This study aimed to investigate the involvement of the Wnt signalling pathway in the pathogenesis of non-obstructive azoospermia (NOA) and to identify potential diagnostic and therapeutic targets. We obtained the gene expression profiles of NOA patients from the GEO database, screened for differentially expressed genes (DEGs) and NOA-associated co-expressing gene modules, then intersected the DEGs with related genes in the Wnt signalling pathway and identified key genes. LASSO regression analysis was used to find hub genes, and qRT-PCR and WB methods were used to verify the expression of key genes in NOA patients. The immune infiltration and GSEA were conducted in order to investigate the relationship between hub genes and immune cells infiltration and NOA-associated pathways; furthermore, we built the miRNA-mRNA-TF regulatory network and predicted possible small molecules drug targets of the hub gene. Four candidate genes were related to NOA: CSNK1G2, GNG3, H2AFB1 and PARD6A. The key hub gene was CSNK1G2 based on the results of the LASSO regression analysis, and its expression level was significantly down-regulated in NOA patients. The immune infiltration analysis and GSEA results showed that the expression level of CSNK1G2 had a close relationship with immune cells infiltration and NOA-related pathways. Furthermore, we built a miRNA-mRNA-TF regulatory network and predicted the possible small molecule drugs of CSNK1G2. Our findings suggest that the Wnt signalling pathway, particularly CSNK1G2, plays a crucial role in the pathogenesis of NOA. CSNK1G2 may be a novel target for the diagnosis and treatment of NOA.

Clinical outcomes after transarterial chemoembolization (TACE) for intermediate–to–advanced hepatocellular carcinoma (HCC) are highly variable, and reliable predictive biomarkers are lacking. Although gut microbiota dysbiosis has been implicated in HCC pathogenesis and immunotherapy response, its role in TACE outcomes remains unclear. This study aimed to delineate gut microbiome remodeling across HCC progression and TACE treatment and to evaluate its association with clinical outcomes. Fecal samples were collected from healthy controls (n = 10), newly diagnosed untreated HCC patients (n = 30), post-TACE HCC patients (n = 29), and a longitudinal cohort of TACE-treated patients (n = 56). Gut microbiota profiles were analyzed using 16S rDNA sequencing. Differential taxa, microbial diversity, functional pathways, and survival associations were assessed using bioinformatics and Kaplan–Meier analyses. Gut microbiome composition differed markedly across healthy controls, untreated HCC, and post-TACE patients. Bacteroides abundance progressively decreased, whereas Prevotella_9 increased across disease progression and treatment. Among TACE-treated patients, progressive disease was characterized by higher Prevotella_9 and lower Bacteroides and Ruminococcus abundance, accompanied by significantly reduced microbial diversity. Kaplan–Meier analysis showed that low Prevotella_9 (P = 0.001) and high Bacteroides (P = 0.001) and Faecalibacterium (P = 0.04) were associated with prolonged progression-free survival, while higher Phascolarctobacterium and Veillonella abundance correlated with shorter overall survival. Functional prediction revealed alterations in pathways related to lipid metabolism, carbohydrate metabolism, and immune regulation. Gut microbiome remodeling is closely associated with HCC progression and TACE outcomes. Specific microbial taxa, particularly Bacteroides and Prevotella_9, were associated with therapeutic response and prognosis; however, these findings are exploratory and warrant We hypothesized that specific microbial taxa and metabolic pathways could serve as predictive biomarkers of TACE efficacy and clinical outcomes.

Abstract Rho GTPase-activating protein 21 (ARHGAP21) plays a role in the occurrence and development of certain cancers, but its function in hepatocellular carcinoma (HCC) remains unclear. In this study, elevated ARHGAP21 expression was observed in both HCC cell lines and tissues and correlated with poor patient prognosis. Knockdown of ARHGAP21 suppressed HCC cell migration and invasion in vitro by regulating the actin cytoskeleton, while overexpression of ARHGAP21 had the opposite effect. In vivo, knockdown of ARHGAP21 inhibited HCC tumorigenesis and metastasis. Mechanistically, we demonstrated that ARHGAP21 directly binds to FLNA, and the PDZ domain of ARHGAP21 functions as a potential mediator of its binding to the 1–1200 aa fragment of FLNA. ARHGAP21 also directly binds to and recruits HSP90α to stabilize FLNA by inhibiting its ubiquitination and degradation. Overexpression of FLNA reversed the cytoskeleton remodeling-related suppression of tumor metastasis in ARHGAP21-knockdown HCC cells. These results revealed that ARHGAP21 promotes cytoskeleton remodeling and stimulates HCC metastasis by inhibiting FLNA ubiquitination and degradation via HSP90α recruitment. Our results position ARHGAP21 as both a potential prognostic marker and a promising therapeutic target in HCC.

