Formyl peptide receptor-2 (FPR2) belongs to the G protein-coupled receptor (GPCR) family and plays a critical role in the development of various tumors. However, the roles and mechanisms of FPR2 in glioblastoma (GBM) remain poorly understood. In this study, we observed significant upregulation of FPR2 in glioma cell lines and tissues, and elevated FPR2 expression levels are correlated with poor patient survival. Furthermore, we found that FPR2 suppresses the autophagy mediated by BECN1 and ATG5 in GBM cells. Using Western blot analysis, we revealed that FPR2 regulates GBM cell invasion via the PI3K/AKT signaling pathway. Additionally, we demonstrated that knocking down FPR2 expression in GBM cells reduced tumor cell migration and invasion in vitro and tumor growth in vivo. The inhibition of FPR2 led to cell cycle arrest at the G2/M phase and increased apoptosis. Finally, our findings indicate that FPR2 may prevent autophagy-induced epithelial‒mesenchymal transition (EMT)-like changes by preventing autophagy-induced degradation of Snail. Our findings suggest that FPR2 promotes GBM cell migration and invasion through the inhibition of autophagy and the activation of the PI3K/AKT signaling pathway, highlighting the potential of inducing autophagy as a therapeutic approach to inhibit invasion in GBM with high FPR2 expression.

BackgroundNeuroglobin (Ngb) is a novel oxygen-binding or sensor protein that is present primarily in neurons and the brain. It plays a critical role in sensing oxygen and hypoxia signals and in transducing intracellular signaling pathways. However, the specific functions and mechanism of Ngb in the glioblastoma remain unclear.MethodsThe expression of Ngb in glioma brain tissues and cells was measured by Western blot, immunohistochemical staining and retrieved from TCGA databases. Loss or gain of function assays, CCK-8 assay, scratch and transwell assay, transmission electron microscopy (TEM) analysis, acridine orange staining, evaluation of fluorescent LC3 puncta, and flow cytometry analysis were conducted to determine the effects of Ngb overexpression or knockdown on glioblastoma multiforme (GBM) cell proliferation, invasion and autophagy, and Ngb/EGFR interactions were verified by glutathione S-Transferase (GST) pull-down assay and co-immunoprecipitation (Co-IP), and the mechanism of Ngb on autophagy was investigated by Western blot. The animal model of glioma was further employed to assess the inhibitory effect of Ngb overexpression on GBM cell growth.ResultsThe study demonstrated that the expression of Ngb was significantly downregulated in glioma tissues and cell lines and that its downregulation was positively correlated with poor patient survival, further demonstrating that Ngb promoted belcin1 and LC3-dependent autophagy in the GBM cells. We found that inhibitory effect of Ngb on cellular invasion is associated with the suppression of EGFR/PI3K/AKT/m-TOR signaling. Furthermore, our study revealed that increasing Ngb expression in GBM cells notably decreased their ability to migrate and invade in vitro and suppressed tumor growth in vivo. The overexpression of Ngb resulted in cell cycle arrest at the S phase and increased apoptosis. Finally, our findings indicated that Ngb increased autophagy, which may inhibit the invasion of glioblastoma multiforme (GBM) by interaction with the amino acid 1-42 domains of Ngb with EGFR.ConclusionsIn this study, our research findings indicated that Ngb promoted autophagy and suppressed the migration and invasion of GBM cells through inactivation of the EGFR/PI3K/AKT/m-TOR signaling pathway, highlighting that autophagy activation may suppress the invasion of GBM cells with low Ngb expression.

An amendment to this paper has been published and can be accessed via the original article.

An amendment to this paper has been published and can be accessed via the original article.

Recent evidences have implicated that SENP3 is a deSUMOylase which possesses neuronal damage effects in cerebral ischemia. However, its role in microglia remains poorly understood. Here, we found that SENP3 was upregulated in the peri-infarct areas of mice following ischemic stroke. Furthermore, knockdown of SENP3 significantly inhibits the expression of proinflammatory cytokines and chemokines in microglial cells. Mechanistically, SENP3 can bind and then mediated the deSUMOylation of c-Jun, which activated its transcriptional activity, ultimately followed by the activation of MAPK/AP-1 signaling pathway. In addition, microglia-specific SENP3 knockdown alleviated ischemia-induced neuronal damage, and markedly diminished infract volume, ameliorated sensorimotor and cognitive function in animals subjected to ischemic stroke. These results indicated SENP3 functions as a novel regulator of microglia-induced neuroinflammation by activating the MAPK/AP-1 signaling pathway via mediating the deSUMOylation of c-Jun. Interventions of SENP3 expression or its interaction with c-Jun would be a new and promising therapeutic strategy for ischemic stroke.

