Clinicopathologic Features and Prognosis of Female Early Breast Cancer With HER2 Low Expression: A Propensity Score Matched Analysis.

Background: Metastatic breast cancer (MBC) patients with low expression of human epidermal growth factor 2 (HER2) have been proven to benefit from HER2 targeted therapy. We aimed to determine how HER2-low status affected survival and metastatic risk as well as how it affected pathological complete response (pCR) in neoadjuvant chemotherapy (NAC) patients. Methods: According to the results of immunohistochemistry (IHC) and in situ hybridization (ISH) testing, 321 female patients were sorted into HER2-low (IHC 1+/2+ with ISH negative) and HER2-zero (IHC 0) groups using propensity score matching (PSM). Overall survival (OS), disease-free survival (DFS), and distant disease-free survival (DDFS) were compared for both groups, while pCR was only analyzed for NAC patients. Results: In total, 97 patients in each group after PSM were included. We discovered that pCR was not associated with HER2 expression status in 45 patients who underwent NAC. Five-year OS in the HER2-low group was significantly higher (98.99%) than in the HER2-zero group (95.87%, P = .044); however, this difference was not reflected in the 5-year DFS (90.61 vs 90.52%, P = .868) and 5-year DDFS (93.67 vs 91.53%, P = .757). Meanwhile, multivariate analysis revealed that HER2-low expression could indicate better OS (P = .047, hazard ratios [HRs] = 16.121, 95% confidence interval [CI] = 1.035-251.046), but it had no prognostic value for DFS or DDFS. Conclusion: When compared with HER2-zero expression, HER2-low expression was not connected to pCR and could not modify metastasis risk in female patients with early-stage breast cancer (BC), but it may prolong patient survival.

Nomogram for predicting survival in patients with mucinous breast cancer undergoing chemotherapy and surgery: a population-based study.

BACKGROUND: The prognosis of patients with mucinous breast cancer (MuBC) is affected by several factors, but the low incidence of MuBC makes it difficult to conduct extensive and in-depth studies. This study was designed to establish a prognostic model and verify its accuracy in patients with MuBC after chemotherapy and surgery to help develop personalized treatment strategies. MATERIALS AND METHODS: Patients with MuBC who underwent chemotherapy and surgery from 2004 to 2015 were identified in the Surveillance, Epidemiology, and End Results (SEER) database. The prognostic factors of patients with MuBC were investigated using a Cox proportional hazards regression analysis. Based on the identified factors, a nomogram was constructed to forecast the overall survival (OS) of patients at 3, 5, and 10 years. Internal (from SEER) and external (from Yunnan Cancer Center, YNCC) verification queues were used to verify the nomogram and demonstrate the predictive capacity of this model. RESULTS: The study comprised 1668 MuBC patients from the SEER database and 107 from the YNCC. The nomogram included four characteristics: age, anatomical stage, surgical method, and radiotherapy. The concordance indices in the training, internal verification, and external verification queues were 0.680, 0.768, and 0.864, respectively. The calibration curves for the nomogram showed excellent agreement between the predictions and observations. This nomogram has good clinical application value according to the decision curve analysis. CONCLUSIONS: The prognosis of patients with MuBC who have undergone chemotherapy and surgery can be forecasted using this nomogram, which would be beneficial to help create individualized treatment plans for the affected patients.

Targeting the KLF5-EphA2 axis can restrain cancer stemness and overcome chemoresistance in basal-like breast cancer.

Ephrin type-A receptor 2 (EphA2) is a member of the tyrosine receptor kinases, a family of membrane proteins recognized as potential anticancer targets. EphA2 highly expressed in a variety of human cancers, playing roles in proliferation, migration, and invasion. However, whether and how EphA2 regulates basal-like breast cancer (BLBC) cell stemness and chemoresistance has not been revealed. Here, KLF5 was proven to be a direct transcription factor for EphA2 in BLBC cells, and its expression was positively correlated in clinical samples from breast cancer patients. The inflammatory factor TNF-α could promote BLBC cell stemness partially by activating the KLF5-EphA2 axis. Moreover, phosphorylation of EphA2 at S897 (EphA2 pS897) induced by TNF-α and PTX/DDP contributes to chemoresistance of BLBC. Furthermore, the EphA2 inhibitor ALW-II-41-27 could effectively reduce EphA2 pS897 and tumor cell stemness in vitro and significantly enhance the sensitivity of xenografts to the chemotherapeutic drugs PTX and DDP in vivo. Clinically, tumor samples from breast patients with less response to neoadjuvant chemotherapy showed a high level of EphA2 pS897 expression. In conclusion, KLF5-EphA2 promotes stemness and drug resistance in BLBC and could be a potential target for the treatment of BLBC.

