ATP citrate lyase (ACLY) is involved in acetyl-coenzyme A synthesis and protein acetylation, thereby increasing lipid metabolism and altering protein metabolism to affect cellular metabolism. Additionally, ACLY is associated with various biological and pathological functions, especially regarding tumorigenesis. It facilitates the progression of various cancer types, including liver, lung, breast, prostate, and colorectal cancers. Mechanisms underlying ACLY-mediated carcinogenesis are under investigation and may not be limited to energy metabolism and biosynthesis. Acetylation modification of specific signaling molecules and transcription factors is considered a potential mechanism of ACLY-mediated tumorigenesis and offers novel insights and potential targets for the clinical treatment of tumors. Furthermore, the antitumor effect of pharmacological ACLY-inhibiting agents, including various small molecules or naturally active compounds, has been reported, albeit their practical application in clinical settings remains limited. This study aims to comprehensively review the oncogenic role of ACLY, with a focus on major collaborators and regulatory genes.

IntroductionChinese holly (Ilex cornutaLindl. ex Paxt) fruit exhibits various biological activities, including heat-clearing and detoxifying, promoting blood circulation to remove stasis, relieving pain and detoxifying, and anti-inflammatory effects. However, its role in inhibiting tumor initiation and progression remains unclear, particularly in melanoma therapy.MethodsIn the present study, a panel of molecular biological approaches, including CCK8 assay, colony formation assay, transwell assay, cell cycle profiling, apoptosis detection, flow cytometry, IHC, Western blot, qPCR, RNAseq and metabonomics were utilized to systematically explore the regulatory effects of CHF on proliferative behaviors and immune evasion potential of melanoma cells.Results and DiscussionWe found that Chinese holly fruit (abbreviated as CHF) extract suppresses the proliferative activity of melanoma by activating the P53-P21 signaling pathway, which downregulates the expression of CDK2 and cyclin family members. Meanwhile, CHF promotes apoptosis by upregulating FAS and GADD45A. Metabolomic profiling revealed that differential metabolites induced by CHF extract treatment were enriched in glucose metabolism, energy metabolism, and the AMPK signaling pathway. Furthermore, CHF extract inhibits PD-L1 expression by suppressing the JAK2-STAT1 signaling pathway, thereby increasing the infiltration of CD3+ and CD8+T cells into tumor tissues and consequently suppressing melanoma immune escape. More importantly, pharmacological administration of CHF extract improves the anti-tumor efficacy of anti-PD-1/PD-L1 immunotherapy, as demonstrated by enhanced T cell infiltration and slower tumor growth in the combination treatment group compared with monotherapy with either agent. Taken together, these findings highlight a crucial role of CHF extract in anti-melanoma effects, and combination with PD-L1 antibody immunotherapy may be an attractive strategy for melanoma treatment.

Bile acids (BAs) represent the terminal products of cholesterol catabolism and are integral to a wide range of physiological processes. The maintenance of BAs homeostasis is essential for human health, with disruptions being implicated in various liver and intestinal disorders. The gut-liver axis, a bidirectional communication network connecting multiple organ systems, plays a crucial role in preserving both metabolic and immune homeostasis. Recent evidence suggests that BAs are key modulators within this axis, influencing intestinal barrier function, immune responses, and the composition of the gut microbiome. This review synthesizes recent advances in our understanding of BAs, including their origins, circulation within the gut-liver axis, and diverse roles in physiology, thereby highlighting the critical functional significance of this BAs-mediated network.

Panax species are globally recognized for their high medicinal and economic value, yet large-scale cultivation is constrained by high production costs, progressive soil acidification, and persistent soil-borne diseases. Although various soil improvement strategies have been tested, a comprehensive synthesis of their comparative effectiveness has been lacking. Here, we conducted a meta-analysis of 1381 observations from 54 independent studies to evaluate the effects of conventional fertilizers, microbial fertilizers, organic amendments, and inorganic amendments on Panax cultivation. Our results demonstrate that microbial fertilizers, organic amendments, and inorganic amendments significantly increased soil pH, thereby ameliorating soil acidification. Among them, organic amendments significantly enhanced the content of soil organic carbon, available nitrogen, and available phosphorus, alongside a notable increase in microbial diversity (Chao1 and ACE indices, which increased by 9% and 17%, respectively). Moreover, our analysis revealed that while microbial fertilizers, organic amendments, and inorganic amendments (except conventional fertilizers) reduced the disease index of Panax plants, organic amendments demonstrated absolute superiority in promoting plant height, root dry weight, root fresh weight, and root length. By quantitatively integrating multi-source evidence, this study provides novel mechanistic insights and practical recommendations that extend beyond local practices, offering guidance for sustainable ginseng cultivation and broader medicinal plant production systems worldwide.

