The far-upstream element-binding protein 2 is correlated with proliferation and doxorubicin resistance in human breast cancer cell lines.

Far-upstream element (FUSE)-binding protein 2 (FBP2) was a member of single-stranded DNA-binding protein family; it played an important role in regulating transcription and post-transcription and is involved in the regulation of C-MYC gene expression in liver tumors. However, the role of FBP2 in breast cancer and its mechanism has not been studied yet. Here, we discovered that FBP2 was up-regulated in breast cancer tissues and breast cancer cell lines. Moreover, immunohistochemistry analysis demonstrated that up-regulated FBP2 was highly associated with tumor grade, Ki-67, and poor prognosis, which was an independent prognostic factor for survival of breast cancer patients. At the cellular level, we found that FBP2 was correlated with cell cycle progression by accelerating G1/S transition, and knockdown of FBP2 could weaken cell proliferation, anchorage-independent cell growth, while enhancing the sensitivity of breast cancer cells to doxorubicin. More importantly, we found that activation of PI3K/AKT pathway could phosphorylate FBP2, and then make FBP2 shuttle from cytoplasm into the nucleus, which was the main mechanism of breast cancer cell proliferation and drug resistance. Taken together, our findings supported the notion that FBP2 might via PI3K/AKT pathway influence breast cancer progression and drug resistance, which might provide a new target for the design of anti-cancer drugs for breast cancer patients.

Decreased expression and prognostic role of cytoplasmic BRSK1 in human breast carcinoma: correlation with Jab1 stability and PI3K/Akt pathway.

OBJECTIVE: Jun activation domain-binding protein 1 (Jab1) was overexpressed in breast cancer, which was involved in degradation of the cyclin-dependent kinase inhibitor p27(Kip1). The objective of this study was to examine the effect of brain specific kinase 1 (BRSK1) expression on Jab1 over-expression and related signaling pathway in breast cancer. METHODS: Immunohistochemical analysis was performed in 95 human breast carcinoma samples and the data were correlated with clinicopathologic features. Furthermore, Western blot analysis was performed for BRSK1 and Jab1 in breast carcinoma samples and cell lines to evaluate their protein levels and molecular interaction. RESULTS: We found that the cytoplasmic BRSK1 expression was inversely associated with Jab1 expression (P<0.01) and correlated significantly with histologic grade (P=0.006), however nuclear BRSK1 expression couldn't obtain similar results. Kaplan-Meier analysis revealed that survival curves of low versus high expressers of cytoplasmic BRSK1 and Jab1 showed a highly significant separation in breast cancer (P<0.01). While in vitro, following release of breast cancer cell lines from serum starvation, the expression of Jab1, phosphor-Akt (p-Akt) was up-regulated, whereas BRSK1 and p27(Kip1) were decreased. Treatment of phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 could diminish Jab1 expression but increase BRSK1 expression. In addition, we employed siRNA technique to knock down Jab1 and/or BRSK1 expression and observed their effects on MDA-MB-231 cell growth. CONCLUSIONS: BRSK1 is a novel tumor suppressor in breast cancer which inversely correlated with Jab1 expression, may involve in the restoring Jab1-induced suppression of p27(Kip1) and may regulate cell cycle through the PI3K/Akt pathway.

Knocking down the expression of adenylate cyclase-associated protein 1 inhibits the proliferation and migration of breast cancer cells.

Adenylate cyclase-associated protein 1 (CAP1) is a conserved protein that was found to be up-regulated in breast cancer and related to the migration of breast cancer. We verified its roles in breast cancer specimens and cell lines. In our results, 71 of 100 specimens of breast cancer showed high levels of CAP1 by immunohistochemistry. Associated with statistical analysis, we saw that CAP1 was related to the grade of breast cancer. In MDA-MB-231, the expression of CAP1 was the highest and by knocking down the expression of CAP1 in MDA-MB-231, its ability for proliferating and migrating apparently decreased and induced changes in morphology, which were related to the arrangement of F-actin. Therefore, CAP1 might be a potential molecular targeted therapy for surgery and immune treatment.

[Expression and clinicopathological significance of Emi1 in breast carcinoma].