To explore how neutrophil extracellular traps (NETs) mediate neuropathic pain in primary Sjögren's syndrome-associated peripheral neuropathy (pSS-PN). We analyzed clinical features in pSS-PN (n = 6) by DN4 Questions, Electromyography examination and sural nerve biopsies from six pSS-PN patients and six traumatic amputees using histology, immunohistochemistry (IHC), transmission electron microscopy (TEM), and immunofluorescence (IF) for NETs markers (cit-H3/MPO). And we created a model of pSS-PN. Pain behaviors were assessed, plasma cit-H3 was measured by ELISA, and hindlimb perfusion was quantified via laser speckle imaging. To inhibit NETosis, DNase I was administered intravenously. PSS-PN patients exhibited neuropathic pain, nerve conduction deficits, reduced nerve fiber density, and inflammatory vasa nervorum injury with significant cit-H3/MPO accumulation. NOD. Aire⁻/⁻ mice developed mechanical allodynia (1.885 vs. 2.497, P < 0.001 vs. C57BL/6 J; 1.885 vs. 2.367 P < 0.01 vs. NOD WT) and thermal hyperalgesia (6.993 vs. 8.585, P < 0.05 vs. C57BL/6 J; 6.93 vs. 8.815 P < 0.05 vs. NOD WT), accompanied by elevated plasma cit-H3 (44.61 vs. 27.49, P < 0.0001 vs. C57BL/6 J; 44.61 vs. 30.96 P < 0.0001 vs. NOD WT), sciatic nerve NETs deposition (44.61 vs. 35.60, P < 0.0001 24 vs. 18 weeks, NOD. Aire⁻/⁻), and increased hindlimb perfusion. DNase I treatment effectively reduced plasma cit-H3, alleviated pain behaviors, mitigated microvascular damage, and normalized perfusion. NETs drive peripheral neuropathy in pSS by inducing vasa nervorum inflammation and microcirculatory dysfunction, leading to neuropathic pain. These findings identify NETs as a key mechanistic link, biomarker, and promising therapeutic target in pSS-PN.

Purpose The purpose of this study was to determine the efficacy and safety of low-dose radiotherapy (LDR) for postoperative local chest wall recurrence of breast cancer. Methods The records of 52 patients with postoperative local chest wall recurrent breast cancer treated at our cancer center from January 2019 to December 2022. The t-test was used to compare the means of the LDR group and non LDR group. Categorical data were compared using the chi-square test. The Kaplan-Meier method were used to determine the factors associated the survival. Results Compared to patients who did not undergo LDR, patients in the LDR group showed a higher incidence of grade I side effects in their skin and soft tissue systems (p = 0.002), a significant reduction in grade II side effects (p < 0.05), and no grade III side effects. Compared with the non LDR group, the complete response rates were 42.3% vs. 38.5%, p = 0.777, the partial response rates were 53.8% vs. 50.0%, p = 0.781, and the objective relief rates were 96.2% vs. 88.5%, p = 0.833, respectively. The 3-year overall survival rate, local recurrence free survival rate, distant metastasis-free survival rate and disease-specific survival rate comparison between LDR group and non LDR group was 54.8% vs. 55.8%, p = 0.845 and 54.2% vs. 52.9%, p = 0.751, 67.9% vs. 51.9%, p = 0.097 and 39.2% vs. 49.6%, p = 0.993, respectively. Conclusion Compared with traditional radiotherapy, LDR pre-irradiation has better tolerance and efficacy in patients with local chest wall recurrence of breast cancer after operation.