Gastric cancer (GC) is one of the most common malignancies with a poor prognosis. The development of novel biomarkers is of utmost importance to screen patients with GC. Molecular mechanism study of GC may provide a research basis for the development of targeted drugs. We identified tRF-29-79MP9P9NH525 (tRF-29) as a GC-associated tRNA-derived fragment (tRF). The specific hair-pin structure reverse primer and amplification primers were first designed and then applied for tRF-29 quantification. Receiver operator characteristic curve, Kaplan-Meier survival curve, and multivariate Cox analysis were applied to analyze the diagnostic and prognostic values of tRF-29 in GC. Ethynyl-2'-deoxyuridine, cell cloning, Transwell assay, and flow cytometry were used to detect the effects of tRF-29 on proliferation, migration, and cell cycle distribution of GC cells. Xenograft tumor formation in NOD-SCID mice was applied in determining tRF-29's effects on tumor growth. Fluorescence in situ hybridization, dual luciferase reporter assay, Western blot, immunohistochemistry, and RNA-binding protein immunoprecipitation were conducted to explore the molecular mechanism underlying tRF-29 regulating GC development. It was found that tissue tRF-29 showed effective diagnostic efficiency in GC and could discriminate different gastric mucosa. Besides, plasma tRF-29 improved GC diagnostic values of common tumor markers and had prognostic values in GC. tRF-29 was found to suppress proliferation and cell cycle progression. tRF-29 inhibited the growth of xenograft tumors. Mechanically, tRF-29 exerted Kinesin family member 14 (KIF14) mRNA destabilization by combining with argonaute 2 (Ago2) and regulated AKT/P27 pathway. In conclusion, tRF-29 inhibited GC progression by combining with Ago2 and regulated AKT/P27 pathway by silencing KIF14 expression. In normal cells, tRF-29, derived from tRNA-ValACC, targets the 3'UTR region of KIF14 mRNA by forming RNA silencing complex with Ago2. Reduced KIF14 results in less phospholation of AKT. Subsequently, the expression of P27 is increased, while the expression of MMP-2 is decreased. Finally, the cell cycle is arrested, and the cell proliferation is suppressed, as well as the metastasis is inhibited. In gastric cancer cells, due to the downregulated of tRF-29, the expression of KIF14 is increased, thus the cell proliferation and metastasis are promoted via AKT pathway.

Protein N-phosphorylation represents one of the principal forms of protein phosphorylation modifications, which has been extensively identified in both prokaryotes and eukaryotes. However, significant knowledge gaps persist regarding its functional implications, sequence motifs, and structural characteristics. Through integrated functional, sequential, and structural analyses of experimentally verified large-scale N-phosphorylation datasets, we found that protein N-phosphorylation broadly participates in diverse biological processes and exhibits close associations with human diseases, particularly cancer. And the high motif conservation between N- and O-phosphorylation in eukaryotes offers novel research perspectives for investigating N-phosphorylation through the lens of O-phosphorylation. Moreover, the structural-sequence pattern analyses demonstrate that relative solvent accessibility at modification sites provides more distinctive characterization of phosphorylation sites than other structural-sequence descriptors. These findings provide evidence supporting the potential role of N-phosphorylation in biological processes and contribute to its further development in biological sciences, analytical chemistry, and medical research.

BACKGROUND: A growing body of evidence has shown that activating spinal cord glial cells (typically astrocytes and microglial cells) is closely related to hyperpathia and persistent pain. OBJECTIVE: To investigate the expression of GFAP and CR3/CD11b in cornu dorsale medullae spinalis of rats with nonbacterial prostatitis, to explore the therapeutic efficacy and action mechanism of intrathecal injection of BNP alleviating chronic neuropathic pain. METHODS: Eighteen male SPF SD rats were randomly divided into sham operation control group, nonbacterial prostatitis group (NBP) and intrathecal injection BNP group, the NBP model was established by intraprostatic injection of CFA, and the spinal cord of L6-S1 segment was extracted seven days after intrathecal injection of BNP; The expression of GFAP and CR3/CD11b in dorsal horn of spinal cord were detected by immunofluorescence and Western blot. RESULTS: The cumulative optical density values of GFAP and CR3/CD11b immunofluorescence assay in the NBP group were higher than those in the sham operation group, with statistical significance (p 0.01); The expression of GFAP and CR3/CD11b in intrathecal injection BNP group were lower than those in NBP group, the differences were statistically significant (p 0.01). Western blot results showed that the expression of GFAP and CR3/CD11B in NBP group were higher than those in sham operation group, with statistical significance (p 0.05). The expression of GFAP and CR3/CD11B in intrathecal injection BNP group were lower than those in NBP group, the differences were statistically significant ( p 0.05). CONCLUSION: Intrathecal injection of BNP can down-regulate the expressions of GFAP and CR3/CD11b in L6-S1 spinal cord of NBP rat model and to further inhibit chronic pain caused by NBP.