OBJECTIVE: To examine the expression and prognostic value of novel oncogene Emi1 in breast cancer. METHODS: Immunohistochemical analysis was performed for 93 human breast carcinoma samples and adjacent normal tissues for detecting the expression of Emi1 and cell proliferative factor Ki-67. Then the data were correlated with clinicopathological features. RESULTS: Emi1 was highly expressed in breast carcinoma tissues compared with adjacent normal tissues. Emi1 expression was significantly associated with histological grade (P = 0.002) , axillary lymph node status (P = 0.017) and ER status (P = 0.038) . However, there was no correlation between Emi1 expression and other factors such as age, tumor size, histology, PR status, HER-2 or P53. Meanwhile similar results were obtained for Ki-67 expression. A marked correlation also existed between Emi1 and Ki-67 expression (Spearman's r² = 0.454, P = 0.002) . CONCLUSION: As a novel breast cancer associated gene, Emil plays an important role in evaluating invasion and metastatic potentiality in breast cancer. And it is also an important prognostic predictor of breast cancer so as to become a potential therapeutic target for breast cancer.

[Prognostic significance of CXCR2 expression in pancreatic ductal carcinoma].

OBJECTIVE: To explore the relationship between the expression of CXC chemokine receptor 2 (CXCR2) and the clinicopathologic features with prognosis in pancreatic ductal carcinoma (PDAC) tissues. METHODS: The CXCR2 expression in 161 PDAC tissues were detected with immunohistochemistry using anti-human CXCR2 antibody and tissues microarray. RESULTS: The expression of CXCR2 in PDAC tumor tissues was higher than that in normal pancreatic tissues (χ(2) = 11.437, P = 0.001). The comparison of clinicopathologic characteristics and immunohistochemistry by χ(2) test analysis showed that a high expression of CXCR2 in PDAC was correlated with vascular invasion (χ(2) = 6.489, P = 0.011) and late TNM stage (χ(2) = 6.205, P = 0.013). Kaplan-Meier survival and Cox regression analyses showed that a high expression of CXCR2 (HR: 5.514, P = 0.016) was an independent prognostic factor. CONCLUSION: A high expression of CXCR2 denotes a poor prognosis in PDAC.

[Expression and prognostic value of galectin-9 in hepatocellular carcinoma patients].

OBJECTIVE: To explore the prognostic value of galectin-9 in patients with hepatocellular carcinoma (HCC). METHODS: Galectin-9 was validated by immunohistochemisty in tissue microarrays from HCC patients (n = 147) and statistically assessed for the prognosis. The serum levels of galectin-9 from another independent cohort including HCC patients (n = 31) were assessed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Patients with a lower expression of galectin-9 had significantly worse prognosis than those with a higher expression. The serum level of galectin-9 of HCC patients (8.36 ± 2.12) µg/L was significantly lower than that in healthy (4.62 ± 1.59 )µg/L and liver cirrhosis controls (5.11 ± 1.92 )µg/L (P < 0.05). Multivariate Cox proportional hazard analysis showed that galectin-9 was an independent marker for predicting a poor prognosis of HCC patients. CONCLUSION: Involved in the poor prognosis of HCC patients, galectin-9 may be a new predictor of recurrence for HCC patients and serve as a high-priority therapeutic target.

Isoproterenol-induced Upregulation of HPSE Accelerates Triple-negative Breast Cancer Cell Proliferation and Migration through Enhancing the Transcriptional Activity of HIF-1α.

BACKGROUND: Triple-negative breast cancer (TNBC) is considered to be the most malignant subtype of breast cancer (BC). Heparanase (HPSE) has been reported to contribute to tumor development, but its potential function in TNBC is not clear. The intention of this study was to investigate whether HPSE affects TNBC progression and to explore the possible mechanisms. METHODS: Bioinformatics analyses were applied to analyze the expression of HPSE in TNBC samples and normal breast samples. The mRNA and protein levels of HPSE in TNBC cells were detected by RT-qPCR and western blot. Function assays, including CCK-8 assay, colony formation assay, transwell assay and wound healing assay, were conducted to validate the effects of HPSE silencing on TNBC cell proliferation and migration. Mechanism experiments were performed to explore the upstream molecular mechanism of HPSE in TNBC cells. RESULTS: Silencing of HPSE suppressed the proliferation and migration of TNBC cells. Moreover, hypoxia-inducible factor-1 alpha (HIF-1α) interacted with the HPSE promoter and promoted the transcription of HPSE. Isoproterenol (ISO), a pharmacological substitute for chronic stress-induced sympathetic activation, was proven to induce HIF-1α upregulation, so as to transcriptionally activate HPSE in TNBC cells. Furthermore, it manifested that ISO facilitated TNBC cell proliferation and migration in an HPSE-dependent way. CONCLUSION: HPSE activated by ISO-induced HIF-1α promoted TNBC cell proliferation and migration, which might offer a novel insight for TNBC treatment.