AimsAurora kinase A (AURKA) has been implicated in promoting myeloid and renal fibrosis. This study aimed to investigate the impact and underlying mechanism of AURKA on liver fibrosis and to assess the therapeutic potential of MLN8237, a small-molecule AURKA inhibitor, in preventing liver fibrosis in mice.MethodsThe research used bioinformatics analysis and immunohistochemistry staining on fibrotic liver tissues from human and mouse models to assess AURKA expression. The cellular localization of AURKA was determined through double immunofluorescence staining in human fibrotic liver tissues and primary mouse hepatic stellate cells. RNA interference and AURKA antagonism were used to examine the effects of AURKA on liver fibrosis, while RNA-sequencing, qRT-PCR, and western blotting were employed to elucidate the potential molecular mechanisms of AURKA on hepatic stellate cell activation.ResultsThe results showed that AURKA was positively correlated with the progression of liver fibrosis and was predominantly expressed in activated HSCs. Silencing AURKA inhibited HSC activation and proliferation, and induced HSC apoptosis, effects that were similar to those observed with MLN8237 treatment. Additionally, silencing AURKA suppressed the glycogen synthase kinase-3β/β-catenin signaling pathway. Pharmacological inhibition of AURKA phosphorylation also resulted in reduced liver fibrosis in vivo.ConclusionIn conclusion, AURKA may promote HSC activation and liver fibrosis through the Wnt/β-catenin pathway, suggesting its potential as a therapeutic target for liver fibrosis.

EphrinA5 belongs to a subclass of ephrin ligands. Abnormal signal transduction of EFNA5 shows a relationship to the development of various tumors. In this study, we explored the level of EFNA5 in hepatoma cells and the influence of up regulation of EFNA5 expression level on the proliferation, invasion, and migration of HepG2 and LM3 cells. Additionally, this work focused on examining its possible mechanism of action, and future impacts on clinical practice. Immunohistochemistry was utilized to explore the connection between EFNA5 and hepatoma. Real-time quantitative polymerase chain reaction was used for determining the expression levels of EFNA5 in several hepatoma cell lines and normal hepatocytes. Cells were transfected with a pCMV3-EFNA5-flag plasmid and an EFNA5 plasmid. The expression efficiency of EFNA5 was identified through qRT-PCR. For the purpose of further identifying cell proliferation, the Cell Counting Kit-8 assay was applied. To identify changes of cell migration and invasion ability, Transwell and Boyden tests were utilized. Western blot was employed to identify the expressions mof EFNA5 and possible downstream molecules. Data acquired from The Cancer Genome Atlas demonstrated that the level of EFNA5 in hepatoma was significantly downregulated in relative to the normal hepatocytes (P < 0.05). Upregulation of EFNA5 expression in hepatoma cells hindered the proliferative, invasive, and migratory ability of cells (P < 0.05). Additionally, EFNA5 downregulated the level of epithelial–mesenchymal transition-related molecules and EGFR. The expression of EFNA5 was low in hepatoma cells. An increase in EFNA5 levels hinders the proliferation, invasion, and migration of hepatoma cells. These effects may occur through inhibition of hepatoma epithelial–mesenchymal transition by EFNA5. Moreover, the study on the mechanisms of proliferation, invasion and metastasis of hepatoma provides a novel theoretical basis, and may influence the clinical practice of tumor treatment in the future.

EFNA4, a member of the Ephrin-A ligand family, may influence hepatocellular carcinoma cells through two distinct mechanisms: one reliant on specific Eph receptor binding and the other independent of receptor involvement. However, EFNA4's influence on HCC via non-Eph receptor pathways remains unclear. In this study, we aimed to investigate the role of EFNA4 in a receptor-independent environment. Firstly, we constructed an environment lacking Eph receptors via CRISPR/Cas9 and found that EFNA4 could still partially promote HCC proliferation and metastasis in vivo and in vitro. Further analyses of apoptosis, ROS, and GPX4 expression revealed that overexpression of EFNA4 would inhibit ferroptosis in HCC. Mechanistically, EFNA4 was positively correlated with SLC7A11 and directly interacted with SLC7A11 in HCC via bioinformatics analysis. We demonstrated that the structural domain (a.a. 161-201) of EFNA4 specifically binds to the domain (a.a. 222-501) of SLC7A11, which led to the deubiquitination of SLC7A11. Subsequently, we found that EFNA4 would recruit the deubiquitinase USP9X, resulting in inhibition of SLC7A11 degradation, which ultimately inhibits ferroptosis and enhances the proliferation and metastasis of HCC. In conclusion, we demonstrated that EFNA4 promotes the proliferation and metastasis of HCC independent of Eph receptors by inhibiting ferroptosis and advancing the deubiquitination of SLC7A11 by recruiting the deubiquitinase USP9X. This indicates that EFNA4 could act as a potential prognostic marker and a prospective therapeutic target in patients with HCC.