Circular RNAs are considered to play important roles in the progression of different cancers such as esophageal squamous cell carcinoma. However, the functions of circular RNAs in esophageal squamous cell carcinoma are still not clear. This study aimed to investigate the role and mechanism of circRNA-0036474 in the progression of esophageal squamous cell carcinoma. The hsa_circ_0036474 expression levels were found to be elevated in both EC109 cells and esophageal squamous cell carcinoma tissue samples. Moreover, knockdown of circRNA-0036474 expression in the EC109 cells induced migration and invasion, characterized by the down-regulation of E-cadherin, and up-regulation of N-cadherin and vimentin. In addition, the over-expressed hsa_circ_0036474 significantly decreased the activity of EC109 cells, elevated E-cadherin expression but declined N-cadherin and vimentin expression. Moreover, over-expressed mir-223-3p levels and interfered RERG expression verified the role of hsa_circ_0036474 in inhibiting the invasion and migration of EC109 cells, reducing the expression of N-cadherin and vimentin, and promoting the expression of E-cadherin. In conclusion, circRNA-0036474 mitigated the progression of esophageal squamous cell carcinoma through regulating mir-223-3p/RERG axis, presenting a potential therapeutic target for the treatment.

Protein N -phosphorylation widely present in nature and participates in various biological functions. However, current knowledge on N -phosphorylation is extremely limited compared to that on O -phosphorylation. In this study, we collected 11,710 experimentally verified N -phosphosites of 7344 proteins from 39 species and subsequently constructed the database Nphos to share up-to-date information on protein N -phosphorylation. Upon these substantial data, we characterized the sequential and structural features of protein N -phosphorylation. Moreover, after comparing of hundreds of learning models, we chose and optimized gradient boosting decision tree (GBDT) models to predict three types of human N -phosphorylation, achieving mean areas under the receiver operating characteristic curve (AUC) of 90.56%, 91.24%, and 92.01% for pHis, pLys, and pArg, respectively. Meanwhile, we discovered 488,825 distinct N -phosphosites in the human proteome. The models were also deployed in Nphos for interactive N -phosphosite prediction. In summary, this work provides new insights and points for both flexible and focused investigations of N -phosphorylation. It will also facilitate a deeper and more systematic understanding of protein N -phosphorylation modification by providing a data and technical foundation. Nphos is freely available at http://www.bio-add.org and http://ppodd.org.cn/Nphos/ .

Abstract Programmed death-ligand 1 (PD-L1), one of the immunosuppressive molecules, overexpresses in multiple cancers and is critical for their immune escape. We previously showed that the nuclear coactivator SRC-1 promoted colorectal cancer (CRC) progression by enhancing CRC cell viability; however, the role of SRC-1 in CRC immune escape is unclear. Here, we demonstrated that SRC-1 was positively correlated with PD-L1 in human CRC specimens. SRC-1 deficiency significantly inhibited PD-L1 expression in both human and murine CRC cells and retarded murine CRC growth in subcutaneous grafts by enhancing CRC immune escape via increasing tumor infiltration and antitumor activity of effector CD8+ T cells. Genetic ablation of SRC-1 in mice also decreased PD-L1 expression in AOM/DSS-induced murine CRC. These results suggest that tumor-derived SRC-1 promotes CRC immune escape by enhancing PD-L1 expression. Mechanistically, SRC-1 activated JAK-STAT signaling by inhibiting SOCS1 expression and coactivated STAT3 and IRF1 to enhance PD-L1 transcription as well as stabilized PD-L1 protein by inhibiting proteasome-dependent degradation mediated by speckle type POZ protein (SPOP). Pharmacological inhibition of SRC-1 improved the antitumor effect of PD-L1 antibody in both subcutaneous graft and AOM/DSS-induced murine CRC models. Taken together, our findings highlight a crucial role of SRC-1 in facilitating CRC immune escape and targeting SRC-1 in combination with PD-L1 antibody immunotherapy may be an attractive strategy for CRC treatment. Citation Format: Yilin Hong, Qiang Chen, Zinan Wang, Yong Zhang, Bei Li, Xu Kong, Pingli Mo, Nengming Xiao, Jianming Xu, Yunbin Ye, Chundong Yu. Nuclear receptor coactivator SRC-1 promotes colorectal cancer immune escape by enhancing PD-L1 transcription and protein stability [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1688.