Rationale: Annexin-A1 (ANXA1) has previously been proposed to play a crucial role in neuronal apoptosis during ischemic stroke injury. Our recent study demonstrated that ANXA1 was modified by SUMOylation, and that this modification was greatly weakened after cerebral ischemia, but its effect on neuronal death and the underlying mechanism have not been fully elucidated. Methods: Mice subjected to middle cerebral artery occlusion were established as the animal model and primary cultured neurons treated with oxygen-glucose deprivation and reperfusion was established as the cell model of ischemic stroke. The Ni2+-NTA agarose affinity pull-down assay was carried out to determine the SUMOylation level of ANXA1. Co-immunoprecipitation assays was utilized to explore the protein interaction. Immunoblot analysis, quantitative real-time PCR, Luciferase reporter assay were performed to identify the regulatory mechanism. LDH release and TUNEL staining was performed to investigate the neuronal cytotoxicity and apoptosis, respectively. Results: In this study, we identified the deSUMOylating enzyme sentrin/SUMO-specific protease 6 (SENP6) as a negative regulator of ANXA1 SUMOylation. Notably, we found that SENP6-mediated deSUMOylation of ANXA1 induced its nuclear translocation and triggered neuronal apoptosis during cerebral ischemic injury. A mechanistic study demonstrated that SENP6-mediated deSUMOylation of ANXA1 promoted TRPM7- and PKC-dependent phosphorylation of ANXA1. Furthermore, blocking the deSUMOylation of ANXA1 mediated by SENP6 inhibited the transcriptional activity of p53, decreased Bid expression, suppressed caspase-3 pathway activation and reduced the apoptosis of primary neurons subjected to oxygen-glucose deprivation and reperfusion. More importantly, SENP6 inhibition by overexpression of a SENP6 catalytic mutant in neurons resulted in significant improvement in neurological function in the mouse model of ischemic stroke. Conclusions: Taken together, the results of this study identified a previously unidentified function of SENP6 in neuronal apoptosis and strongly indicated that SENP6 inhibition may provide therapeutic benefits for cerebral ischemia.

Background: Previous studies reported that N-myc downstream-regulated gene 1 (NDRG1) was upregulated in various cancer tissues and decreased expression of miR-188-3p and miR-133b could suppress cell proliferation, metastasis, and invasion and induce apoptosis of cancer cells. However, the molecular mechanism of NRDG1 involved in hepatocellular carcinoma (HCC) tumorigenesis is still unknown. Methods: The expressions of miR-188-3p, miR-133b, and NRDG1 in HCC tissues and cells were quantified by qRT-PCR and Western blot. MTT assay and transwell invasion assay were performed to evaluate cell growth and cell migration, respectively. Luciferase reporter assay were performed to determine whether miR-188-3p and miR-133b could directly bind to NRDG1 in HCC cells. Results: The results showed that NRDG1 was upregulated and these 2 microRNAs were downregulated in HCC tissues. NRDG1 was negatively correlated with miR-188-3p and miR-133b in HCC tissues. MiR-188-3p and miR-133b were demonstrated to directly bind to 3′UTR of NRDG1 and inhibit its expression. Upregulation of miR-188-3p and miR-133b reduced NRDG1 expression in hepatocellular carcinoma cell lines, which consequently inhibited cell growth and cell migration. Conclusions: Our finding suggested that miR-188-3p and miR-133b exert a suppressive effect on hepatocellular carcinoma proliferation, invasion, and migration through downregulation of NDRG1.

