Detection of doxycycline by using a tapered droplet structure fiber sensor.

The abuse of doxycycline (DC) can lead to residues in animals and water environments, which severely threaten human health; however, currently accepted detection methods are generally complicated and cannot be used for real-time detection. Therefore, developing a method for rapid real-time detection of DC microcontent residues is highly important. Herein, based on the Mach-Zehnder interference, we propose a simple tapered droplet structure fiber sensor with a high detection sensitivity. By modifying the sensing region with a molecularly imprinted polymer film of DC, this sensor realizes the specific detection of DC and has a detection sensitivity of 58.81 pm/ppm for DC in a large concentration range of 0-300 ppm. This sensor can be used to detect DC microcontent in aqueous solutions in real time.

Challenging the nexus of power: The gaming dilemma of collaboration between government and enterprises in environmental management.

This study presents a novel approach to analysing environmental governance by Chinese governments through the lens of a tripartite evolutionary game model. The key novelty of our research lies in the explicit incorporation of a reputation mechanism into the evolutionary game analysis, which significantly influences government decision-making, environmental governance strategies, and the dynamics of the relationship between government and polluting enterprises. By assessing the marginal effects of conventional governance and mobilization-based governance on the environmental mechanism, as well as the collusion behaviours between government and polluting enterprises, our study sheds light on previously unexplored aspects of environmental governance. Our findings indicate that the reputation mechanism plays a crucial role within the evolutionary game system of environmental governance, exerting a substantial impact on government decision-making. Furthermore, we demonstrate that policy interventions, such as increasing the cost of penalties under regulatory policies, can encourage compliance strategies among enterprises. Additionally, our research highlights the high sensitivity of reputation signals towards local government's environmental governance strategies, directly impacting their credibility and influencing the adoption of proactive environmental governance strategies. Moreover, we emphasize the role of the central environmental inspection system as a means to facilitate the transmission of environmental governance pressures between central and local governments, ultimately fostering a green development concept and promoting coordinated development between the economy and ecological civilization. Overall, this study provides valuable insights into the intricacies of environmental governance in China and underscores the importance of reputation mechanisms and policy interventions in promoting sustainable development.

Unravelling the veil of appearance anxiety: exploring social media use among Chinese young people.

The purpose of this study is to explore the relationship between appearance anxiety and social media use among Chinese adolescents. Using a grounded theory approach, the study conducted two-round online interviews with ten Chinese university students and subsequently constructed a theoretical model of social media appearance anxiety among Chinese young people. The results of the study indicate that social media has a dual impact on appearance anxiety. On one hand, increased social media engagement amplifies appearance anxiety by shaping aesthetic standards and fostering comparative environments. On the other hand, diverse aesthetic perspectives and authentic presentations on social media partially alleviate appearance anxiety by promoting acceptance of unique appearances and boosting self-confidence. It is emphasized in this study that there should be an in-depth understanding of the dual impact and complicated relationship of social media on the daily lives of Chinese adolescents to further develop relevant strategies that promote healthy social media behavior among youth. Furthermore, this study calls for efforts to actively promote the healthy image and psychological well-being of adolescents while alleviating the negative impact of appearance anxiety and overall mental health. Such efforts are needed to ensure a positive and healthy development for the younger generation.

The mRNA stability of NCAPG2, a novel contributor to breast invasive carcinoma, is enhanced by the RNA-binding protein PCBP2.