A prognostic nomogram based on risk assessment for invasive micropapillary carcinoma of the breast after surgery.

PURPOSE: Invasive micropapillary carcinoma (IMPC) is one of the rare subtypes of breast cancer. This study aimed to explore a predictive nomogram model for IMPC prognosis. METHODS: A total of 1855 IMPC patients diagnosed after surgery between 2004 and 2014 were identified from the Surveillance, Epidemiology and End Results (SEER) database to build and validate nomogram. A nomogram was created based on univariate and multivariate Cox proportional hazards regression analysis. Receiver operating characteristic (ROC) curves were used to demonstrate the accuracy of the prognostic model. Decision curve analysis (DCA) was performed to evaluate the safety of the model in the range of clinical applications, while calibration curves were used to validate the prediction consistency. RESULTS: Cox regression analysis indicated that age ≥62 at diagnosis, negative ER status, and tumor stage were considered adverse independent factors for overall survival (OS), while patients who were married, white or of other races, received chemotherapy or radiotherapy, had a better postoperative prognosis. The nomogram accurately predicted OS with high internal and external validation consistency index (C index) (0.756 and 0.742, respectively). The areas under the ROC curve (AUCs) of the training group were 0.787, 0.774 and 0.764 for 3, 5 and 10 years, respectively, while those of the validation group were 0.756, 0.766 and 0.762, respectively. The results of both DCA and calibration curves demonstrated the good performance of the model. CONCLUSIONS: A nomogram for IMPC of the breast patients after surgery was developed to estimate 3, 5 and 10 years-OS based on independent risk factors. This model has good accuracy and consistency in predicting prognosis and has clinical application value.

Pivotal models and biomarkers related to the prognosis of breast cancer based on the immune cell interaction network.

The effect of breast cancer heterogeneity on prognosis of patients is still unclear, especially the role of immune cells in prognosis of breast cancer. In this study, single cell transcriptome sequencing data of breast cancer were used to analyze the relationship between breast cancer heterogeneity and prognosis. In this study, 14 cell clusters were identified in two single-cell datasets (GSE75688 and G118389). Proportion analysis of immune cells showed that NK cells were significantly aggregated in triple negative breast cancer, and the proportion of macrophages was significantly increased in primary breast cancer, while B cells, T cells, and neutrophils may be involved in the metastasis of breast cancer. The results of ligand receptor interaction network revealed that macrophages and DC cells were the most frequently interacting cells with other cells in breast cancer. The results of WGCNA analysis suggested that the MEblue module is most relevant to the overall survival time of triple negative breast cancer. Twenty-four prognostic genes in the blue module were identified by univariate Cox regression analysis and KM survival analysis. Multivariate regression analysis combined with risk analysis was used to analyze 24 prognostic genes to construct a prognostic model. The verification result of our prognostic model showed that there were significant differences in the expression of PCDH12, SLIT3, ACVRL1, and DLL4 genes between the high-risk group and the low-risk group, which can be used as prognostic biomarkers.

Prognostic Factor Analysis and Model Construction of Triple-Negative Metaplastic Breast Carcinoma After Surgery.