Prevention of the nuclear translocation of ANXA1 with Tat-NTS was recently reported to alleviate neuronal injury and protect against cerebral stroke. However, the role that Tat-NTS plays in the occurrence and development of gliomas still needs to be elucidated. Therefore, human glioblastoma (GB) cells were treated with various concentrations of Tat-NTS for 24 h, and cell proliferation, migration and invasion were assessed with CCK-8 and Transwell assays. The nuclear translocation of ANXA1 was evaluated by subcellular extraction and immunofluorescence, and protein expression levels were detected by Western blot analysis. In addition, the activity of MMP-2/9 was measured by gelatin zymography. The results revealed that Tat-NTS significantly inhibited the nuclear translocation of ANXA1 in U87 cells and inhibited the proliferation, migration and invasion of GB cells. Tat-NTS also suppressed cell cycle regulatory proteins and MMP-2/-9 activity and expression. Moreover, Tat-NTS reduced the level of p-p65 NF-κB in U87 cells. These results suggest that the Tat-NTS-induced inhibition of GB cell proliferation, migration and invasion is closely associated with the induction of cell cycle arrest, downregulation of MMP-2/-9 expression and activity and suppression of the NF-κB signaling pathway. Thus, Tat-NTS may be a potential chemotherapeutic agent for the treatment of GB.

ANXA1, which can bind phospholipid in a calcium dependent manner, is reported to play a pivotal role in tumor progression. However, the role and mechanism of ANXA1 involved in the occurrence and development of malignant glioma are still not well studied. Therefore, we explored the effects of ANXA1 on normal astrocytes and glioma cell proliferation, apoptosis, migration and invasion and the underlying mechanisms. We found that ANXA1 was markedly up-regulated in glioma cell lines and glioma tissues. Down-regulation of ANXA1 inhibited normal astrocytes and glioma cell proliferation and induced the cell apoptosis, which suggested that the consequences of loss of Annexin 1 are not specific to the tumor cells. Furthermore, the siRNA-ANXA1 treatment significantly reduced tumor growth rate and tumor weight. Moreover, decreasing ANXA1 expression caused G2/M phase arrest by repressing expression levels of cdc25C, cdc2 and cyclin B1. Interestingly, ANXA1 did not affect the expressions of β-catenin, GSK-3β and NF-κB, the key signaling molecules associated with cancer progression. However, siRNA-ANXA1 was found to negatively regulate phosphorylation of AKT and the expression and activity of MMP2/-9. Finally, the decrease of cell proliferation and invasiveness induced by ANXA1 down-regulation was partially reversed by combined treatment with AKT agonist insulin-like growth factor-1 (IGF-1). Meanwhile, the inhibition of glioma cell proliferation and invasiveness induced by ANXA1 down-regulation was further enhanced by combined treatment with AKT inhibitor LY294002. In summary, these findings demonstrate that ANXA1 regulates proliferation, migration and invasion of glioma cells via PI3K/AKT signaling pathway.

Objective:To investigate the effect of microRNA (miRNA, miR)-188-3p on N-myc downstream regulated gene 1(NDRG1) and its role in the proliferation activity of hepatocarcinoma cells (HCC).Methods:Collected 21 cases of HCC tissue specimens and 13 cases of adjacent cancer tissues that were surgically resected and pathologically confirmed by the Department of Hepatobiliary and Pancreatic Surgery, Wuhan Central Hospital from February 2018 to October 2019, HepG2 cells were cultured in vitro. In this study, the miR-188-3p was predicted with bioinformatics and identified with dual luciferase report system. Expression of miR-188-3p and NDRG1 was determined with real-time quantitative polymerase chain reaction (Real-time PCR) and Western blotting after transfection of miR-188-3p. The proliferation of HepG2 cells was detected in vitro by CCK-8 assay. Results:MiR-188-3p can inhibit NDRG1 expression by binding to 3’untranslated regions (3’UTR) of NDRG1 mRNA. miR-188-3p can negatively control the mRNA and protein expression of NDRG1 (0.56±0.04 vs.1.12±0.13, t=10.777, P<0.01、0.43±0.07 vs. 0.88±0.15, t=9.123, P<0.05). The proliferation of HepG2 cells was negatively controlled by miR-188-3p(0.76±0.07 vs. 1.26±0.19, t=7.509, P<0.05). Conclusion:MiR-188-3p could effectively inhibit the proliferation of HCC through targting NDRG1, suggesting miR-188-3p could serve as an innovative therapeutic strategy in terms of HCC.

The abnormal expression of HPV16 E6/E7 activates oncogenes and/or inactivates tumor suppressor genes, resulting in the selective growth and malignant transformation of cancer cells. miR-4454 was selected by sequencing due to its abnormal high expression in HPV16 E6/E7 positive CaSki cell compared with HPV16 E6/E7 negative C33A cell. Overexpression of miR-4454 enhances cervical cancer cell invasion and migration. ABHD2 and NUDT21 are identified as a target gene of miR-4454.The effects of ABHD2 and NUDT21 on migration and invasion of CaSki and C33A cells were determined. The dual luciferase and RT-qPCR assays confirmed that miR-4454 might regulate its targets ABHD2 and NUDT21 to promote the proliferation, invasion and migration, whereas, inhibit the apoptosis in CaSki and C33A cells.