Background: Acute myocardial infarction (AMI) remains one of the most fatal diseases worldwide. Persistent ischemia and hypoxia are implicated as significant mechanisms in the development of AMI. However, no hypoxia-related gene targets of AMI have been identified to date. This study aimed to identify potential genes and drugs for AMI using bioinformatics analysis. Materials and Methods: Two datasets both related to AMI (GSE76387 and GSE161427) were downloaded from the Gene Expression Omnibus to identify differentially expressed genes (DEGs) between AMI and sham mice. Gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed. A protein-protein interaction (PPI) network was constructed to identify hub genes using Cytoscape. Candidate genes were identified by the intersection of hub genes and hypoxia-related genes. Western blotting was used to validate the candidate genes in the AMI mouse model. Furthermore, the Drug-Gene Interaction Database was used to predict potential therapeutic drugs targeting all hub genes. Results: Fifty-three upregulated and 16 downregulated genes closely related to AMI were identified. The DEGs were primarily enriched in protein, heparin, and integrin binding. KEGG analysis suggested that focal adhesion, PI3K-Akt signaling pathway, and extracellular matrix-receptor interaction are crucial pathways for AMI. The PPI network analysis identified 14 hub genes, two of which were hypoxia-related. Several agents were found to have therapeutic potential for AMI. Conclusion: This study suggests that connective tissue growth factors and the collagen family members may be candidate targets in treating AMI. Agents targeting these candidates may be potential treatments.

Background and Objective: SPC24 was reported to be correlated with the development of many cancers. However, its role in renal cancer was unclear. Our aim was to explore the role of SPC24 in kidney renal clear cell carcinoma (KIRC) and kidney renal papillary cell carcinoma (KIRP) in types of renal cancer. Methods: SPC24 expressions in KIRC and KIRP were firstly analyzed. Subsequently, the correlation between SPC24 expression and TNM staging of KIRC and KIRP and the accuracy of SPC24 in diagnosing KIRC and KIRP were explored. Moreover, the correlation between SPC24 expression and prognosis of KIRC and KIRP were analyzed. Univariate and multivariate analyses were performed to identify prognostic factors in KIRC and KIRP, and nomograms were constructed. The correlation between SPC24 expression and immune cell infiltration, immune molecules, microsatellite instability (MSI), and tumor mutational burden (TMB) were further explored. Finally, the correlations between SPC24 expression and prognosis of KIRC based on different immune cell enrichment were analyzed. Results: SPC24 was significantly up-regulated in multiple cancers, especially KIRC and KIRP. SPC24 expression was significantly correlated with the TNM stage of KIRC and KIRP, and upregulated SPC24 suggested a worse prognosis. Besides, SPC24 possesses good accuracy in diagnosing KIRC and KIRP. The SPC24-based nomograms displayed satisfactory efficacy in KIRC and KIRP. Moreover, we found that SPC24 expression was closely correlated with immune cell infiltration, immune molecules, and TMB in KIRC, and up-regulated SPC24 revealed poor prognosis based on different immune cell enrichment. Conclusion: SPC24 has the potential to be a biomarker predicting the prognosis and/or immune infiltration of KIRC and KIRP.