Objective: The study aimed to analyze the prognostic factors of patients with triple-negative (TN) metaplastic breast carcinoma (MpBC) after surgery and to construct a nomogram for forecasting the 3-, 5-, and 8-year overall survival (OS). Methods: A total of 998 patients extracted from the Surveillance, Epidemiology, and End Results (SEER) database were assigned to either the training or validation group at random in a ratio of 7:3. The clinical characteristics of patients in the training and validation sets were compared, and multivariate Cox regression analysis was used to identify the independent risk variables for the OS of patients with TN MpBC after surgery. These selected parameters were estimated through the Kaplan-Meier (KM) curves using the log-rank test. The nomogram for predicting the OS was constructed and validated by performing the concordance index (C-index), receiver operating characteristics (ROC) curves with area under the receiver operating characteristic curves (AUC), calibration curves, and decision curve analyses (DCAs). Patients were then stratified as high-risk and low-risk, and KM curves were performed. Results: Multivariate Cox regression analysis indicated that factors including age, marital status, clinical stage at diagnosis, chemotherapy, and regional node status were independent predictors of prognosis in patients with MpBC after surgery. Separate KM curves for the screened variables revealed the same statistical results as with Cox regression analysis. A prediction model was created and virtualized via nomogram based on these findings. For the training and validation cohorts, the C-index of the nomogram was 0.730 and 0.719, respectively. The AUC values of the 3-, 5-, and 8-year OS were 0.758, 0.757, and 0.785 in the training group, and 0.736, 0.735, and 0.736 for 3, 5, and 8 years in the validation group, respectively. The difference in the OS between the real observation and the forecast was quite constant according to the calibration curves. The generated clinical applicability of the nomogram was further demonstrated by the DCA analysis. In all the training and validation sets, the KM curves for the different risk subgroups revealed substantial differences in survival probabilities (P <0.001). Conclusion: The study showed a nomogram that was built from a parametric survival model based on the SEER database, which can be used to make an accurate prediction of the prognosis of patients with TN MpBC after surgery.

The Interaction of NTN4 and miR-17-92 Polymorphisms on Breast Cancer Susceptibility in a Chinese Population.

INTRODUCTION: Genome-wide association studies have identified a genetic variant rs17356907 in netrin 4 (NTN4) as a risk locus of breast cancer (BC) in Europeans. NTN4 is a target gene of miR-17-92 cluster that is an oncogenic miRNA in BC development. We aimed to replicate the rs17356907 in a Chinese population and examine the interaction of NTN4 and miR-17-92 on BC susceptibility. MATERIALS AND METHODS: The rs17356907 in NTN4 and 3 additional polymorphisms in the promoter of miR-17-92 (ie, rs9588884, rs982873, and rs1813389) were determined in 415 patients with BC and 420 healthy controls using a TaqMan assay. The expression levels of NTN4 in BC and normal tissues were performed using the quantitative reverse transcription-PCR. RESULTS: With reference to the rs17356907AA genotype, the GG genotype was associated with a decreased risk of BC with an adjusted OR of 0.38 (95% CI: 0.20-0.74). With reference to the rs17356907AA-rs982873CT/CC genotypes, the rs17356907 AG/GG-rs982873CT/CC genotypes were associated with a borderline decreased risk of BC with an adjusted OR of 0.67 (95% CI: 0.48-0.93). Gene-gene interaction analysis showed that the rs17356907-rs982873-rs9588884-rs1813389 was the best model on BC susceptibility. Furthermore, the rs17356907GG genotype displayed higher levels of NTN4 mRNA. CONCLUSIONS: The NTN4 rs17356907 may have a single and interactive effect with miR-17-92 polymorphisms on the risk of BC.

Overexpression of ING3 is associated with attenuation of migration and invasion in breast cancer.

Inhibitor of growth 3 (ING3) has been identified as a potential cancer drug target, but little is known about its role in breast cancer. Thus, the present study aimed to investigate ING3 expression in breast cancer, its clinical value, and how ING3 influences the migration and invasion of breast cancer cells. The Cancer Genome Atlas and UALCAN databases were used to analyze ING3 expression in cancer tissues and normal tissues. Survival analysis was performed using the UALCAN, UCSC Xena and KM-plot databases. In addition, reverse transcription-quantitative PCR and western blot analyses were performed to detect ING3 mRNA and protein expression levels. ING3 was overexpressed via lentiviral vector transfection, while the Transwell and wound healing assays were performed to assess the cell migratory and invasive abilities. Protein interaction and pathway analyses were performed using the GeneMANIA and Kyoto Encyclopedia of Genes and Genomes databases, respectively. The results demonstrated that ING3 expression was significantly lower in cancer tissues compared with normal tissues (P<0.05). In addition, luminal A and human epidermal growth factor receptor 2 (HER2)-enriched breast cancer tissues expressed lower levels of ING3 compared with normal breast tissues. Notably, statistically significant differences were observed in long-term survival between patients with luminal A (P=0.04) and HER2-enriched (P=0.008) breast cancer, with high and low expression levels of ING3. The results of the Transwell migration and invasion assays demonstrated that overexpression of ING3 significantly inhibited the migratory and invasive abilities of MCF7 (P<0.05) and HCC1937 (P<0.05) cells. The results of the wound healing assay demonstrated that the percentage wound closure significantly decreased in cells transfected with LV5-ING3 compared with the negative control group at 12 h (P<0.05) and 24 h (P<0.01). The PI3K/AKT, JAK/STAT, NF-κB and Wnt/ß-catenin pathways are the potential pathways regulated by ING3. Notably, overexpression of ING3 inhibited migration and invasion in vitro. However, further studies are required to determine whether ING3 regulates the biological behavior of breast cancer via tumor-related pathways.

