Inflammatory Factor Levels and Clinical Characteristics of Mental Disorders in Patients with Sheehan Syndrome.

Background: Sheehan's syndrome often occurs in women aged 20 to 40 years. Bleeding is the main cause of the disease. This syndrome is rarely reported in the literature either in China or abroad, and it is rare in psychiatric clinic. Objective: To investigate the inflammatory factors levels and clinical characteristics of mental disorders in patients with Sheehan's syndrome in order to improve rational clinical diagnosis and treatment and reduce the occurrence of mental disorders. Design: This was a retrospective study. Setting: This study was performed in the Department of Endocrinology of Xingtai People' s Hospital in China. Participants: A total of 100 patients with Sheehan's syndrome admitted to Xingtai People's Hospital, China, from 2016 to 2021 were included in the study. According to the occurrence of mental disorders during treatment, they were divided into the psychological disorder group (PS group), psychological disorder during treatment group (TPS group) and non-psychological disorder group (NPS group). Methods: The clinical data of the 3 groups were retrospectively analyzed to explore the levels of inflammatory factors and clinical characteristics of mental disorders in patients with Sheehan's syndrome. Results: In the PS group, compared with the other 2 groups, onset to diagnosis time was longer (P < .05). There was a statistical difference in systolic blood pressure (SBP) among the 3 groups. The SBP in the PS group was the lowest, and that in the TPS group was higher than in the PS group and lower than in the NPS group (P < .05). Compared with TPS group, in the PS group the diastolic blood pressure (DBP), blood sodium, blood glucose, free triiodothyronine (FT3), free thyroxine (FT4), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were not significantly different, but were lower than in the NPS group (P < .05). There was no significant difference in age, disease course, body mass index (BMI), thyroid-stimulating hormone (TSH), cortisol, adrenocorticotropic hormone (ACTH), growth hormone (GH), Prolactin (PRL), follicle-stimulating hormone( FSH), luteinizing hormone (LH ) and estradiol (E2) in the 3 groups. In the treatment process, the amount of hydrocortisone administered on the first, second day, and third day and the first 3 days in the TPS group were significantly higher than in the NPS group, and the increased rate of serum sodium on the first day in the TPS group was significantly higher than in the NPS (P < .05). Conclusion: Mental health illnesss are more likely to occur in patients with Sheehan's syndrome who are not diagnosed in time for various reasons, in patients with obvious anterior pituitary dysfunction, and in patients with high levels of inflammatory factors, large doses of glucocorticoid at the early stage of the disease and rapid increase of serum sodium at the first day of treatment.

A Comprehensive Overview of the Antibiotics Approved in the Last Two Decades: Retrospects and Prospects.

Due to the overuse of antibiotics, bacterial resistance has markedly increased to become a global problem and a major threat to human health. Fortunately, in recent years, various new antibiotics have been developed through both improvements to traditional antibiotics and the discovery of antibiotics with novel mechanisms with the aim of addressing the decrease in the efficacy of traditional antibiotics. This manuscript reviews the antibiotics that have been approved for marketing in the last 20 years with an emphasis on the antibacterial properties, mechanisms, structure-activity relationships (SARs), and clinical safety of these antibiotics. Furthermore, the current deficiencies, opportunities for improvement, and prospects of antibiotics are thoroughly discussed to provide new insights for the design and development of safer and more potent antibiotics.

A multicenter study to develop a non-invasive radiomic model to identify urinary infection stone in vivo using machine-learning.

Urolithiasis is a common urological disease, and treatment strategy options vary between different stone types. However, accurate detection of stone composition can only be performed in vitro. The management of infection stones is particularly challenging with yet no effective approach to pre-operatively identify infection stones from non-infection stones. Therefore, we aimed to develop a radiomic model for preoperatively identifying infection stones with multicenter validation. In total, 1198 eligible patients with urolithiasis from three centers were divided into a training set, an internal validation set, and two external validation sets. Stone composition was determined by Fourier transform infrared spectroscopy. A total of 1316 radiomic features were extracted from the pre-treatment Computer Tomography images of each patient. Using the least absolute shrinkage and selection operator algorithm, we identified a radiomic signature that achieved favorable discrimination in the training set, which was confirmed in the validation sets. Moreover, we then developed a radiomic model incorporating the radiomic signature, urease-producing bacteria in urine, and urine pH based on multivariate logistic regression analysis. The nomogram showed favorable calibration and discrimination in the training and three validation sets (area under the curve [95% confidence interval], 0.898 [0.840-0.956], 0.832 [0.742-0.923], 0.825 [0.783-0.866], and 0.812 [0.710-0.914], respectively). Decision curve analysis demonstrated the clinical utility of the radiomic model. Thus, our proposed radiomic model can serve as a non-invasive tool to identify urinary infection stones in vivo, which may optimize disease management in urolithiasis and improve patient prognosis.