Non-SMC condensin II complex subunit G2 (NCAPG2) is one of the three non-SMC subunits in condensin II, which plays a vital role in regulating chromosome condensation and segregation. Although the tumor-promoting role of NCAPG2 has been reported in several solid malignancies, its function in breast invasive carcinoma (BRCA) remains unknown. Data both from GEPIA and GSE36295 indicated that NCAPG2 mRNA expression was abnormally upregulated in cancer tissues, which was further verified in 40 paired BRCA and para-carcinoma samples. Kaplan-Meier Plotter further illustrated that BRCA patients with higher NCAPG2 expression have a poorer prognosis. Functional experiments carried out in two BRCA cell lines (MCF-7 and T-47D) showed that NCAPG2-silenced BRCA cells acquired less aggressive behavior - weakened growth and metastasis both in vitro and in vivo. Label-free proteomics quantified the protein expression patterns in MCF-7 cells, and the results revealed 684 differentially expressed proteins (|log2FC| > 1 and P < 0.05) downstream to NCAPG2. Interestingly, poly(C)-binding protein 2 (PCBP2), an RNA binding protein previously known to increase RNA stability of its target genes, was found to directly bind to and protect NCAPG2 mRNA from degradation-PCBP2 knockdown accelerated the degradation half-life time of NCAPG2 mRNA from approximately 8 h to 5 h. Taken together, our study indicates that NCAPG2 acts as a novel contributor to BRCA growth and metastasis under the regulation of PCBP2, providing insights into BRCA treatment.

What makes Chinese adolescents "trapped" in severe mental illness? An interactionist perspective on self and identity.

The aim of this study was to explore the self and identity perspectives among Chinese adolescents with severe mental illness (SMI), with a focus on their illness experience and subjective meaning of a formal diagnosis. Thirty-one Chinese adolescents were interviewed and the interview data were analysed strictly according to principles suggested by the constructivist grounded theory approach. Five theoretical codes emerged in this study, including changes of personal values and beliefs, accumulated persistent developmental challenges and personal stresses, ineffective coping strategies and development, symptoms and development of mental illness, and changed perceptions and understandings of self. A proposed model of "The dynamic interactions of Chinese adolescents' identity and mental illness", was constructed and visualized. The results revealed that adolescents' identity formation is a fluctuating and non-linear process, but tends to be predominantly negative. The negative self, as informed by long-term ineffective coping with accumulated persistent developmental challenges and stressful events, develops towards a more serious status of negative identity and contributes to relapse symptoms, although this impact occurs variably with perceived personal characteristics. Besides, some participants who had achieved a state of "Buddha-like numbness" made a conscious decision to live a seemingly normal life while coexisting with their illness. The study also highlighted the positive aspects of identity formation that can arise from the experience of illness, including an enhanced sense of realism and increased empathy. Our findings will imply much the need for person-centred treatment plan and services that take into account of individual situations.

The Association of Food Groups and Consumption Time with Hyperuricemia: The U.S. National Health and Nutrition Examination Survey, 2005-2018.

Hyperuricemia (HUA) is associated with a wide range of diseases and increases the public health burden on society as a whole. In addition to genetic variation, diet plays a crucial role in the prevention and treatment of HUA as an important modifiable behavior. The purpose of this study is to investigate whether food groups and consumption time are associated with HUA. A total of 41,230 participants from the National Health and Nutrition Examination Survey between 2005 and 2018 were included in the study. All meals, including breakfast, lunch, and dinner, were obtained according to their corresponding Food Patterns Equivalents Database dietary data. The binary logistic regression model was used to analyze the relationship between food groups, food consumption time and HUA. We found that the intake of fruit (mixed in various forms) (OR = 0.942, 95% CI: 0.909-0.976) or freshly squeezed juices (OR = 0.915, 95% CI: 0.859-0.975), milk (OR = 0.839, 95% CI: 0.808-0.872), and eggs (OR = 0.881, 95% CI: 0.839-0.924), poultry (OR = 1.055, 95% CI: 1.033-1.077) and seafood high in n-3 fatty acids (OR = 1.068, 95% CI: 0.1.018-1.120) at dinner, eating refined grains at breakfast (OR = 0.954, 95% CI: 0.924-0.985) and dinner (OR = 0.962, 95% CI: 0.944-0.980), eating whole grains (OR = 0.908, 95% CI: 0.845-0.976) at lunch, consuming alcoholic beverages or foods at breakfast (OR = 0.748, 95% CI: 0.564-0.990)/lunch (OR = 1.118, 95% CI: 1.008-1.240)/dinner (OR = 1.127, 95% CI: 1.073-1.185) were associated with HUA. Eating particular meals at particular times of the day was related to a lower risk of HUA.