Study on the Effects of Estradiol in Staphylococcus epidermidis Device-Related Capsule Formation.

BACKGROUND: Capsular contracture, mainly caused by Staphylococcus epidermidis (S. epidermidis) biofilm formation, is a complex problem for breast cancer patients who undergo surgical prosthetic breast reconstruction. Estradiol has been reported to be involved in the formation of bacterial biofilms. Thus, the underlying mechanism of estradiol in capsular contracture needs to be investigated. METHODS: Biofilm-related gene expressions were measured by qRT-PCR after sterilizing the silicone with bacterial suspension and E2 treatment in vitro. Rat models were established with bilateral ovariectomy operations and estradiol subcutaneous injections. The effects of estradiol on capsular contracture were detected by monitoring serum estradiol levels, bacterial infection rate in organs, biofilm formation and capsular contracture in vivo; inflammatory factors in vivo were examined as well. Biofilm on the silicone implants was observed under a scanning electron microscope. RESULTS: Both positive regulatory genes and negative regulatory genes were increased by the high concentration of estradiol, suggesting that estradiol can promote the formation of biofilm by not only positive but also negative regulations. High estradiol levels increased bacterial infection rate in organs, biofilm formation and capsular contracture. Further, high estradiol caused a large number of inflammatory cells to infiltrate and caused serious inflammatory reactions that aggravate the immune imbalances of the host. CONCLUSION: High estradiol levels contribute to increasing capsular contracture caused by S. epidermidis biofilm formation. NO LEVEL ASSIGNED: This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.

Overexpression of serum exosomal HOTAIR is correlated with poor survival and poor response to chemotherapy in breast cancer patients.

To investigate the source of serum exosomal HOTAIR, to uncover the diagnostic and prognostic values of serum exosomal HOTAIR, and to discern the expression of serum exosomal HOTAIR between neoadjuvant chemotherapy and response to tamoxifen therapy. Samples were collected from the Third Affiliated Hospital of Kunming Medical University, Tumor Hospital of Yunnan. Exosomes were isolated from serum, cell culture medium and tumor tissues. We used transmission electron microscopy and western immunoblotting assay to characterize exosomes, and real-time PCR (qPCR) to assess HOTAIR expression. Neoadjuvant chemotherapy and tamoxifen therapy were carried out according to established guidelines. Breast cancer patients expressed higher serum exosomal HOTAIR than did healthy individuals (P\0.001). Serum exosomal HOTAIR levels 3 months after surgery were markedly decreased compared with levels before surgery (P\0.001), and the expression level of exosomal HOTAIR in cell culture medium increased with time in both breast cancer cell lines (72 h greater than 48 h greater than 24 h, 48 h vs 24 h [ [P less than 0.05]; 72 h vs 24 h [P less than 0.01]. Expression of serum exosomal HOTAIR in nude mice was notably greater than in the mock control group (P less than 0.001). The results of the ROC analysis revealed an AUC for serum exosomal HOTAIR of 0.9178 with a 95% CI of 0.8407-1.017 (P less than 0.01). The AUC for the CA15-3 cell line was 0.7378 (95% CI, 0.5585-0.9170; P = 0.03). High expression of exosomal HOTAIR led to a worse disease-free survival (P = 0.0481) and overall survival (P = 0.0463). In the high-expression chemotherapy group, six patients achieved a partial response (PR) and eight demonstrated stable disease (SD) and nine patients achieved PR and two SD in the low-expression group (P = 0.048). In the low-expression tamoxifen group, one patient had a recurrence of breast cancer and another 10 patients exhibited no recurrence, while six showed recurrence, and seven had none in the highexpression group (P = 0.035). We isolated exosomes successfully, and demonstrated that serum exosomal HOTAIR originated from primary breast cancer tissue. We conclude that serum exosomal HOTAIR exhibits the potential to be a diagnostic and prognostic biomarker. High expression of serum exosomal HOTAIR was also correlated with poor neoadjuvant chemotherapy and response to tamoxifen therapy.