Long non-coding RNA SNHG8 promotes prostate cancer progression through repressing miR-384 and up-regulating HOXB7.

BACKGROUND: Multiple long non-coding RNAs (lncRNAs) have been demonstrated to function as vital regulators in the progression of prostate cancer (PCa). In the present study, we aimed to probe the function of lncRNA small nucleolar RNA host gene 8 (SNHG8) in PCa progression. METHODS: A quantitative real-time polymerase chain reaction and western blotting were utilized to measure SNHG8, microRNA-384 (miR-384) and homeobox B7 (HOXB7) expression. Call-couting kit-8 and bromodeoxyuridine experiments were employed to evaluate PCa cell proliferation. Transwell experiments were performed to detect PCa cell migration and invasion. Dual-luciferase reporter experiments and RNA immunoprecipitation experiments were conducted to determine the targeting relationships among miR-384, SNHG8 and HOXB7. RESULTS: SNHG8 was up-regulated in PCa tissues and cells. Silencing of SNHG8 suppressed the proliferation, migration and invasion of PCa cells. SNHG8 functioned as a molecular sponge to repress miR-384. The effects of SNHG8 knockdown on PCa cell proliferation, migration and invasion were counteracted by miR-384 inhibition. HOXB7 was confirmed to be a target gene of miR-384. SNHG8 knockdown repressed HOXB7 expression via targeting miR-384. CONCLUSIONS: SNHG8 promotes PCa cell proliferation, migration and invasion via decoying miR-384 and up-regulating HOXB7.

A novel long non-coding RNA PCLN16 facilitates androgen receptor signaling in prostate cancer.

The prostate cancer (PCa) poses serious threat to men's health. The androgen receptor (AR) is essential for normal prostate development and prostate cancer progression. We identified a novel lncRNA PCLN16 which is significantly correlated with AR signaling during prostate cancer progression. The AR-regulated PCLN16 was abundantly overexpressed in localized or metastatic prostate cancer tissues and AR-dependent cell lines. PCLN16 silence suppressed AR signaling and tumor growth. PCLN16 interacted with Huntingtin interacting protein 1 (HIP1) transcript to reduce HIP1 degradation. Therefore, PCLN16 could augment AR signaling via a novel positive feedback loop. Our experiments support an oncogenic role for PCLN16 and suggest that PCLN16 might serve as a potential target for therapeutic intervention.

Hijacking monopolar spindle 1 (MPS1) for various cancer types by small molecular inhibitors: Deep insights from a decade of research and patents.

Monopolar spindle 1 (MPS1) has garnered significant attention due to its pivotal role in regulating the cell cycle. Anomalous expression and hyperactivation of MPS1 have been associated with the onset and advancement of diverse cancers, positioning it as a promising target for therapeutic interventions. This review focuses on MPS1 small molecule inhibitors from the past decade, exploring design strategies, structure-activity relationships (SAR), safety considerations, and clinical performance. Notably, we propose prospects for MPS1 degraders based on proteolysis targeting chimeras (PROTACs), as well as reversible covalent bonding as innovative MPS1 inhibitor design strategies. The objective is to provide valuable information for future development and novel perspectives on potential MPS1 inhibitors.

Stochastic modeling of SIS epidemics with logarithmic Ornstein-Uhlenbeck process and generalized nonlinear incidence.

In this paper, we investigate a stochastic SIS epidemic model with logarithmic Ornstein-Uhlenbeck process and generalized nonlinear incidence. Our study focuses on the construction of stochastic Lyapunov functions to establish the threshold condition for the extinction and the existence of the stationary distribution of the stochastic system. We also derive the exact expression of the density function around the quasi-endemic equilibrium, which provides valuable insight into the transmission and progression of the disease within a population. Our findings demonstrate the importance of considering the impact of stochasticity on the spread of epidemics, particularly in the presence of complex incidence mechanisms and stochastic environmental factors. Additionally, the stochastic threshold reveals that ordinary differential equation models and white noise models underestimate the severity of disease outbreaks, while our proposed the stochastic epidemic model with logarithmic Ornstein-Uhlenbeck process accurately captures real-world scenarios.