Background: CDP-diacylglycerol synthase 1 (CDS1), a functional protein regulating cell growth and lipid synthesis, is implicated in cancer development. Despite its potential role, the impact of CDS1 in hepatocellular carcinoma (HCC) remains elusive. This study aimed to explore the role of CDS1 on HCC progression. Finally, we elucidated whether CDS1 affects HCC pathogenesis and its associated signal transduction.Methods: CDS1 expression was assessed in tissue samples, correlating with clinical characteristics and prognostic outcomes in HCC. Vector, CDS1 overexpression, si-CDS1-2, and si-CDS1-3 groups were established using primary liver cancer tissues, adjacent normal tissues, human HCC cells, liver epithelial cells, and RNA/proteins extracts. In vitro and in vivo experiments were performed to determine the biological function and molecular basis of CDS1, including Cell Counting Kit-8, cell cycle, and 5ethynyl-2 '-deoxyuridine assays for proliferation, Transwell and Boyden assays for invasion and metastasis. Moreover, apoptosis assay, quantitative real-time polymerase chain reaction, and western blotting were shown. Results: Analysis of The Cancer Genome Atlas datasets revealed a significant increase in CDS1 expression in HCC, suggesting a potential influence on liver cancer cell growth, invasion, and apoptosis. Immunohistochemical analysis revealed elevated CDS1 protein levels in HCC samples compared to adjacent tissues. Furthermore, western blotting revealed a plausible carcinogenic role of CDS1 in HCC linked to the RAC-Alpha Serine/Threonine-Protein Kinase (AKT)-Mechanistic Target of Rapamycin (mTOR) signaling pathway. Finally, experimental findings confirmed that CDS1 promotes HCC proliferation, invasion, and metastasis while inhibiting apoptosis, potentially through the AKT-TSC2-mTOR pathway.Conclusions: CDS1 modulates the proliferation, migration, and invasion of liver cancer cells, impeding normal apoptotic processes. The underlying mechanism includes the activation of the AKT-TSC2-mTOR signaling pathway.

Terpenoids are essential for plants to adapt for specific ecological niches which are also extensively used in industries of flavor, fragrance, spice, and medicine. Dendrobium catenatum, belonging to epiphytic orchids, is a traditional medicinal plant of high economic value due to its natural abundance in secondary metabolites beneficial for humans. However, knowledge is lacking about the genetic structure of terpenoids and terpenes-mediated stress response in D. catenatum. In this study, terpene synthase DcTPS was mined as an evolutionary gene using phylogenomics in D. catenatum and relative species, and the function of this gene was characterized by transient overexpression in tobacco leaves. Subsequently, co-expression network analysis and machine learning were used to identify transcription factors closely related to DcTPS. Expression changes of DcTPS in response to environmental stresses were also conducted. All these results provided new insights into DcTPS-mediated molecular mechanism of terpenoid accumulation and environmental adaptation in D. catenatum, which will be valuable to guide the cultivation of high-quality medicinal plants and development of terpenoids-related industrial products.

Transarterial embolization, the first-line treatment for hepatocellular carcinoma, does not always lead to promising outcomes in all patients. A better understanding of how the immune lymphocyte changes after transarterial embolization might be the key to improve the efficacy of transarterial embolization. However, there are few studies evaluating immune lymphocytes in transarterial embolization patients. Therefore, we aimed to evaluate the short- and long-term effects of transarterial embolization on lymphocyte subsets in patients with hepatocellular carcinoma to identify those that predict transarterial embolization prognosis. Peripheral blood samples were collected from 44 patients with hepatocellular carcinoma at the following time points: 1 d before the initial transarterial embolization, 3 d after the initial transarterial embolization, and 1 mo after the initial transarterial embolization and subjected to peripheral blood mononuclear cell isolation and flow cytometry. Dynamic changes in 75 lymphocyte subsets were recorded, and their absolute counts were calculated. Tumor assessments were made every 4 to 6 wk via computed tomography or magnetic resonance imaging. Our results revealed that almost all lymphocyte subsets fluctuated 3 d after transarterial embolization, but only Tfh and B cells decreased 1 mo after transarterial embolization. Univariate and multivariate Cox regression showed that high levels of Th2 and conventional killer V delta 2 cells were associated with longer progressive-free survival after transarterial embolization. Longer overall survival after transarterial embolization was associated with high levels of Th17 and viral infection-specific V delta 1 cells and low levels of immature natural killer cells. In conclusion, transarterial embolization has a dynamic influence on the status of lymphocytes. Accordingly, several lymphocyte subsets can be used as prognostic markers for transarterial embolization. Transarterial embolization, a locoregional therapy for patients with hepatocellular carcinoma, exerts a dynamic influence on lymphocyte subsets, while several lymphocyte subsets could be prognostic markers for transarterial embolization.

