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.

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.

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.

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.

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.

LAMP1 expression is associated with poor prognosis in breast cancer.

Lysosome associated membrane protein-1 (LAMP1) is a heavily glycosylated lysosomal membrane protein, which is able to protect the lysosomal membrane from intracellular proteolysis. LAMP1 has been implicated in cancer development and progression. However, LAMP1 expression in breast cancer (BC) and its relationship with the clinical parameters of BC has not yet been fully investigated. In the present study, LAMP1 expression in BC was characterized by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) on 20 pairs of fresh-frozen BC and corresponding non-cancerous tissues. In addition, tissue microarray immunohistochemistry (TMA-IHC) was conducted on 143 BC and matched non-cancerous tissue samples. The results of RT-qPCR and TMA-IHC demonstrated that LAMP1 expression in BC tissues was significantly higher than in corresponding non-cancerous tissues. Furthermore, LAMP1 protein expression levels were significantly associated with histological grade (P=0.047), estrogen receptor expression (P=0.003), progesterone receptor expression (P=0.002), molecular classification (P=0.022), lymph node metastasis (P=0.033) and tumor-node-metastasis (TNM) stage (P=0.012). Multivariate analysis using Cox regression models and Kaplan-Meier survival curves demonstrated that LAMP1 expression (P=0.037), molecular classification (P=0.017) and TNM stage (P=0.003) were independent prognostic factors for overall survival. The above data suggested that LAMP1 expression is associated with malignant attributes of BC and may serve as a novel prognostic factor for patients with BC.

Overexpression of SYF2 promotes cell proliferation and correlates with poor prognosis in human breast cancer.

SYF2, a known cell cycle regulator, is reported to be involved in cell cycle arrest by interacting with cyclin-D-type binding protein 1. In the present study, we investigated the role of SYF2 in human breast cancer (BC) progression. SYF2 was highly upregulated in BC tissues and cell lines, as per Western blot and immunohistochemistry analysis. The SYF2 expression level had a significant correlation with the tumor grade and Ki-67 expression. In vitro starvation-refeeding experiment and SYF2-siRNA transfection assay demonstrated that SYF2 could promote proliferation of BC cells, while SYF2 knockdown resulted in cells cycle arrest at G1/S phase, reducing the cell growth rate of BC cells. These results indicated that SYF2 promotes human BC progression by accelerating the BC cells' proliferation. SYF2 could be a novel therapeutic target in human BC therapies.

High Eg5 expression predicts poor prognosis in breast cancer.

Eg5 is a motor protein belonging to the kinesin-5 family and has been suggested to exert important function in tumors. In this study, we determined the mRNA and protein expression levels of Eg5 in cancerous and non-cancerous breast tissue by quantitative real-time polymerase chain reaction (qRT-PCR) and tissue microarray immunohistochemistry analysis (TMA-IHC) respectively. The results of 20 fresh-frozen BC samples demonstrated that Eg5 mRNA levels were significantly higher in BC tissues compared with corresponding non-cancerous tissue (p = 0.0009). TMA-IHC analysis in 127 BC tissues revealed that Eg5 expression obviously correlated with clinicopathologial parameters, including tumor grade (p = 0.004), ER status (p = 0.030), Ki67 status (p = 0.005), molecular classification (p = 0.026), N stage (p = 0.015), and TNM stage (p = 0.001). Kaplan-Meier survival curve indicated that high Eg5 expression (p = 0.012), Ki67 status (p = 0.014) and TNM stage (p = 0.026) were independent factors to predict poor prognosis for patients with breast cancer. Our data suggest that Eg5 is not only overexpressed in BC, it may be also served as a potential prognostic marker.

Aldehyde dehydrogenase 1 expression is correlated with poor prognosis in breast cancer.

Breast cancer (BC) is one of the most common cancers worldwide, and is a major cause of death in women. Aldehyde dehydrogenase 1 (ALDH1) is a marker of stem cells and cancer stem cells, and its activity correlates with the outcome of various tumors, including BC. This study aimed to analyze the relationship between ALDH1 expression and clinicopathological characters in BC and the prognostic significance of ALDH1.We used quantitative reverse-transcription PCR (qRT-PCR) to detect ALDHA1 mRNA levels in 25 fresh frozen BC samples and matched noncancerous samples. Immunohistochemistry on tissue microarrays was used to analyze protein expression in 137 paraffin-embedded BC tissues and corresponding noncancerous tissues. STATA 16.0 software was used for statistical analysis.The results suggested that levels of both ALDH1 mRNA and protein in BC were significantly higher than in corresponding adjacent breast samples (3.856 ±â€Š0.3442 vs 1.385 ±â€Š0.1534, P < .001; 52.6% vs 25.5%, P < .001, respectively). ALDH1 protein expression was also significantly associated with histological grade (P  =  .017), tumor size (P  =  .017), and tumor-node-metastasis (TNM) stage (P  =  .038). Multivariate analysis using the Cox regression model demonstrated that ALDH1 expression (P  =  .024), molecular typing (P  =  .046), and TNM classification (P  =  .034) were independent predictive factors for the outcome of BC. Kaplan-Meier analysis and the log-rank test indicated that patients with high ALDH1 expression, triple-negative BC, and advanced TNM stage had a reduced overall survival time.These data suggest that ALDH1 could be used as a prognostic factor for BC and may provide a useful therapeutic target in the treatment of BC.

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.

Downregulated PIRH2 Can Decrease the Proliferation of Breast Cancer Cells.