Background: C5orf46 has been found to have antibacterial and anti-inflammatory effects via sequencing and microarray technologies, but its effects on cancer are unclear. Methods: C5orf46 expression in renal cancer patients and cell lines was measured by quantitative polymerase chain reaction (qPCR). RNA sequencing data and clinicopathological information from renal cancer patients extracted from The Tumor Genome Atlas (TCGA) were analyzed to evaluate the prognostic value of C5orf46. The role of C5orf46 in vitro was verified by migration, proliferation and apoptosis experiments in renal cancer cell lines. Furthermore, the transcriptome of renal cancer cell lines with C5orf46 knocked down was sequenced to analyze potential signaling network pathways. Finally, the possible mechanisms of C5orf46 involvement in renal cancer development were analyzed by evaluating the immune microenvironment, mutation status and methylation levels. Results: C5orf46 was highly expressed in renal cancer and was an independent prognostic factor. In vitro cell experiments showed that inhibition of C5orf46 expression could reduce renal cancer cell proliferation and migration and increase apoptosis. Transcriptomic sequencing after knockdown of C5orf46 in renal cancer cells revealed that it is involved in the malignant phenotype and immune microenvironment regulation of renal cancer. Finally, public databases suggest that C5orf46-related immune cell infiltration, mutational potential, and low methylation levels may contribute to poor prognosis in renal cancer. Conclusion: These findings suggest that C5orf46 is associated with renal cancer progression and could be a potential target for improving renal cancer prognosis.

Given that myc was known to be a cancer-causing gene in several cancers including kidney renal clear cell carcinoma (KIRC). We aimed to construct myc-regulated genes (MRGs)-based prognostic signature. We obtained the mRNA expression and clinical data of KIRC from The Cancer Genome Atlas (TCGA) database and MRGs from the Molecular Signature Database (MSigDB). Then, a prognostic signature consisting of 8 MRGs (IRF9, UBE2C, YBX3, CDKN2B, CKAP2L, CYFIP2, FBLN5, and PDLIM7) was developed by differential expression analysis, cox regression analysis, and least absolute shrinkage and selection operator (lasso) analysis. Patients with KIRC were divided into high- and low-risk groups based on risk scores of MRGs-based signatures. Patients in the high-risk group showed inferior clinical characteristics and survival. In addition, the risk score was an independent prognostic factor for KIRC, and the risk score=based nomogram displayed satisfactory performance to predict the survival of KIRC. The MRGs-based signature is also correlated with immune cell infiltration and the mRNA expression of important immune checkpoints (IDO2, PDCD1, LAG3, FOXP3, and TIGIT). The tumor mutation burden (TMB) landscape between the high- and low-risk groups showed higher levels of TMB in the high-risk group than in the low-risk group and that higher levels of TMB predicted a poorer prognosis in KIRC. Furthermore, patients with KIRC in the high-risk group are more likely to experience immune escape. At last, we found patients with KIRC in the high-risk group were more sensitive to several chemotherapy drugs such as sunitinib, gefitinib, nilotinib, and rapamycin than patients with KIRC in the low-risk group. Our study successfully constructed and validated an MRGs-based signature that can predict clinical characteristics, prognosis, level of immune infiltration, and responsiveness to immunotherapy and chemotherapy drugs in patients with KIRC.

SNHG10 is a long non-coding RNA (lncRNA) found to be overexpressed in multiple human cancers including prostate cancer (PC). However, the underlying mechanisms of SNHG10 driving the progression of PC remains unclear. In this study, we investigated the role of SNHG10 in PC and found that SNHG10 expression was significantly increased in datasets extracted from The Cancer Genome Atlas. Increased expression of SNHG10 was related to advanced clinical parameters. Receiver operating curve analysis revealed the significant diagnostic ability of SNHG10 (AUC = 0.805). In addition, immune infiltration analysis, and GSEA showed that SNHG10 expression was correlated with oxidative phosphorylation and immune infiltrated cells. Finally, we determined that SNHG10 regulated cell proliferation, migration, and invasion of PC in vitro. In conclusion, our data demonstrated that SNHG10 was correlated with progression and immune infiltration, and could serve as a prognostic biomarker for PC.

Background Long noncoding RNAs (lncRNAs) are closely related to the occurrence and development of cancer. Gastric adenocarcinoma-associated, positive CD44 regulator, long intergenic noncoding RNA (GAPLINC) is a recently identified lncRNA that can actively participate in the tumorigenesis of various cancers. Here, we investigated the functional roles and mechanism of GAPLINC in renal cell carcinoma (RCC) development. Methods Differentially expressed lncRNAs between RCC tissues and normal kidney tissues were detected by using a microarray technique. RNA sequencing was applied to explore the mRNA expression profile changes after GAPLINC silencing. After gain- and loss-of-function approaches were implemented, the effect of GAPLINC on RCC in vitro and in vivo was assessed by cell proliferation and migration assays. Moreover, rescue experiments and luciferase reporter assays were used to study the interactions between GAPLINC, miR-135b-5p and CSF1. Results GAPLINC was significantly upregulated in RCC tissues and cell lines and was associated with a poor prognosis in RCC patients. Knockdown of GAPLINC repressed RCC growth in vitro and in vivo, while overexpression of GAPLINC exhibited the opposite effect. Mechanistically, we found that GAPLINC upregulates oncogene CSF1 expression by acting as a sponge of miR-135b-5p. Conclusion Taken together, our results suggest that GAPLINC is a novel prognostic marker and molecular therapeutic target for RCC.