ARHGAP25 suppresses the development of breast cancer by an ARHGAP25/Wnt/ASCL2 feedback loop.

Downregulation of ARHGAP25 was found in the tumor samples from breast cancer patients and five breast cancer cell lines. However, its precise role and molecular mechanisms in breast cancer remain completely unknown. Herein, we found that knockdown of ARHGAP25 in breast cancer cells promoted proliferation, migration and invasion of breast cancer cells. Mechanistically, ARHGAP25 silence facilitated the activation of the Wnt/ß-catenin pathway and the upregulation of its downstream molecules (including c-Myc, Cyclin D1, PCNA, MMP2, MMP9, Snail and ASCL2) by directly regulating Rac1/PAK1 in breast cancer cells. In vivo xenograft experiments indicated ARHGAP25 silence promoted tumor growth and activated the Wnt/ß-catenin pathway. In contrast, overexpression of ARHGAP25 in vitro and in vivo impeded all of the above cancer properties. Intriguingly, ASCL2, a downstream target of the Wnt/ß-catenin pathway, transcriptionally repressed the expression of ARHGAP25 and therefore constituted a negative feedback loop. Moreover, bioinformatics analysis indicated that ARHGAP25 was significantly correlated with tumor immune cell infiltration and the survival of patients with different immune cell subgroups in breast cancer. Collectively, our work revealed that ARHGAP25 suppressed tumor progression of breast cancer. It provides a novel insight for the treatment of breast cancer.

LAPTM5 regulated by FOXP3 promotes the malignant phenotypes of breast cancer through activating the Wnt/ß­catenin pathway.

Breast cancer remains the most common malignancy and the leading cause of cancer­associated mortality in women worldwide. Lysosomal protein transmembrane 5 (LAPTM5), a lysosomal membrane protein, plays an important role in several human malignancies. However, the biological functions and mechanism of LAPTM5 in breast cancer remain unclear. In the present study, the potential tumor­promoting effect of LAPTM5 was predicted by bioinformatics analysis. LAPTM5 was highly expressed in breast cancer clinical specimens. Moreover, in vitro studies demonstrated that cell proliferation, migration and invasion, as well as the process of epithelial­mesenchymal transition (EMT) were promoted by LAPTM5 overexpression and were suppressed by LAPTM5 downregulation in vitro. The tumor­promoting effects of LAPTM5 were also confirmed by xenograft tumor assay in vivo. It was found that the tumor­promoting effects of LAPTM5 were partly dependent on the activation of the Wnt/ß­catenin signaling pathway. Furthermore, dual­luciferase and chromatin immunoprecipitation assays verified that the transcription factor forkhead box protein 3 (FOXP3) directly bound to the promoter of LAPTM5 and negatively regulated its expression. Taken together, the present findings indicated that LAPTM5, negatively regulated by FOXP3, promoted the malignant phenotypes of breast cancer through activating the Wnt/ß­catenin signaling pathway.

TRG16, targeted by miR-765, inhibits breast cancer stem cell-like properties via regulating the NF-κB pathway.