Ac2-26, a mimetic peptide of Annexin-A1, plays a vital role in the anti-inflammatory response mediated by astrocytes. In this study, we aimed to explore the underlying mechanisms of Ac2-26-mediated anti-inflammatory effect. Specifically, we investigated the inhibitory effects of Ac2-26 on lipopolysaccharide (LPS)-induced astrocyte migration and on pro-inflammatory cytokines and chemokines expressions, as well as one glutathione (GSH) reductase mRNA and total intracellular GSH levels in LPS-induced astrocytes. Additionally, we investigated whether mitogen-activated protein kinases (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathway were involved in this process. Finally, we evaluated the analgesic effect of Ac2-26 in complete Freund's adjuvant (CFA)-induced inflammatory pain model. Our results demonstrated that Ac2-26 inhibited LPS-induced astrocytes migration, reduced the production of pro-inflammatory mediators [tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 (MIP-1α)] and upregulated GSH reductase mRNA and GSH levels in LPS-induced astrocytes in vitro. This process was mediated through the p38, JNK-MAPK signaling pathway, but not dependent on the NF-κB pathway. Furthermore, the p38 and JNK inhibitors mimicked the effects of Ac2-26, whereas a p38 and JNK activator anisomycin partially reversed its function. Finally, Ac2-26 treatment reduced CFA-induced activation of astrocytes and production of inflammatory mediators in the spinal cord. These results suggest that Ac2-26 attenuates pain by inhibiting astrocyte activation and the production of inflammatory mediators; thus, this work presents Ac2-26 as a potential drug to treat neuropathic pain.

Objective To evaluate the effect of Annexin-A1 mimetic peptide Ac2-26 on activation of astrocytes in rats.Methods The primarily cultured astrocytes from the cortex of fetal Sprague-Dawley rats after 4 passages were divined into 4 groups (n =24 each) using a random number table method:control group (C group),LPS group,LPS+scramble peptide group (LPS+Src group) and LPS+Ac2-26 group.LPS was added to LPS group with the final concentration of 1 mg/ml.LPS at the final concentration of 1 mg/ml and scramble peptide at the final concentration of 3.3 mmol/L were added to LPS+Src group.LPS at the final concentration of 1 mg/ml and Ac2-26 at the final concentration of 3.3 mmol/L were added to LPS+Ac2-26 group.After 24-h incubation,the cell survival rate was measured by CCK-8 assay,the migration was determined by Transwell assay,the concentrations of tumor necrosis factor-alpha (TNF-α),interleukin-1 beta (IL-1β),monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 a (MIP-1a) in the supernatant were measured (by enzyme-linked immunosorbent assay),and the expression of glial fibrillary acidic protein (GFAP),extracellular signal-regulated kinase (ERK),phosphorylated ERK (p-ERK),c-Jun N-terminal kinase (JNK),phosphorylated JNK (p-JNK),p38 mitogen-activated protein kinase (p38MAPK),and phosphorylated p38MAPK (p-p38MAPK) in astrocytes was detected by Western blot.Results Compared with group C,the expression of GFAP was significantly up-regulated,and the cell mobility,concentrations of TNF-α,IL-1β,MCP-1 and MIP-1α in the supernatant,p-ERK/ERK ratio,p-JNK/JNK ratio and p-p38MAPK/p38MAPK ratio were increased (P＜0.05),and no siguificant change was found in the cell survival rate in group LPS (P＞0.05).Compared with group LPS,the expression of GFAP was significantly down-regulated,and the cell mobility,concentrations of TNF-α,IL-1β,MCP-1 and MIP-1α in the supernatant,p-JNK/JNK ratio and p-p38MAPK/p38MAPK ratio were decreased in group LPS+Ac2-26 (P＜0.05),and no significant change was found in the parameters mentioned above in group LPS+Src (P＞0.05).Conclusion Ac2-26 can inhibit activation of astrocytes and produces anti-inflammatory effect in rats.

