasis stage (P<0.001). Additionally, univariate and multivariate analyses indicated that circRNA_0000285 may be an independent prognostic factor for the outcome of patients with NPC. The present data indicated that circRNA_0000285 may be a novel biomarker for NPC and is involved in NPC radiosensitivity.