Previous studies reported that cancer stem cells (CSCs) might be responsible for drug resistance and cancer progression. Transformation-Related Gene 16 Protein (TRG16), a pseudokinase, was reported to be a suppressor in some types of cancer and its overexpression impaired hepatocellular carcinoma cell stemness. However, the function of TRG16 in BC remains unclear. We found that TRG16 expression was significantly downregulated in BC tissues compared with adjacent tissues (n = 40; P < 0.001) and BC patients with lower expression of TRG16 had a worse prognosis. Forced expression of TRG16 inhibited BC stem cell-like properties as evidenced by decreased CD44-positive cells (CSC marker), reduced mammosphere quantity, and downregulated Nanog, aldehyde dehydrogenase, octamer-binding transcription factor 4, and SRY-box transcription factor 2 expression (CSC markers). Moreover, TRG16 overexpression inhibited self-renewal and invasion capabilities of BC cells in vitro as well as tumor growth in vivo but increased cisplatin sensitivity. However, TRG16 silencing had the opposite effects. Further mechanistic studies revealed that TRG16 was targeted and negatively regulated by miR-765, a facilitator of BC progression. TRG16 could suppress the activation of the NF-κB pathway in BC cells, which is a positive pathway in BC progression and contributes to the maintenance of cancer cell stemness. In conclusion, the results above demonstrate that TRG16, negatively regulated by miR-765, may inhibit the BC progression by regulating BC stem cell-like properties and this inhibition may be mediated by the NF-κB pathway. Our findings indicate that TRG16 may be a potential therapeutic targetable node for BC. TRG16, negatively regulated by miR-765, may inhibit the BC progression through regulating BC stem cell-like properties and this inhibition may be mediated by the NF-κB pathway.

SEZ6L2, regulated by USF1, accelerates the growth and metastasis of breast cancer.

Breast cancer (BC) is the second cause of cancer-related mortality in women. Seizure related 6 homolog like 2 (SEZ6L2), a protein presented on cell surface, is involved in tumor development. It was found to be highly expressed in BC, however, its role in BC remains unclear. Herein, we aimed to explore the role of SEZ6L2 in BC. Firstly, the correlationship between SEZ6L2 expression and the clinic pathological characteristics of patients diagnosed with BC was analyzed. Subsequently, the role of SEZ6L2 was further explored using MTT, transwell invasion, flow cytometry, colony formation and wound healing assays. The result showed that the level of SEZ6L2 was remarkably correlated with the TNM stage, HER-2 status and lymph node metastasis of BC. Knockdown of SEZ6L2 significantly suppressed the proliferation of BC cells and induced cell cycle arrest at G1 phase. In addition, SEZ6L2 knockdown repressed their migration and invasion. On the contrary, SEZ6L2 overexpression performed the opposite effects. Furthermore, SEZ6L2 also accelerated the in vivo tumorigenesis of BC cells. Additionally, according to bioinformatics resources, we identified upstream transcription factor 1 (USF1) as a transcriptional factor which bound to the promoter of SEZ6L2 and positively regulated its transcription. In conclusion, this study demonstrated that SEZ6L2 was transcriptionally regulated by USF1 and was involved in the growth and metastasis of BC cells. Revealing the role of SEZ6L2 in BC provides additional knowledge for the pathogenesis of BC, which may benefit to BC therapy.

Diamond formation mechanism in chemical vapor deposition.

It is a key challenge to prepare large-area diamonds by using the methods of high-pressure high-temperature and normal chemical vapor deposition (CVD). The formation mechanism of thermodynamically metastable diamond compared to graphite in low-pressure CVD possibly implies a distinctive way to synthesize large-area diamonds, while it is an intriguing problem due to the limitation of in situ characterization in this complex growth environment. Here, we design a series of short-term growth on the margins of cauliflower-like nanocrystalline diamond particles, allowing us to clearly observe the diamond formation process. The results show that vertical graphene sheets and nanocrystalline diamonds alternatively appear, in which vertical graphene sheets evolve into long ribbons and graphite needles, and they finally transform into diamonds. A transition process from graphite (200) to diamond (110) verifies the transformation, and Ta atoms from hot filaments are found to atomically disperse in the films. First principle calculations confirm that Ta-added H- or O-terminated bilayer graphene spontaneously transforms into diamond. This reveals that in the H, O, and Ta complex atmosphere of the CVD environment, diamond is formed by phase transformation from graphite. This subverts the general knowledge that graphite is etched by hydrogen and sp3 carbon species pile up to form diamond and supplies a way to prepare large-area diamonds based on large-sized graphite under normal pressure. This also provides an angle to understand the growth mechanism of materials with sp2 and sp3 electronic configurations.