ATRX is a predictive marker for endocrinotherapy and chemotherapy resistance in HER2-/HR+ breast cancer through the regulation of the AR, GLI3 and GATA2 transcriptional network.

Drug resistance in breast cancer (BC) is a clinical challenge. Exploring the mechanism and identifying a precise predictive biomarker for the drug resistance in BC is critical. Three first-line drug (paclitaxel, doxorubicin and tamoxifen) resistance datasets in BC from GEO were merged to obtain 1,461 differentially expressed genes for weighted correlation network analysis, resulting in identifying ATRX as the hub gene. ATRX is a chromatin remodelling protein, therefore, ATRX-associated transcription factors were explored, thereby identifying the network of AR, GLI3 and GATA2. GO and KEGG analyses revealed immunity, transcriptional regulation and endocrinotherapy/chemotherapy resistance were enriched. Moreover, CIBERSORT revealed immunity regulation was inhibited in the resistance group. ssGSEA showed a significantly lower immune status in the ATRX-Low group compared to the ATRX-High group. Furthermore, the peaks of H3K9me3 ChIP-seq on the four genes were higher in normal tissues than in BC tissues. Notably, the frequency of ATRX mutation was higher than BRCA in BC. Moreover, depressed ATRX revealed worse overall survival and disease-free survival in the human epidermal growth factor receptor 2 (HER2)-/hormone receptor (HR)+ BC. Additionally, depressed ATRX predicted poor results for patients who underwent endocrinotherapy or chemotherapy in the HER2-/HR+ BC subgroup. A nomogram based on ATRX, TILs and ER exhibited a significantly accurate survival prediction ability. Importantly, overexpression of ATRX significantly inhibited the IC50 of the three first-line drugs on MCF-7 cell. Thus, ATRX is an efficient predictive biomarker for endocrinotherapy and chemotherapy resistance in HER2-/HR+ BC and acts by suppressing the AR, GLI3 and GATA2 transcriptional network.

Overexpression of forkhead box J2 can decrease the migration of breast cancer cells.

The prognosis of breast cancer patients with metastases is generally poor, so it is essential to elucidate related molecules mechanisms. Forkhead Box J2 (FOXJ2) is a member of Forkhead Box transcription factors, many of which have been reported to participate in tumor migration and invasion. In this study, we showed the expression of FOXJ2 was higher in primary breast cancer tissues without lymph nodes metastases than those with, and there was statistical significance between the expression of FXOJ2 and the clinical factors. Hence, we identified a novel function of metastasis, which was not previously known for FOXJ2. Overexpression of FOXJ2 decreased the motility property of highly migrative MDA-MB-231 cells in vitro by wound healing assays and trans-well migration assays, and it was concurrent with the increased expression of epithelial marker E-cadherin and the decreased expression of mesenchymal marker vimentin by Western blot analysis, reverse transcription PCR analysis, and immunofluorescence analysis. Consistent with these observations, the repression of FOXJ2 in weakly metastatic MCF-7 cells remarkably promoted cellular motility. Our study demonstrates that FOXJ2 can inhibit the metastasis of human breast cancer by regulating the EMT key markers E-cadherin and vimentin.

LncRNA TTN-AS1 confers tamoxifen resistance in breast cancer via sponging miR-107 to modulate PI3K/AKT signaling pathway.

OBJECTIVE: Tamoxifen resistance of breast cancer (BC) is a significant hindrance in clinical therapy. The long-noncoding RNA (lncRNA) TTN-AS1 has been reported as a crucial tumor promoting factor in various cancers. In this study, we set out to discover the specific pathologic regulatory mechanisms of tamoxifen-resistance in breast cancer. METHODS: MTT assay was conducted to evaluate the cell viability of the breast cancer cell lines MCF-7 and MCF-7/TAM. QRT-PCR and western blot assay were performed to estimate the expression of TTN-AS1, miR-107 and related proteins. Flow cytometry was conducted to identify degree of apoptosis and cell cycle. The invasive ability was estimated by transwell chamber assay. RESULTS: Our findings revealed that TTN-AS1 can enhance tamoxifen-resistance in BC cells and augment the invasive ability of tamoxifen-resistant breast cancer cells by down-regulating miR-107, and thereby encourage the development of drug-resistant BC. Further investigation indicates that lncRNA TTN-AS1 worsens the course of tamoxifen-resistant BC by regulating zinc and ring finger 2 (ZNRF2) via miR-107 and activating the PI3K/AKT pathway. CONCLUSION: Our findings suggest that the lncRNA TTN-AS1 can encourage tamoxifen-resistance in BC by modulating the miR-107/ZNRF2 axis and stimulating the PI3K/AKT pathway.