From Structure Modification to Drug Launch: A Systematic Review of the Ongoing Development of Cyclin-Dependent Kinase Inhibitors for Multiple Cancer Therapy.

Herein, we discuss more than 50 cyclin-dependent kinase (CDK) inhibitors that have been approved or have undergone clinical trials and their therapeutic application in multiple cancers. This review discusses the design strategies, structure-activity relationships, and efficacy performances of these selective or nonselective CDK inhibitors. The theoretical basis of early broad-spectrum CDK inhibitors is similar to the scope of chemotherapy, but because their toxicity is greater than the benefit, there is no clinical therapeutic window. The notion that selective CDK inhibitors have a safer therapeutic potential than pan-CDK inhibitors has been widely recognized during the research process. Four CDK4/6 inhibitors have been approved for the treatment of breast cancer or for prophylactic administration during chemotherapy to protect bone marrow and immune system function. Furthermore, the emerging strategies in the field of CDK inhibitors are summarized briefly, and CDKs continue to be widely pursued as emerging anticancer drug targets for drug discovery.

Insights into stimuli-responsive diselenide bonds utilized in drug delivery systems for cancer therapy.

Due to the complexity and particularity of cancer cell microenvironments, redox responsive drug delivery systems (DDSs) for cancer therapy have been extensively explored. Compared with widely reported cancer treatment systems based on disulfide bonds, diselenide bonds have better redox properties and greater anticancer efficiency. In this review, the significance and application of diselenide bonds in DDSs are summarized, and the stimulation sensitivity of diselenide bonds is comprehensively reported. The potential and prospects for the application of diselenide bonds in next-generation anticancer drug treatment systems are extensively discussed.

Analysis of the correlation between plasma coagulation factor VII, PAI-1, and uric acid with insulin resistance and macrovascular complications in elderly patients with type 2 diabetes.

BACKGROUND: To analyze the correlations between plasma coagulation factor VII (FVII), plasma plasminogen activator inhibitor-1 (PAI-1), uric acid, and insulin resistance (IR) and diabetic macroangiopathy (DMAP) in elderly patients with type 2 diabetes mellitus (T2DM). METHODS: The clinical data of 112 elderly T2DM patients admitted to our hospital between March 2017 and March 2020 were enrolled. Subgroups were allocated based on the inclusion and exclusion criteria, body mass index (BMI), homeostasis model assessment (HOMA)-IR and the presence of DMAP. The patients were allocated as the study objects (T2DM group, n=90), simple obesity (BMI ≥25 kg/m2, n=25), simple non-obese (BMI <25 kg/m2, n=22), obesity with DMAP (n=24), and non-obese with DMAP (n=19). Meanwhile, data from 50 healthy controls from physical examinations were employed. The levels of FVII, PAI-1, HOMA-IR and uric acid were determined. Pearson correlation analysis was used to measure the correlations, and the receiver operating characteristic (ROC) curve was used to determine the predictive value of detection indexes. RESULTS: The levels of FVII, PAI-1, and uric acid in the T2DM group were higher than those of the control group (P<0.05). In terms of the levels of FVII, PAI-1, and uric acid: simple non-obese group < simple obese group < non-obese with DMAP group < obese with DMAP group (P<0.05). The levels of FVII, PAI-1, and uric acid in T2DM patients were positively correlated with BMI and Homeostasis model assessment (HOMA)-IR (P<0.05). The ROC curve results showed that the area under the curve (AUC) for FVII, PAI-1, and uric acid separately, as well as a combination of the three were 0.930, 0.831, 0.888, and 0.997, respectively. CONCLUSIONS: FVII, PAI-1, and uric acid levels are elevated in elderly T2DM patients. The levels of FVII, PAI-1, and uric acid are closely related to IR in elderly T2DM patients. The combination of TFVII, PAI-1, and uric acid levels can be used as an effective measure to predict patients with DMAP. Furthermore, the levels of these markers should be promptly measured in a clinical setting for early intervention and improvement of the patient's outcomes.

BZW1 promotes cell proliferation in prostate cancer by regulating TGF-ß1/Smad pathway.