LINC00982 Inhibits the Proliferation, Migration, and Invasion of Breast Cancer Cells Through the miR-765/DPF3 Axis.

Breast cancer (BC) is one of the most frequently occurring malignant tumors in female adults. The long intergenic nonprotein coding RNA 00982 (LINC00982) has been regarded as a cancer suppressor in several human cancers. However, the function and the underlying mechanisms of LINC00982 have not been studied in BC. The present study found that LINC00982 was significantly downregulated in BC tumor tissues, and the low LINC00982 level predicts a poor prognosis of BC. Through the overexpression and suppression of LINC00982 in two BC cell lines, we found that LINC00982 could inhibit cell proliferation, migration, and invasion by suppressing the activity of the signal transducer and activator of transcription 3 (STAT3)/nuclear factor kappa B (NF-κB) signal pathway. Furthermore, luciferase reporter assay has been used to verify that LINC00982 functions as a molecular sponge for miR-765, which could target DPF3. The relative expression of miR-765 decreased with LINC00982 overexpressing, and DPF3 increased at the same time. In addition, the suppression of cell malignant phenotype caused by overexpression of LINC00982 can be reversed by inhibition of DPF3. To verify the function of LINC00982 in vivo, the BC cells were implanted in nude mice and the results suggested the tumor growth and malignant phenotype were suppressed by LINC00982. In this study, we prove that LINC00982 regulates the growth and development of BC through STAT3/NF-κB signal pathway, mediated by the miR-765/DPF3 axis. LINC00982 may function as a target molecule to take part in the prognosis and therapy of BC.

CKAP2L, transcriptionally inhibited by FOXP3, promotes breast carcinogenesis through the AKT/mTOR pathway.

Cytoskeleton-associated protein 2-like (CKAP2L) is a mitotic spindle protein and its high expression is reported to be associated with the poor prognosis of cancer patients. Interestingly, TNMplot website analysis indicated that CKAP2L expression was significantly higher in breast cancer (BC) tissues than in normal breast tissues (P < 0.001). Thus, this study was conducted to investigate the role of CKAP2L in breast carcinogenesis and its underlying molecular mechanisms. The mRNA and protein expression levels of CKAP2L in 40 paired fresh BC and para-carcinoma specimens were first analyzed, and the results confirmed the high expression of CKAP2L in BC tissues. Functional studies revealed that CKAP2L silencing dramatically suppressed the proliferation, migration, and invasion, induced cell cycle arrest and apoptosis of BC cells in vitro, and inhibited the growth of xenografted tumors in vivo. However, CKAP2L overexpression produced the opposite results. Mechanically, CKAP2L could activate the AKT/mTOR signaling pathway in BC cells accompanied by increased phosphorylation levels of AKT, mTOR, and p70S6K in CKAP2L-overexpressed cells. Forkhead box protein P3 (FOXP3), a transcription factor with tumor-suppressive properties, was proved to negatively regulate CKAP2L expression in BC cells through binding to the promoter of CKAP2L and inhibiting its transcription. In summary, the present study demonstrates that CKAP2L, transcriptionally regulated by FOXP3, activates the AKT/mTOR signaling pathway and promotes breast carcinogenesis. CKAP2L may serve as a promising target of therapeutic intervention for BC.

Chrysin prevents lipopolysaccharide-induced acute lung injury in mice by suppressing the IRE1α/TXNIP/NLRP3 pathway.