Up-regulation of long noncoding RNA MBNL1-AS1 suppresses breast cancer progression by modulating miR-423-5p/CREBZF axis.

Breast cancer is the leading cause of cancer-related death among females, which is required to be solved urgently. Recent studies have found significant changes in a large number of genes and their transcriptional levels during breast cancer development, which are often closely related to the abnormal expression of long noncoding RNAs (lncRNAs). Herein, our study found that MBNL1-AS1 was down-regulated both in breast cancer tissues and cell lines, and it functioned as a tumor suppressor to inhibit cancer cell proliferation, migration, and invasion. MiR-423-5p was found to be a target of MBNL1-AS1 with an inverse relationship: an increase in miR-423-5p could counteract the inhibitory effect induced by MBNL1-AS1 on cancer cell promotion. Further, CREBZF was negatively regulated by miR-423-5p. Accordingly, CREBZF knockdown could impair the hindrance of cancer cell growth mediated by low miR-423-5p expression. Also, MBNL1-AS1 influenced the PI3K/AKT pathway, which was associated with cell proliferation and apoptosis, by regulating CREBZF. As a result, our work illustrated the tumor suppressor role of MBNL1-AS1 in breast cancer via upregulating miR-423-5p-targeted CREBZF. Thereby, the evidence indicates the complete understanding of the role of MBNL1-AS1/miR-423-5p/CREBZF axis in the regulation of breast cancer development, which could be used as a biomarker for predicating survival among breast cancer patients.

EphA8 inhibits cell apoptosis via AKT signaling and is associated with poor prognosis in breast cancer.

Erythropoietin­producing hepatocellular receptors (Ephs) comprise the largest subfamily of receptor tyrosine kinases and have been reported to be involved in a variety of biological cellular processes, including tumorigenesis and cancer progression. The present study aimed to determine the expression levels and clinicopathological significance of EphA8 in breast cancer (BC) using immunohistochemistry analysis of tissue microarrays. The results of the present study revealed that EphA8 expression levels were upregulated in BC tissue and were associated with tumor size and TNM stage. In addition, upregulated expression levels of EphA8 were identified to be a poor prognostic biomarker for patients with BC. The knockdown of EphA8 expression using short hairpin RNA resulted in increased levels of apoptosis as well as decreased proliferation, migration and invasion of BC cells both in vivo and in vitro. The knockdown of EphA8 also decreased the phosphorylation of AKT, which was accompanied by downregulation of Bcl­2 expression levels and upregulation of p53, Caspase­3 and Bax expression levels. Moreover, knockdown of EphA8 expression increased the chemosensitivity of BC cells to paclitaxel. In conclusion, the results of the present study indicated that EphA8 may be a useful prognostic marker in BC and that knockdown of EphA8 may represent a novel strategy in adjuvant chemotherapy for the treatment of BC.

Real-Time Mask Identification for COVID-19: An Edge-Computing-Based Deep Learning Framework.

During the outbreak of the Coronavirus disease 2019 (COVID-19), while bringing various serious threats to the world, it reminds us that we need to take precautions to control the transmission of the virus. The rise of the Internet of Medical Things (IoMT) has made related data collection and processing, including healthcare monitoring systems, more convenient on the one hand, and requirements of public health prevention are also changing and more challengeable on the other hand. One of the most effective nonpharmaceutical medical intervention measures is mask wearing. Therefore, there is an urgent need for an automatic real-time mask detection method to help prevent the public epidemic. In this article, we put forward an edge computing-based mask (ECMask) identification framework to help public health precautions, which can ensure real-time performance on the low-power camera devices of buses. Our ECMask consists of three main stages: 1) video restoration; 2) face detection; and 3) mask identification. The related models are trained and evaluated on our bus drive monitoring data set and public data set. We construct extensive experiments to validate the good performance based on real video data, in consideration of detection accuracy and execution time efficiency of the whole video analysis, which have valuable application in COVID-19 prevention.

JAB1 expression is associated with inverse expression of p27(kip1) in hepatocellular carcinoma.