BACKGROUND AND AIMS: We undertook this study to investigate the influence of PIRH2 (p53-induced RING-H2) protein on the proliferation and cell cycle of breast cancer cell lines. METHODS: PIRH2 expression was detected by Western blot analysis, immunohistochemistry (IHC) and Kaplan-Meier curve analysis. Cell proliferation was assessed by cell counting kit-8 (CCK-8). Cell cycle control was analyzed by flow cytometry. RESULTS: PIRH2 was up-regulated in breast cancer tissues and cell lines and up-regulated PIRH2 was highly associated with tumor size, grade, ER, and Ki-67. Moreover, Kaplan-Meier curve showed that up-regulated PIRH2 was related to the poor overall survival of patients with breast carcinoma. When the expression of PIRH2 was inhibited by siRNA transfection, cell proliferation was reduced. In addition, the number of G0/G1 phase cells was increased, but G2/M cells were not affected significantly. CONCLUSION: Decrease of PIRH2 expression in the breast cancer cell line MDA-MB-231 resulted in reduced tumor cell growth via the inhibition of cell proliferation and the interruption of cell cycle transition.

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.

Upregulated PFTK1 promotes tumor cell proliferation, migration, and invasion in breast cancer.

PFTK1 was a cell division cycle 2-related serine/threonine protein kinase, which was up-regulated in breast cancer tissues and breast cancer lines. And up-regulated PFTK1 was highly associated with grade, axillary lymph node status, and Ki-67. Moreover, Kaplan-Meier curve showed that up-regulated PFTK1 was related to the poor breast carcinoma patients' overall survival. Here, we first discovered and confirmed that cyclin B was a new interacting protein of PFTK1, and the complex might increase the amount of DVL2, which triggers Wnt/ß-catenin signaling pathway. Furthermore, knockdown of PFTK1 attenuated cell proliferation, anchorage-independent cell growth, and cell migration and invasion by inhibiting the transcriptional activation of ß-catenin for cyclin D1, MMP9, and HEF1, whereas exogenous expression of PFTK1 might promote MDA-MB-231 cells proliferation, migration, and invasion via promoting PFTK1-DVL2-ß-catenin axis. Our findings supported the notion that up-regulated PFTK1 might promote breast cancer progression and metastasis by activating Wnt signaling pathway through the PFTK1-DVL2-ß-catenin axis.

Expression of HAX1 and Ki-67 in breast cancer and its correlations with patient's clinicopathological characteristics and prognosis.

OBJECTIVE: This study aimed to investigate the HS-1-associated protein X-1 (HAX1) and Ki-67 expression in the breast cancer and its clinical significance. METHODS: Breast cancer tissues and tumor-adjacent tissues were collected from 81 patients, and immunohistochemistry was conducted to detect the HAX1 and Ki-67 expression. The correlations of HAX1 expression with demographics, clinicopathological characteristics and prognosis were evaluated. RESULTS: HAX1 was highly expressed in the breast cancer, and its expression was related to the degree of breast cancer differentiation (P=0.002), lymph nodes metastasis (P=0.008) and progesterone receptor (PR) (P=0.021), but not with the age, tumor size, histological type, estrogen receptor (ER), HER2 and p53. HAX1 expression was positively related to Ki-67 expression in the breast cancer (r(2)=0.394, P=0.019). In addition, a higher HAX-1 expression was related to a lower 10-year survival rate. CONCLUSION: HAX1 is a new protein related to the breast cancer and probably plays an important role in the invasion and metastasis of breast cancer. Thus, HAX1 may be used as a potential target for the therapy of breast cancer.

High expression of RAB27A and TP53 in pancreatic cancer predicts poor survival.

RAB27A is a member of Rab family GTPases involved in cellular vesicle trafficking, and TP53 has recently been implicated in regulating the exosome secretion pathway. Because exosome secretion plays an important role in modulating tumor microenvironment and invasive growth, we hypothesized that RAB27A and TP53 expression might be associated with aggressive behavior in pancreatic ductal adenocarcinoma (PDAC), one of the most deadly human malignancies. We determined protein expression of RAB27A and TP53 in 265 pancreatic tissues (186 carcinomas and 79 normal or benign tissues) by immunohistochemistry analysis on tissue microarray and found their expression was correlated with patients' clinical parameters and overall survival. We found that RAB27A and TP53 protein expression was significantly higher in cancerous tissues compared to normal and benign tissues. High RAB27A protein expression (RAB27A+) was significantly associated with tumor stage and vascular invasion. No correlation between RAB27A and TP53 expression was observed. Patients with high RAB27A expression and high TP53 expression had a poor overall survival. Our data indicate that RAB27A expression is an independent prognostic marker for PDAC, and RAB27A-regulated exosome secretion pathway may represent a novel therapeutic target in pancreatic cancer .

Prognostic value of Rab27B nuclear expression in gastrointestinal stromal tumors.

Rab proteins of the endocytosis and exocytosis pathways both play critical roles in cancer progression, and Rab27B has a significant relationship with several types of human cancer. However, the association between Rab27B expression and clinical features to determine its clinicopathological significance in gastrointestinal tumor (GIST) has not been investigated. To examine the expression of Rab27B in GIST and investigate the association between its expression and patient prognosis, immunohistochemistry analysis with tissue microarray was used to evaluate expression of Rab27B in 162 patients with GIST. The relationship between Rab27B expression and patient prognosis was analyzed. High nuclear staining of Rab27B was detected in 88 of 162 (54.32%) GIST tissues. Positive staining of Rab27B was significantly associated with tumor size (P = 0.006), mitotic index (P = 0.013), Armed Forces Institute of Pathology Miettinen risk classification (P = 0.002), and tumor grade (P = 0.021). Kaplan-Meier survival curves showed that GIST patients with low Rab27B nuclear expression (P = 0.038) and mitotic index <5 per 50 high-power fields (P = 0.029) had a more favorable prognosis. These findings indicate that Rab27B nuclear expression is correlated with several clinicopathological features of GIST patients, and it may serve as an unfavorable prognostic marker.