Acute lung injury (ALI) remains a serious challenge in the intensive care unit. Inflammation plays a key role in the progression of ALI. Chrysin (CHR) is a natural flavonoid with anti-inflammatory functions. We investigated the anti-inflammatory effects in a mouse model of ALI induced by lipopolysaccharide (LPS), and identified the underlying mechanisms of its action. Following CHR administration, mice were challenged with LPS intratracheally for 6 h to induce ALI. Compared to mice challenged with LPS alone, the presence of CHR showed a reduction in the development of lung injuries, as confirmed by histopathological observation. Pre-treatment with CHR attenuated inflammation by reducing the production of myeloperosidase (MPO), and pro-inflammatory cytokine levels in the lung and bronchoalveolar lavage fluid (BALF). Furthermore, CHR improved lung edema by reducing the vascular permeability, as demonstrated by less evans blue staining in the lung tissue and low levels of protein in BALF. In addition, our results proved that CHR improved the antioxidant capacity by increasing the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the lung tissue. Results of western blot assays suggested that CHR suppressed the LPS-induced expression of glucose-regulated protein 78 (GRP78) and phosphorylated inositol-requiring enzyme 1α (p-IRE1α). We also found that CHR suppressed the expression of thioredoxin interaction protein (TXNIP), nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) and cleaved caspase-1. In conclusion, CHR improved vascular permeability and mitigated the inflammatory response of lung tissue by suppressing the IRE1α/TXNIP/NLRP3 pathway, thereby alleviating LPS-induced ALI in the lungs of mice.

Clinical and imaging characteristics of breast ductal carcinoma in situ with microinvasion.

BACKGROUND: We analyzed the clinical and imaging characteristics of patients with breast ductal carcinoma in situ with microinvasion (DCISM) and breast ductal carcinoma in situ (DCIS). METHODS: We analyzed the records of 40 patients diagnosed with DCISM and 61 patients with DCIS who were hospitalized at Shengjing Hospital (Shenyang, China) from January 2009 to June 2016. The size, hardness, and degree of calcification of tumors were determined by mammography and ultrasonography. RESULTS: In all, 37 DCISM patients and 45 DCIS patients showed clinical palpable masses (92.5% vs 73.77%, P = 0.018). Mammography showed that the mean size of tumor was larger in DCISM patients than that of DCIS patients (3.13 ± 1.51 vs 2.68 ± 1.77, P = 0.030). Ultrasound examination revealed calcification shadows in the solid tumor mass in 17 DCISM cases and 11 DCIS patients (42.5 vs 18.03%, P = 0.007). Furthermore, estrogen receptor positivity and progesterone receptor positivity were more common in DCIS patients (32.5% vs 54.10%, P = 0.033; 22.5% vs 45.90%, P = 0.017), and the percentage of menopausal patients were higher in DCISM patients than that of DCIS patients (70.00% vs 47.54%, P = 0.026). CONCLUSION: Clinically palpable and calcified tumor masses on sonography are more commonly encountered in DCISM lesions.

The long noncoding RNA HOTTIP promotes breast cancer cell migration, invasiveness, and epithelial-mesenchymal transition via the Wnt-ß-catenin signaling pathway.

Long noncoding RNA HOTTIP (HOXA transcript at the distal tip) has recently been reported to have a role in the proliferation of various cancer cells, yet its role in cell migration, invasiveness, and the EMT (epithelial-mesenchymal transition) in breast cancer and the potential mechanisms remain unknown. Breast cancer cell lines MDA-MB-231 and MDA-MB-468 were transfected with shRNA (short hairpin RNA) that specifically targeting HOTTIP. We observed a remarkable decrease in migration and invasiveness in these two breast cancer cell lines after knock-down of HOTTIP by shHOTTIP. We also demonstrated that the EMT of these two breast cell lines was suppressed after HOTTIP knock-down, as evidenced by increased E-cadherin levels, and decreased levels of N-cadherin, Snail, and Twist. Moreover, HOTTIP silencing also suppressed tumor metastasis in nude mice in vivo. In addition, we found that the expression of ß-catenin was significantly decreased in breast cancer cells after knock-down of HOTTIP. In a further rescue experiment using overexpression of ß-catenin, the rates of cell migration, invasiveness, and EMT of HOTTIP-silenced breast cancer cells were promoted, disclosing a potential role of the Wnt-ß-catenin signaling pathway in this process. Overall, we discovered the positive regulatory function of HOTTIP in the migration, invasiveness, and EMT of breast cancer cells, via regulating the Wnt-ß-catenin pathway.