肿瘤的早期检测对于肿瘤的早期发现、诊断及治疗具有重要意义.基于硅纳米线、石墨烯、二硫化钼的纳米场效应晶体管生物传感器,由于灵敏度高和特异性好、分析速度快、免标记、廉价、能够微型化和一体化等优点,能够检测肿瘤相关标志物微RNA和蛋白质等,在肿瘤的早期检测中可以发挥重要作用.

Objective To explore the expression and clinical significance of the long non-coding RNA anti-differentiation antagonizing noncoding RNA (DANCR) in the patients with intrahepatic metastasis of hepatocellular carcinoma (HCC).Methods The tumor tissues,pre-and post-operative plasma samples of 24 HCC intrahepatic metastasis patients undergoing resection,the tumor tissues and plasma samples of 24 HCC patients,and the plasma samples of 24 healthy volunteers were collected from the Central Hospital of Wuhan between Jan.2015 and Oct.2017.The expression of DANCR mRNA level was detected by quantitative real-time quantitative polymerase chain reaction (PCR) in the tumor tissues and plasma samples.The relationship of DANCR mRNA expression with clinicopathological characteristics was analyzed.Results The expression levels of DANCR mRNA in the tumor tissues (2.85 ± 0.23 vs.1.63 ±0.16,P＜0.01) and the plasma (0.043 ±0.007 vs.0.018 ±0.005,P＜0.01) of the patients with intrahepatic metastasis of HCC were significantly higher than those of HCC patients.In addition,the DANCR mRNA expression was significantly lower after surgical resection than that in patients with intrahepatic metastasis of HCC before surgery (0.035 ±0.006 vs.0.012 ±0.004,P ＜0.05).The expression of DANCR mRNA in tumor tissues of patients with HCC intrahepatic metastasis was correlated with the size of primary tumor (P ＜ 0.05),chronic hepatitis B history (P ＜ 0.05) and Child-Pugh grade (P ＜ 0.05).Conclusion DANCR expression is closely related to the development of HCC.

Breast cancer is the most common cancer type in female. As microRNAs play vital role in breast cancer, this study aimed to explore the molecular mechanism and clinical value of miR-21 in breast cancer. qRT-PCR was performed to detect miR-21 levels in plasma of 127 healthy controls, 82 benign breast tumor, 252 breast cancer patients, as well as in breast cancer cell lines. Transwell and wound healing assay were used to analyze breast cancer metastasis in response to miR-21 inhibitor. Colony formation and eFluor™ 670 based flow cytometric analysis were used to test breast cancer proliferation following miR-21 inhibitor treatment. Leucine zipper transcription factor-like 1 (LZTFL1), the target gene of miR-21 was predicted by MIRDB, TargetScan 5.1, PicTar and miRanda. Survival analysis of LZTFL1 levels in breast cancer prognosis was estimated with the Kaplan–Meier method by log-rank test according to data from the Cancer Genome Atlas. Luciferase activity assay was performed to confirm the regulation of miR-21 on LZTFL1. LZTFL1 siRNA and miR-21 inhibitor were co-transfected to breast cancer cells, then cell proliferation, migration and epithelial–mesenchymal transition (EMT) makers were tested. BALB/c nude mice were injected in situ with Hs578T cells stably overexpressing miR-21. Breast tumor growth, metastasis and the expression of EMT markers or LZTFL1 were detected in vivo. Plasma miR-21 levels were elevated in breast cancer patients compared with healthy controls and benign breast tumor patients, and the miR-21 levels were significantly decreased after surgery comparing with pre operation in 44 patients. Inhibition of miR-21 suppressed cell proliferation and metastasis in breast cancer cells. LZTFL1 was identified as a novel target gene of miR-21. Knockdown of LZTFL1 overcame the suppression of miR-21 inhibitor on cell proliferation, metastasis and the expression of EMT markers in breast cancer cells. miR-21 overexpression promoted breast cancer cell proliferation and metastasis in vivo. These results indicate that plasma miR-21 level is a crucial biomarker for breast cancer diagnosis and targeting miR-21–LZTFL1–EMT axis might be a promising strategy in breast cancer therapy. Retrospectively registered.