BACKGROUND/AIMS: Recent studies have shown that overexpression of c-jun activation domain binding protein 1 (JAB1) and reduced expression of p27(kip1) are associated with advanced tumor stage and poor prognosis in several human cancers. Here, We investigated the functional role and correlation of JAB1 and p27(kip1) in hepatocellular carcinoma (HCC). METHODOLOGY: Immunohistochemical study for JAB1, p27(kip1) was performed on 76 cases of HCC and adjacent nontumorous tissues. 6 Fresh specimens of HCC and the adjacent liver tissue were collected for Western blot analysis. The influence of As2O3 on HCC SMMC-7721 cells, was detected by flow cytometry and Hochest staining. The expression and subcellular localization of p27(kip1) and JAB1 were investigated by Western blot and immunofluorescence. RESULTS: The expression of JAB1 was higher but p27(kip1) was lower in HCC than that in adjacent liver tissue. As2O3 treatment inhibited the growth of SMMC-7721 cells. In As2O3-treated cells, p27(kip1) expression was increased while JAB1 was decreased. The location of p27(kip1) and JAB1 were transferred from cytoplasm to nucleus. CONCLUSIONS: In HCC, JAB1 was inversely correlated with p27(kip1). As2O3 attenuated the expression of JAB1, disturbed the location and expression of p27(kip1), which may participate in regulating the growth of human hepatoma cells.

[Effects of adenoviral-mediated melanoma differentiation associated gene-7/IL-24 on growth and apoptosis of breast cancer cells].

OBJECTIVE: To investigate the effects of adenovirus melanoma differentiation associated gene-7 (mda-7)/IL-24 on the growth and apoptosis of human breast cancer cells. METHODS: Human breast cancer cells of the lines MCF-7 and MD-MBA-453 were cultured and transfected with purified adenovirus mda-7/IL-24. 48 h later, Western blotting was used to detect the protein expression of mda-7/IL-24 in the MCF-7 cells. The growth of Ad-mda-7/IL-24 in the MCF-7 cells was assayed by crystal violet staining and MTT method. The apoptotic effect of Ad-mda-7/IL-24 in the MCF-7 and MDA-MB-453 cells was detected by Hoechst staining and annexin V method. Nude mice were inoculated with MCF-7 cells and randomly divided into 2 groups to be injected with Ad-mda-7/IL-24 of PBS. The size of tumor was observed. RESULTS: Western blotting showed that mda-7/IL-24 was expressed in the transfected MCF-7 cells. Crystal violet staining and MTT method showed that Ad-mda-7/IL-24 dose and time-dependently inhibited the growth of the MCF-7 and MDA-MB-453 cells. Hochst staining and annexin V test indicated obvious apoptosis of the breast cancer cells. The size of tumor of the nude mice injected with Ad-mda-7/IL-24 was significantly smaller than that of the control mice. CONCLUSION: Ad-mda-7/IL-24 effectively inhibits the growth of breast cancer cells and induces its apoptosis.

[Expression and significance of c-jun-activation-domain binding protein (JAB1) in hepatocellular carcinoma].

OBJECTIVE: to investigate the expression of c-jun-activation-domain binding protein (JAB1) in hepatocellular carcinoma (HCC) and the clinicopathologic significance thereof. METHODS: Immunohistochemistry was used on 76 specimens of HCC tissues and native liver tissues adjacent to the HCC tissues, and 10 specimens of normal liver tissues near the liver angioma to detect the expression of JAB1 and the cell proliferative factor Ki67. RESULTS: The expression rate of JAB1 in the HHC tissues was 68.85%, significantly higher than that in the adjacent liver tissues and normal liver tissues near liver angioma (38.72% and 34.36% respectively, both P < 0.001). The expression of JAB1 was correlated with the histological differentiation, serum alpha-fetoprotein level, and metastasis (P = 0.000, 0.015, and 0.000), but not with gender, age, tumor size, serum HBsAg, and existence of necrosis and cirrhosis. The expression rate of Ki67 protein in the HCC tissues was 41.45%, significantly higher than that in the adjacent liver tissues and normal liver tissues near liver angioma (2.11% and 2.01% respectively, both P < 0.001). There was a positive correlation between JAB1 and Ki67 (P < 0.001). CONCLUSION: JAB1 is highly expressed in HCC and may play an important role in the oncogenesis and development of HCC. JAB1 may be used as a marker for neoplastic change in liver cells and thus has potential clinicopathologic value.

Suppression of Kpnß1 expression inhibits human breast cancer cell proliferation by abrogating nuclear transport of Her2.