Diagnostic value of endoscopic appearance during ductoscopy in patients with pathological nipple discharge.

BACKGROUND: To explore the features of ductoscopic appearance that may be diagnostic in patients with pathologic nipple discharge (PND) and to discuss the diagnostic criteria for intraductal tumors. METHODS: We reviewed 247 patients with PND but without a palpable mass who were evaluated using either surgical biopsy or excision. Data concerning patient age, duration of discharge, discharge color, and the details of endoscopic appearance were analyzed according to the pathological results. RESULTS: The postoperative diagnosis in 61 patients (24.70%) was a nonmass lesion, and 186 patients (76.52%) had an intraductal tumor. Among those with intraductal lesions, 10 patients (4.05%) had a malignant tumor, including 4 (1.62%) with ductal carcinoma in situ and 6 (2.43%) with invasive ductal carcinoma. On univariate analysis, patients of older age with spontaneous and bloody discharge were more likely to suffer from intraductal lesions. On logistic regression analysis, bloody nipple discharge, morphology, and a broad lesion base revealed by ductoscopy showed a statistically significant correlation with malignancy (p = 0.001, p < 0.001, p = 0.022, respectively). CONCLUSIONS: Both clinical features and endoscopic appearance are significant for the precise diagnosis of an intraductal lesion seen on ductoscopy. The endoscopic features of bloody discharge, morphology, and a broad lesion base are independent risk factors for malignancy and represent new criteria for the diagnosis of patients with PND.

Circulating microRNA-451 as a predictor of resistance to neoadjuvant chemotherapy in breast cancer.

OBJECTIVE: We aimed to explore the potential application of circulating microRNA-451 (miR-451) in serum in predicting the resistance to neoadjuvant chemotherapy (NACT) in breast cancer (BC). METHODS: Eighty-two BC patients who underwent NACT were recruited in our study, including 41 NACT-sensitive patients (NACT-sensitive group) and 41 NACT-resistant patients (NACT-resistant group). Additionally, 60 healthy subjects were selected as normal controls. Epirubicin-resistant MCF-7 BC cell line (MCF-7/EPI) and docetaxel-resistant MCF-7 BC cell line (MCF-7/DOC) were cultured in our study. MTT assay was applied to calculate the survival rates of MCF-7 cells, MCF-7/DOC cells and MCF-7/EPI cells. The expression levels of miR-451 in normal controls, NACT-sensitive group, NACT-resistant group, MCF-7 cells, MCF-7/DOC cells and MCF-7/EPI cells were measured by qRT-PCR method. RESULTS: The proliferation rates of both the MCF-7/DOC and MCF-7/EPI cells were significantly restrained at the drug concentration of 10 ng/ml, 50 ng/ml, 100 ng/ml and 200 ng/ml. However, the proliferation rates of MCF-7/DOC and MCF-7/EPI cells both increased significantly at the drug concentration of 500ng/ml. Furthermore, the IC50 of MCF-7/DOC cells was 23.603 ng/ml and the IC50 of MCF-7/EPI cells was 3.209 ng/ml. The relative expression of miR-451 was significantly lower in both the NACT-resistant group and the NACT-sensitive group than the normal control group. We also found that the relative expression level of miR-451 was significantly lower in the NACT-resistant group than that in the NACT-sensitive group. The expression of miR-451 in the MCF-7/EPI and the MCF-7/DOC cell lines was significantly lower than that in the MCF-7 cell lines. CONCLUSION: We supported the view that the relative expression level of miR-451 was lower in the NACT-resistant BC patients, suggesting the circulating miR-451 may have a functional significance in predicting the resistance to NACT in BC patients. We laid a foundation for further research on the resistance to NACT in BC treatment.