Epigenetically altered miR­193a­3p promotes HER2 positive breast cancer aggressiveness by targeting GRB7.

Emerging evidence has demonstrated that microRNAs (miRNAs/miRs) have various biological functions in the development of human epidermal growth factor receptor 2 (HER2) positive breast cancer. The aim of the present study is to reveal the mechanism of miR­193a­3p inhibiting the progress of HER2 positive breast cancer. The expression of miR­193a­3p was evaluated by quantitative polymerase chain reaction (PCR). The methylation status of miR­193a­3p was evaluated by PCR and pyrosequencing analysis. Overexpression of miR­193a­3p and growth factor receptor bound protein 7 (GRB7) combined with in vitro tumorigenic assays were conducted to determine the carcinostatic capacities of miR­193a­3p in HER2 positive breast cancer cells. The association between miR­193a­3p and GRB7 was determined by luciferase reporter assay. Protein level was evaluated using western blot analysis. miR­193a­3p was downregulated in HER2 positive breast cancer cells and clinical tissues. Methylation­mediated silencing led to decreased expression of miR­193a­3p in HER2 positive breast cancer. Overexpression of miR­193a­3p could inhibit proliferation, migration and invasion of breast cancer cells. Overexpression of GRB7 could abolish this effect. miR­193a­3p could directly target the 3' untranslated region of GRB7. miR­193a­3p could directly or indirectly target extracellular signal­regulated kinase 1/2 (ERK1/2) and forkhead box M1 (FOXM1) signaling. In conclusion, it was identified that silencing of miR­193a­3p through hypermethylation can promote HER2 positive breast cancer progress by targeting GRB7, ERK1/2 and FOXM1 signaling. The function of miR­193a­3p in HER2 positive breast cancer implicates its potential application in therapy.

A Genetic Variant of rs145204276 in the Promoter Region of Long Noncoding RNA GAS5 Is Associated With a Reduced Risk of Breast Cancer.

INTRODUCTION: Growth arrest-specific 5 (GAS5), downregulated in breast cancer (BC), functions as a tumor suppressor by affecting tumor growth and cell apoptosis in vivo and in vitro. This study was designed to determine whether an insertion (ins)/deletion (del) polymorphism (rs145204276 AGGCA/-) in the promoter region of GAS5 was a susceptibility gene to the occurrence of BC. PATIENTS AND METHODS: A hospital-based case-control study was conducted and the GAS5 rs145204276 genotype was analyzed in 575 sporadic BC patients and 602 controls to test the association between the polymorphism and BC risk. Further functional analysis was performed to evaluate the effect of the polymorphism on the promoter activity and GAS5 expression levels using quantitative polymerase chain reaction and dual luciferase reporter assay. RESULTS: The prevalence of BC was lower in carriers with rs145204276 ins/del and del/del genotypes compared with those with ins/ins genotype (adjusted odds ratio [OR], 0.74; 95% confidence interval [CI], 0.58-0.92; P = .009). An allelic test for association with BC was also significant (del vs. ins: adjusted OR, 0.78; 95% CI, 0.65-0.93; P = .007). Genotype-phenotype analysis revealed that individuals with rs145204276 ins/del and del/del genotypes expressed significantly higher levels of GAS5. Luciferase reporter analysis revealed that rs145204276 del allele enhanced the promoter activity of GAS5. CONCLUSION: The rs145204276 del allele might protect against the development of BC via inducing the promoter activity by binding to transcriptional factor specificity protein 1, and finally resulting in higher levels of GAS5.

Tunicamycin suppresses breast cancer cell growth and metastasis via regulation of the protein kinase B/nuclear factor-κB signaling pathway.