Background DLEU2 is a long noncoding RNA considered important in the progression of many cancers. However, correlations between DLEU2 and kidney renal clear cell carcinoma (KIRC) and liver hepatocellular carcinoma (LIHC) have rarely been reported. Methods We first analysed the expression of DLEU2 across cancers and the correlation between DLEU2 and the clinical features of KIRC and LIHC by using the “ggplot2” package in R and searched the Oncomine database and Timer website platform. We verified the expression of DLEU2 in the GEO dataset (GSE105261 and GSE45267). Receiver operating characteristic (ROC) curves were drawn using the “pROC” and “ggplot2” packages in R, and we constructed a DLEU2-based prognostic nomogram for KIRC and LIHC by using the “survival” and “rms” packages in R. Then, we analysed the correlation between DLEU2 expression and prognosis in R as well as the correlation between DLEU2 and immune cell infiltration in the TIMER database. Finally, we explored the causes of DLEU2 upregulation in the UCSC Xena and UALCAN databases. Results We found that DLEU2 was upregulated in many cancers, including KIRC and LIHC. Expression of DLEU2 is associated with tumour stage, grade, lymphatic metastasis, and distant metastasis in KIRC as well as alpha-fetoprotein (AFP), tumour stage, grade, lymphatic metastasis, and distant metastasis in LIHC. DLEU2 is an adverse factor for the prognosis of KIRC and LIHC. In addition, DLEU2 has moderate accuracy in diagnosing KIRC and LIHC and predicting their prognosis. Moreover, we found that expression of DLEU2 correlated positively with immune cell infiltration in KIRC and LIHC, and upregulation of DLEU2 in KIRC and LIHC suggests a poor prognosis based on immune cells analysis. Genetic and epigenetic analyses of DLEU2 indicate that copy number variations (CNVs) and methylation contribute to the upregulation of DLEU2. Conclusion The long noncoding RNA DLEU2 has the potential to predict the prognosis and immune infiltration of KIRC and LIHC.

Background: Circular RNAs (circRNAs), a type of noncoding RNA, are associated with the occurrence and development of cancers. In recent years, their potential as biomarkers for bladder cancer (BC) has attracted increased attention. Aims: To reveal the value of circRNAs in the prognosis of BC. Methods: Relevant studies were collected to extract the clinicopathological data and overall survival (OS) of patients with BC. We then evaluated their tumor-related clinicopathological indicators using pooled odds ratio (OR) and 95% confidence interval (CI). Hazard ratio (HR) and 95% CI were used to estimate the OS of BC patients who expressed abnormal circRNAs. Results: The results indicate that seven circRNAs (circMYLK, circASXL1, hsa_circ_0000144, circ-VANGL1, circGprc5a, circZFR, and circ-cTFRC) whose expression was upregulated in tumor tissues, are associated with poor clinicopathological features (tumor/node/metastasis [TNM] stage: OR = 4.86, 95% CI: 2.53-9.34; histological grade: OR = 3.71, 95% CI: 2.37-5.79; lymph node metastasis: OR = 3.23; 95% CI: 2.15-4.88; recurrence: OR = 5.33; 95% CI: 2.27-12.52) and poor prognoses (OS: HR = 1.69; 95% CI: 1.17-2.44). We also found that seven circRNAs (circMTO1, circ-ITCH, circUBXN7, circFNDC3B, circ-ZKSCAN1, circPICALM, and circACVR2A) that were downregulated in tumors were associated with better clinicopathological indicators (TNM stage: OR = 0.23, 95% CI: 0.14-0.38; histological grade: OR = 0.21, 95% CI: 0.13-0.33; lymph node metastasis: OR = 0.26; 95% CI: 0.15-0.47) and better prognoses (OS: HR = 0.42; 95% CI: 0.30-0.58). Conclusion: Our results suggest that certain circRNAs are related to the clinicopathological characteristics and prognosis of BC patients, and may potentially be used as biomarkers.

[This corrects the article DOI: 10.3892/ol.2019.9967.].

[This corrects the article DOI: 10.3892/ol.2019.9967.].