Ribonucleic acid interference (RNAi) based on microRNA (miRNA) may provide efficient and safe therapeutic opportunities. However, natural microRNAs can not easily be regulated and usually cause few phenotypic changes. Using the engineering principles of synthetic biology, we provided a novel and standard platform for the generation of tetracycline (Tet)-inducible vectors that express artificial microRNAs in a dosage-dependent manner. The vector generates a Pol II promoter-mediated artificial microRNA which was flanked by ribozyme sequences. In order to prove the utility of this platform, we chose β-catenin and HIF-1α as the functional targets and used the bladder cancer cell lines 5637 and T24 as the test models. We found that the Tet-inducible artificial microRNAs can effectively silence the target genes and their downstream genes, and induce anti-cancer effects in the two bladder cancer cell lines. These devices can inhibit proliferation, induce apoptosis, and suppress migration of the bladder cancer cell lines 5637 and T24. The Tet-inducible synthetic artificial microRNAs may represent a kind of novel therapeutic strategies for treating human bladder cancer.

TINCR is a well-known lncRNA which acts as a master regulator in somatic differentiation development. However, it is still unclear whether TINCR is also involved in caner occurrence and progression. In this study, we observed that TINCR was up-regulated in bladder cancer tissues and cells and contributed to oncogenesis and cancer progression. Silencing TINCR expression inhibited cell proliferation and promoted apoptosis in vitro, indicating that TINCR may be the potential therapeutic target for treating bladder urothelial carcinoma. Thus we used the synthetic biology approach to create theophylline controllable RNAi-based genetic switches which silenced TINCR in a dosage-dependent manner. Both RNAi-OFF and ON switches can be used to quantitatively control the expression of TINCR in bladder cancer to suppress the progression of bladder cancer. These findings suggest that lncRNA-TINCR could promote bladder cancer development and progression and artificial control of its expression through inducible RNAi may represent a new kind of therapeutic strategy for treating human bladder cancer.

Background Plasmodium berghei has been used as a preferred model for studying human malaria, but only a limited number of disease-associated genes of P. berghei have been reported to date. Identification of new disease-related genes as many as possible will provide a landscape for better understanding the pathogenesis of P. berghei . Methods Network module analysis method was developed and applied to identify disease-related genes in P. berghei genome. Sequence feature identification, gene ontology annotation, and T-cell epitope analysis were performed on these genes to illustrate their functions in the pathogenesis of P. berghei . Results 33,314 genes were classified into 4,693 clusters. 4,127 genes shared by six malaria parasites were identified and are involved in many aspects of biological processes. Most of the known essential genes belong to shared genes. A total of 63 clusters consisting of 405 P. berghei genes were enriched in rodent malaria parasites. These genes participate in various stages of parasites such as liver stage development and immune evasion. Combination of these genes might be responsible for P. berghei infecting mice. Comparing with P. chabaudi , none of the clusters were specific to P. berghei . P. berghei lacks some proteins belonging to P. chabaudi and possesses some specific T-cell epitopes binding by class-I MHC, which might together contribute to the occurrence of experimental cerebral malaria (ECM). Conclusions We successfully identified disease-associated P. berghei genes by network module analysis. These results will deepen understanding of the pathogenesis of P. berghei and provide candidate parasite genes for further ECM investigation.