Breast cancer is one of the most common metastatic tumor types. Reports have suggested that Tunicamycin may inhibit the aggressiveness of cancer cells by promoting their apoptosis. In the present study, the inhibitory effects of Tunicamycin were investigated and the potential molecular mechanism underlying the Tunicamycin-inhibited growth and aggressiveness of breast cancer cells was explored. In vitro assays demonstrated that Tunicamycin significantly inhibited growth and arrested the cell cycle of breast cancer cells in a dose-dependent manner, compared with control cells. Results revealed that Tunicamycin treatment suppressed the migration and invasion of breast cancer cells. Significantly increased apoptosis of breast cancer cells was observed subsequent to Tunicamycin treatment, as compared with control cells. Mechanism analysis demonstrated that Tunicamycin inhibited the protein kinase B (Akt) and nuclear factor-κB (NF-κB) signaling pathways, whilst Akt overexpression significantly cancelled out the Tunicamycin-inhibited growth and aggressiveness of breast cancer cells, as compared with control cells. In vivo assays revealed that Tunicamycin treatment significantly inhibited tumor growth and significantly prolonged the survival of tumor-bearing mice, compared with the PBS-treated group. In conclusion, these results indicate that Tunicamycin may inhibit the growth and aggressiveness of breast cancer cells via regulation of the Akt/NF-κB signaling pathway.

Opposite response to hypoxia by breast cancer cells between cell proliferation and cell migration: A clue from microRNA expression profile.

The majority of tumors possess the features of hypoxia. It is generally accepted that hypoxia is a negative prognostic factor for cancer. Low levels of oxygen are able to modify basic cell metabolism status. Elucidating the basic response, including cell proliferation and migration, to hypoxia by cancer cells is important for understanding the role of hypoxia in the development of cancer. In the present study, CoCl2 stimulation was used to simulate hypoxia. A microRNA (miRNA/miR) array was used to systematically detect the changes in miRNA expression profiles. Following treatment with CoCl2 for 12 h, 15 miRNAs were markedly upregulated and 10 miRNAs were markedly decreased compared with the control. After 24 h CoCl2 incubation, 15 miRNAs were increased and 3 miRNAs were decreased compared with the control. Among them, 7 miRNAs were upregulated and 2 miRNAs were downregulated at 12 and 24 h following CoCl2 stimulation. The potential roles of these miRNA were reviewed and it was identified that the majority of them are associated with cell proliferation and migration. Additional experiments demonstrated that CoCl2 incubation inhibited the proliferation of MCF-7 cells but promoted cell migration. miR-491 may be a key miRNA for hypoxia-inhibited cell proliferation, as it was identified that hypoxia induced the downregulation of B-cell lymphoma-extra large in a miR-491-dependent manner. As the target of miR-302a, CXCR4 may be a key protein for hypoxia-promoted cell migration. In the present study, it was identified that in the early stage of hypoxia, cell proliferation was inhibited but cell migration was promoted. These results support the hypothesis that hypoxia may be a driving force for tumor cell escape from the primary tumor site to other organs, or other sites of the same organ.

Circular RNA hsa_circ_0001982 Promotes Breast Cancer Cell Carcinogenesis Through Decreasing miR-143.

Circular RNAs (circRNAs) are a type of noncoding RNAs generated from back-splicing, which have been verified to mediate multiple tumorigenesis. With the development of high-throughput sequencing, massive circRNAs are discovered in tumorous tissue. However, the potential physiological effect of circRNAs in breast cancer is still unknown. The purpose of this study is to investigate the expression profile of circRNA in breast cancer tissue and explore the in-depth regulatory mechanism in breast cancer tumorigenesis. In the present study, we screened the circRNA expression profiles in breast cancer tissue using circRNA microarray analysis. Totally 1705 circRNAs were identified to be significantly aberrant. Among these dysregulated circRNAs, hsa_circ_0001982 was markedly overexpressed in breast cancer tissue and cell lines. Bioinformatics analysis predicted that miR-143 acted as target of hsa_circ_0001982, which was confirmed by Dual-luciferase reporter assay. Loss-of-function and rescue experiments revealed that hsa_circ_0001982 knockdown suppressed breast cancer cell proliferation and invasion and induced apoptosis by targeting miR-143. In summary, our study preliminarily investigates the circRNA expression in breast cancer tissue and explores the role of competing endogenous RNA (ceRNA) mechanism in the progression, providing a novel insight for breast cancer tumorigenesis.