Breast cancer (BC) is one of the most fatal diseases and poses critical health problems worldwide. However, its mechanisms remain unclear. Consequently, there is an urgency to investigate the mechanisms involved in BC initiation and progression and identify novel therapeutics for its prevention and treatment. In this study, we identified karyopherin ß-1 (Kpnß1) as a possible novel therapeutic target for BC. Western blotting was used to evaluate the expression of Kpnß1 in four pairs of tumorous and adjacent non-tumorous tissues. The results revealed that the protein level of Kpnß1 was higher in the cancer samples compared with those in the corresponding normal samples. Immunohistochemistry was performed on 140 BC cases and indicated that Kpnß1 was significantly associated with clinical pathological variables. Kaplan-Meier curve revealed that high expression of Kpnß1 was related to poor BC patient prognosis. A starvation and re-feeding assay was used to imitate the cell cycle using the SKBR-3 cell line, indicating that Kpnß1 plays a critical role in cell proliferation. The Cell Counting Kit-8 assay revealed that SKBR-3 cells treated with Kpnß1-siRNA (siKpnß1) grew more slowly than the control cells, while flow cytometry revealed that low-Kpnß1 expressing SKBR-3 cells exhibited increased BC cell apoptosis. Furthermore, the interaction between Kpnß1 and Her2 was clearly observed by immunoprecipitation, indicating that Kpnß1-knockdown abrogated nuclear transport of Her2. In summary, our findings revealed that Kpnß1 is involved in the progression of BC and may be a useful therapeutic target.

Knockdown of Ran GTPase expression inhibits the proliferation and migration of breast cancer cells.

Breast cancer is the second leading cause of cancer­associated mortality in women worldwide. Strong evidence has suggested that Ran, which is a small GTP binding protein involved in the transport of RNA and protein across the nucleus, may be a key cellular protein involved in the metastatic progression of cancer. The present study investigated Ran gene expression in breast cancer tissue samples obtained from 140 patients who had undergone surgical resection for breast cancer. Western blot analysis of Ran in breast cancer tissues and paired adjacent normal tissues showed that expression of Ran was significantly increased in breast cancer tissues. Immunohistochemistry analyses conducted on formalin­fixed paraffin­embedded breast cancer tissue sections revealed that Ran expression was associated with tumor histological grade, nerve invasion and metastasis, vascular metastasis and Ki­67 expression (a marker of cell proliferation). Kaplan­Meier survival analysis showed that increased Ran expression in patients with breast cancer was positively associated with a poor survival prognosis. Furthermore, in vitro experiments demonstrated that highly migratory MDA­MB­231 cancer cells treated with Ran­si­RNA (si­Ran), which knocked down expression of Ran, exhibited decreased motility in trans­well migration and wound healing assays. Cell cycle analysis of Ran knocked down MDA­MB­231 cells implicated Ran in cell cycle arrest and the inhibition of proliferation. Furthermore, a starvation and re­feeding (CCK­8) assay was performed, which indicated that Ran regulated breast cancer cell proliferation. Taken together, the results provide strong in vitro evidence of the involvement of Ran in the progression of breast cancer and suggest that it could have high potential as a therapeutic target and/or marker of disease.

Dyrk1B overexpression is associated with breast cancer growth and a poor prognosis.

Dyrk1B, also called minibrain-related kinase (Mirk), is a member of the dual-specificity tyrosine phosphorylation-regulated kinase (Dyrk)/minibrain family of dual-specificity protein kinases. It is a serine/threonine kinase involved in the regulation of tumor progression and cell proliferation. In this study, the role of Dyrk1B in breast cancer development was investigated. The expression of Dyrk1B was detected by Western blot and immunohistochemistry staining, both of which demonstrated that Dyrk1B was overexpressed in breast cancer tissues and cells. Statistical analysis showed that the extent of Dyrk1B expression was associated with multiple clinicopathologic factors, including tumor size, grade, estrogen receptor status, and Ki-67 expression, and that high expression predicted a poor prognosis. The growth of breast cancer cells was inhibited significantly after knockout of DYRK1B by small interfering RNA (siRNA). Moreover, FoxO1 could be phosphorylated by Dyrk1B, and then FoxO1 was shuttled from the cell nucleus into the cytoplasm, which might be the mechanism of Dyrk1B-mediated survival in breast cancer cells. The results suggest that Dyrk1B plays a key role in the progression of breast cancer and provides a new target for breast cancer therapy.