Recently, basic leucine zipper and the W2 domain-containing protein 1 (BZW1) are reported to be implicated in tumor progression. However, the role of BZW1 in prostate cancer remains unknown. This study is aimed to investigate the expression of BZW1 and its influence on cell proliferation in prostate cancer. Then, the expression levels of BZW1 were measured in 136 cases of prostate cancer and matched adjacent non-cancerous prostate tissues by quantificational real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). The effect of BZW1 on cell proliferation was further explored. QRT-PCR analysis showed that the mRNA levels of BZW1 in prostate cancer were significantly greater compared with those in matched adjacent non-cancerous prostate tissues (P< 0.001). IHC results showed that the high-expression rates of BZW1 in prostate cancer and matched adjacent non-cancerous prostate tissues were 68.4% and 32.4%, and the difference was statistically significant (P< 0.001). BZW1 high expression significantly correlated with T stage, lymph node metastasis, prostate-specific antigen (PSA) and Gleason score (P< 0.05). Patients with BZW1 high expression presented unfavorable prognosis compared with those with BZW1 low expression (P= 0.002). In addition, CCK-8 and colony formation assays revealed that BZW1 overexpression significantly promoted cell proliferation in vitro. Tumor xenograft has shown that BZW1 knockdown significantly inhibited tumor growth in vivo. Moreover, BZW1 overexpression activated the TGF-ß1/Smad1/Smad3 pathway. Therefore, these data indicate that BZW1 overexpression predicts poorer prognosis and promotes cell proliferation in prostate cancer by regulating TGF-ß1/Smad pathway.

Current Landscape and Future Perspective of Oxazolidinone Scaffolds Containing Antibacterial Drugs.

The widespread use of antibiotics has made the problem of bacterial resistance increasingly serious, and the study of new drug-resistant bacteria has become the main direction of antibacterial drug research. Among antibiotics, the fully synthetic oxazolidinone antibacterial drugs linezolid and tedizolid have been successfully marketed and have achieved good clinical treatment effects. Oxazolidinone antibacterial drugs have good pharmacokinetic and pharmacodynamic characteristics and unique antibacterial mechanisms, and resistant bacteria are sensitive to them. This Perspective focuses on reviewing oxazolidinones based on the structural modification of linezolid and new potential oxazolidinone drugs in the past 10 years, mainly describing their structure, antibacterial activity, safety, druggability, and so on, and discusses their structure-activity relationships, providing insight into the reasonable design of safer and more potent oxazolidinone antibacterial drugs.

Foresight regarding drug candidates acting on the succinate-GPR91 signalling pathway for non-alcoholic steatohepatitis (NASH) treatment.

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, and it is a liver manifestation of metabolic syndrome, with a histological spectrum from simple steatosis to non-alcoholic steatohepatitis (NASH). NASH can evolve into progressive liver fibrosis and eventually lead to liver cirrhosis. The pathological mechanism of NASH is multifactorial, involving a series of metabolic disorders and changes that trigger low-level inflammation in the liver and other organs. In the pathogenesis of NASH, the signal transduction pathway involving succinate and the succinate receptor (G-protein-coupled receptor 91, GPR91) regulates inflammatory cell activation and liver fibrosis. This review describes the mechanism of the succinate-GPR91 signalling pathway in NASH and summarizes the drugs that act on this pathway, with the aim of providing a new approach to NASH treatment.

Esculin and ferric citrate-incorporated sturgeon skin gelatine as an antioxidant film for food packaging to prevent Enterococcus faecalis contamination.

Herein, a sturgeon skin gelatine film combined with esculin and ferric citrate was developed as an edible food packaging material to prevent Enterococcus faecalis (E. faecalis) contamination. E. faecalis is able to hydrolyse esculin in the film, and then the hydrolysed product, esculetin, combines with ferric citrate to form a brown-black phenol iron complex. This phenomenon can be observed easily after 48 h of contamination under visible light, and it can be determined under 365 nm ultraviolet light with high sensitivity. With the addition of esculin and ferric citrate, the film showed better mechanical properties and water vapour permeability than those of the unmodified gelatine. When an increased amount of esculin was added, an increase in thermal stability, antioxidant activity, and antioxidant stability of the film was observed. These physicochemical characteristics are beneficial for developing a packaging material for food storage that mitigates foodborne illness caused by E. faecalis.