目的 探讨2型糖尿病及其糖尿病肾病患者血清中4种肿瘤标志物(AFP、CEA、CA125和CA199)的水平变化.方法 收集2型糖尿病患者207例(T2DM组)、2型糖尿病肾病患者45例(DKD组),选取同期健康体检者231例作为对照组,采用雅培i2000全自动生化分析仪检测4种肿瘤标志物.比较3组4种血清肿瘤标志物水平.根据糖化血红蛋白(HbA1c)水平将2型糖尿病患者进行再分组,比较各组间4种肿瘤标志物水平.同时利用Spearman秩相关法分析空腹血糖 、HbA1c和4种肿瘤标志物之间的相关性.结果T2DM患者的血清CEA、CA125和CA199水平较对照组明显增高.与对照组和T2DM组相比,DKD患者血清中CA125和CA199水平均显著增高.不同HbA1c水平组CA125和CA199水平比较,差异有统计学意义(P<0.05).空腹血糖 、HbA1c与CEA、CA125、CA199之间呈正相关(P<0.05).结论 2 型糖尿病及其糖尿病肾病患者部分血清肿瘤标志物水平升高 . 空腹血糖 、HbA1c 与 CEA 、CA125 、CA199 之间呈正相关 ,且血糖控制不理想时 ,CA199 和 CA125 水平升高更明显 .

Nowadays, vitamin D is known to have functions beyond bone formation, including inhibiting angiogenesis and promoting tumor apoptosis. CYP27B1 and group-specific component (GC), the main enzyme responsible for the degradation and transport of active vitamin D, play important role in many cancer-related cellular processes. Relationships between CYP27B1 and GC polymorphisms and cancer susceptibility have been widely investigated, whereas the results are inconsistent. We strictly searched EMBASE, PubMed, Web of Science, WanFang and CNKI electronic databases for relevant studies exploring the associations of GC (rs4588 and rs7041) and CYP27B1 (rs4646537, rs3782130) polymorphisms with cancer risks according to search strategy. Thirty-two studies published in 13 articles involving 15713 cases and 17304 controls were included. Our analyses suggested that rs4588 and rs7041 polymorphisms were significantly associated with overall cancer risk. Stratification analyses of ethnicity indicated that rs4588 polymorphism significantly increased cancer risk in Caucasians and Asians, while rs7041 polymorphism significantly increased cancer risk in Asians. When studies were stratified by cancer type, our results indicated that rs4588 significantly increased the risk of breast cancer and digestive system tumor, but not in prostate cancer and non-small cell lung cancer, while rs7041 significantly increased the risk of non-small cell lung cancer. Above associations were noteworthy findings as evaluated by false-positive report probabilities (FPRPs). There were no associations of rs4646537 and rs3782130 with overall cancer risks. Associations between CYP27B1 and GC polymorphisms and cancer risks were examined, and additional large samples are necessary to validate our results.

Background: Carnitine palmitoyl transferase 1A (CPT1A) is the rate-limiting enzyme of fatty acid oxidation. It is overexpressed in advanced breast cancer and leads to poor survival. Here we aimed to examine the serum levels of CPT1A in a large-scale study and develop CPT1A as a biomarker for the early diagnosis of breast cancer. Methods: An ELISA was conducted to detect serum CPT1A levels in 432 breast cancer patients, 200 patients with benign breast disease, and 400 healthy controls in a training set and a test set. Receiver operating characteristic curves were generated, and binary logistic regression analyses were performed to evaluate the effectiveness of CPT1A, CA15-3, CEA, and CA125 as biomarkers in breast cancer diagnosis and to develop novel diagnostic panels. Findings: Serum CPT1A levels were significantly higher in breast cancer patients than in patients with benign breast disease or in healthy controls. CPT1A levels were even more significantly elevated in serum from advanced or triple-negative breast cancer cases and were decreased in paired post-operative samples compared with pre-operative samples. CPT1A exhibited a higher efficacy in differentiating breast cancer patients from healthy controls (area under the curve, AUC: training set, 0.870; test set, 0.901) than did CA15-3, CEA, or CA125. The panel combining CPT1A with CA15-3, CEA, and CA125 was more effective in breast cancer diagnosis (AUC: training set, 0.908; test set, 0.909) than CPT1A alone. Interpretation: CPT1A can be a novel serum biomarker for the diagnosis and disease monitoring of breast cancer.Funding Statement: The work was supported by National Science Foundation of China (81802653), Research Fund of Hubei Province Public Health Bureau (WJ2015MB144) and Research Fund of Wuhan Public Health Bureau (WX15A12 and WX18Y11). Declaration of Interests: No potential conflicts of interest were disclosed.Ethics Approval Statement: The study was approved by the ethics committee of the two hospitals. Written informed consent was obtained from every participant for the use of blood samples and medical records for research purposes.