A promising antiviral candidate drug for the COVID-19 pandemic: A mini-review of remdesivir.

Remdesivir (GS-5734), a viral RNA-dependent RNA polymerase (RdRP) inhibitor that can be used to treat a variety of RNA virus infections, is expected to be an effective treatment for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. On May 1, 2020, The U.S. Food and Drug Administration (FDA) has granted Emergency Use Authorization (EUA) for remdesivir to treat COVID-19 patients. In light of the COVID-19 pandemic, this review presents comprehensive information on remdesivir, including information regarding the milestones, intellectual properties, anti-coronavirus mechanisms, preclinical research and clinical trials, and in particular, the chemical synthesis, pharmacology, toxicology, pharmacodynamics and pharmacokinetics of remdesivir. Furthermore, perspectives regarding the use of remdesivir for the treatment of COVID-19 are also discussed.

High expression of SMYD3 indicates poor survival outcome and promotes tumour progression through an IGF-1R/AKT/E2F-1 positive feedback loop in bladder cancer.

The AKT/mTOR pathway is critical for bladder cancer (BC) pathogenesis and is hyper-activated during BC progression. In the present study, we identified a novel positive feedback loop involving oncogenic factors histone methyltransferase SMYD3, insulin-like growth factor-1 receptor (IGF-1R), AKT, and E2F-1. SMYD3 expression was significantly up-regulated in BC tumors and positively associated with histological grade, lymph node metastasis, and shorter patient survival. Depletion of SMYD3 inhibited BC cell proliferation, colony formation, migration, invasion, and xenograft tumor growth. Mechanistically, SMYD3 inhibition led to the diminished AKT/mTOR signaling activity, thereby triggering deleterious effects on BC cells. Furthermore, SMYD3 directly activates the expression of IGF-1R, a critical activator of AKT in BC, by inducing hyper-methylation of histone H3-K4 and subsequent chromatin remodeling in the IGF-1R promoter region. On the other hand, E2F-1, a downstream factor of the AKT pathway, binds to the E2F-1 binding motifs at the SMYD3 promoter and consequently induces SMYD3 transcription and expression. Thus, SMYD3/IGF-1R/AKT/E2F-1 forms a positive feedback loop leading to the hyper-activated AKT signaling. Our findings provide not only profound insights into SMYD3-mediated oncogenic activity but also present a unique avenue for treating BC by directly disrupting this signaling circuit.

VHL-HIF-2α axis-induced SMYD3 upregulation drives renal cell carcinoma progression via direct trans-activation of EGFR.

It has been well established that the von Hippel-Lindau/hypoxia-inducible factor α (VHL-HIFα) axis and epidermal growth factor receptor (EGFR) signaling pathway play a critical role in the pathogenesis and progression of renal cell carcinoma (RCC). However, few studies have addressed the relationship between the two oncogenic drivers in RCC. SET and MYND domain-containing protein 3 (SMYD3) is a histone methyltransferase involved in gene transcription and oncogenesis, but its expression and function in RCC remain unclear. In the present study, we found that SMYD3 expression was significantly elevated in RCC tumors and correlated with advanced tumor stage, histological and nuclear grade, and shorter survival. Depletion of SMYD3 inhibited RCC cell proliferation, colony numbers, and xenograft tumor formation, while promoted apoptosis. Mechanistically, SMYD3 cooperates with SP1 to transcriptionally promote EGFR expression, amplifying its downstream signaling activity. TCGA data analyses revealed a significantly increased SMYD3 expression in primary RCC tumors carrying the loss-of-function VHL mutations. We further showed that HIF-2α can directly bind to the SMYD3 promoter and subsequently induced SMYD3 transcription and expression. Taken together, we identify the VHL/HIF-2α/SMYD3 signaling cascade-mediated EGFR hyperactivity through which SMYD3 promotes RCC progression. Our study suggests that SMYD3 is a potential therapeutic target and prognostic factor in RCC.

Long non-coding RNA mortal obligate RNA transcript suppresses tumor cell proliferation in prostate carcinoma by inhibiting glucose uptake.

A previous study reported the decreased expression of long non-coding RNA mortal obligate RNA transcript (lncRNA MORT) in 16 types of cancer, while the functionality of lncRNA MORT in cancer biology remains unknown. Therefore, the present study was conducted to characterize the functionality of lncRNA MORT in prostate carcinoma, a common cancer type worldwide. lncRNA MORT expression level was downregulated in tumor tissues compared with that in the adjacent healthy tissues of patients with prostate carcinoma. Expression of lncRNA MORT in tumor tissues was influenced by tumor size, but not by tumor metastasis. Overexpression of lncRNA MORT inhibited glucose uptake and glucose transporter 1 (GLUT-1) expression in prostate carcinoma cell lines; GLUT-1 overexpression upregulated glucose uptake and attenuated the effects of lncRNA MORT overexpression on glucose uptake, but did not significantly affect the expression of lncRNA MORT. Overexpression of lncRNA MORT inhibited, while GLUT-1 overexpression promoted the proliferation of prostate carcinoma cells. In addition, GLUT-1 overexpression attenuated the effects of lncRNA MORT on cell proliferation. Therefore, lncRNA MORT may inhibit cancer cell proliferation in prostate carcinoma by preventing glucose uptake.

A meta-analysis of the relationship between vitamin D receptor gene ApaI polymorphisms and polycystic ovary syndrome.

BACKGROUND: Emerging evidence from pre-clinical and clinical studies has shown that vitamin D (VD) plays an important role in the pathogenesis of polycystic ovary syndrome (PCOS). Potentially functional ApaI polymorphism of vitamin D receptor (VDR) gene has been implicated in PCOS risk, but individually published studies have yielded inconclusive results. OBJECTIVES: Studies on the associations of VDR gene polymorphisms with PCOS susceptibility reported conflicting results. The objective of this study was to perform a systematic meta-analysis to clarify this issue. MATERIAL AND METHODS: We searched for all publications regarding the associations mentioned above in PubMed, Web of Science, Embase, and China National Knowledge Infrastructure (CNKI) databases updated up to April 2017. A meta-analysis of the overall odds ratios (ORs) with 95% confidence interval (CI) was calculated with the fixed or random effect model. RESULTS: A total of 7 studies fulfilling the inclusion criteria were included in this meta-analysis (1,350 cases and 960 controls). Pooled ORs showed a significant association between ApaI polymorphism and PCOS risk in all 4 genetic models. Subgroup analysis by ethnicity showed that ApaI polymorphism was associated with the risk of PCOS in Asians (aa vs AA: OR = 1.54, 95% CI = 1.04-2.28, p = 0.03). However, ApaI polymorphism (a vs A: OR = 1.34, 95% CI = 1.00-1.79, p = 0.02; aa+Aa vs AA: OR = 1.36, 95% CI = 1.04-1.79, p = 0.03) was associated with the risk of PCOS in Caucasians. CONCLUSIONS: Our meta-analysis demonstrated that PCOS risk was significantly associated with VDR gene ApaI polymorphism. However, due to the relatively small sample size in this meta-analysis, further studies with a larger sample size should be conducted to confirm the findings.

The deregulation of miR-133b is associated with poor prognosis in bladder cancer.

BACKGROUND: MicroRNAs (miRNAs) are single-stranded, endogenous, non-coding RNAs that are increased or decreased in almost all cancer types, and they paly crucial roles in the tumorigenesis as well as development. MATERIALS AND METHODS: 90 patients diagnosed with bladder cancer were enrolled in the present study. The bladder cancer tissues or adjacent normal tissues were obtained from the tumor area or adjacent normal zone. The expression level of miR-133b was examined by quantitative real-time polymerase chain reaction assay (qRT-PCR). Survival curves were displayed by the Kaplan-Meier method, and differences between two survival curves were calculated by the log-rank test. RESULTS: The expression levels of miR-133b in bladder tissues were significantly decreased when compared with the matched adjacent normal bladder tissues (P < 0.05). Moreover, miR-133b expression levels are significantly associated with lymphatic invasion (P = 0.026), distant metastasis (P = 0.025), tumor grade (P = 0.038), as well as the muscle invasion status (P < 0.001). The log-rank test indicated that patients with decreased miR-133b expression underwent poorer overall survival (P = 0.007). Furthermore, multivariate Cox regression analysis showed that the expression level of miR-133b (P = 0.024) was an independent factor for predicting the overall survival in patients with bladder cancer. CONCLUSIONS: The present study showed that miR-133b might be associated with bladder cancer progression, and its down-regulation might be a biomarker for poor prognosis of bladder cancer.