OBJECTIVE:To investigate the role of Rho GTPase-activating protein 21 (ARHGAP21) in regulating the migration and metastasis of non-small cell lung cancer (NSCLC) cells.METHODS:TCGA, CPTAC database were used to analyze the correlation of ARHGAP21 expression level in NSCLC and the patients' prognosis. The expression of ARHGAP21 in clinical specimens of NSCLC tissues was examined using Western blotting and immunohistochemistry. The effect of ARHGAP21 knockdown on migration ability of lung cancer cell lines was examined using Transwell assay and wound healing assay. A nude mouse model with injection of lung cancer H1299 cells via the tail vein was used to examine the effect of ARHGAP21 knockdown on the metastatic ability of the tumor cells. The possible mechanism of ARHGAP21 was predicted by bioinformatics analysis and verified using Western blotting.RESULTS:A low ARHGAP21 expression was associated with poor prognosis of patients with NSCLC (P < 0.05). ARHGAP21 expression was significantly downregulated in lung cancer tissues as compared with the adjacent tissues (P < 0.001). In cultured lung cancer cells, ARHGAP21 knockdown obviously promoted the migration ability of the cells (P < 0.001). In the nude mouse models, injection of H1299 cells with ARHGAP21 knockdown, as compared with the negative control cells, resulted in a greater number of metastatic lung cancer nodules (P < 0.05), which expressed higher levels of N-cadherin and vimentin. Bioinformatic analysis showed a close correlation of ARHGAP21 with APC, GSK3β, and Axin (P < 0.001). Western blotting showed that ARHGAP21 knockdown significantly decreased ubiquitination of β-catenin, upregulated N-cadherin and activated the WNT signaling pathway in the lung cancer cells.CONCLUSION:ARHGAP21 downregulation can significantly promote the migration and metastatic ability of NSCLC possibly as a result of WNT signaling pathway activation, which reduces the ubiquitination of β-catenin by affecting the expressions of APC, GSK3β, and Axin.

Hepatocellular carcinoma (HCC) is one of the common major malignancies worldwide and has the third highest mortality rate of any malignancy. The current field of treatment for hepatocellular carcinoma is multidisciplinary in involvement and a combination of therapeutic approaches, among which immunotherapy is the treatment modality for advanced hepatocellular carcinoma. This review provides new ideas for developing immunotherapy regimens and improving the efficacy of immunotherapy for patients with advanced liver cancer by summarising the progress of intestinal flora in the immunotherapy of patients with liver cancer.

Abstract Background ​Histone arginine methylation is an important feature in bladder cancer that affects prognosis and therapeutic response. However, the investigation of molecular subtypes based upon histone arginine methylation is still being exploited. Methods From the TCGA database, we obtained the RNA sequencing and somatic mutation results of 412 bladder cancer patients. To identify molecular subtypes associated with histone arginine methylation, consensus clustering was performed. These histone arginine methylation-associated subtypes were compared in terms of prognosis, clinical features, immune cell infiltration, and somatic mutation profiles. Moreover, we utilized the CTRP and GDSC databases to examine how drug sensitivity is related to mRNA expression of HAM-related genes. Results Based on our findings, bladder cancer could be divided into histone arginine methylation-low (HAM-low) and histone arginine methylation-high (HAM-high) subtypes with distinctive clinicopathological characteristics, tumor microenvironment and prognostic. There is a dismal prognosis associated with high histone arginine methylation subtypes and a high frequency of oncogene mutations in these subtypes. Conversely, histone arginine methylation-low subtypes are associated with a better clinical outcome and a lower frequency of oncogene mutations. There was a correlation between the HAM-high subtype and the immune-hot phenotype, while the HAM-low subtype was associated with the immune-cold phenotype. As well, we develop and validate a prognostic model associated with histone arginine methylation that has good predictive power. The results of drug sensitivity tests revealed that HAM-related genes are associated with resistance to most drugs. A positive correlation was found between XAV939 or Cetuximab and HAM-related gene expression, suggesting that these agents may be beneficial to patients who fall into the HAM-high subgroup of BC patients. Conclusion ​In summary, we have established a novel bladder classification based on histone arginine methylation subtypes. This classification has significant consequences for the estimation of prognosis and drug sensitivity, as well as the tumor microenvironment.

Background Long non-coding RNAs (lncRNAs) have emerged as biomarkers and important regulators of tumor development and progression. PANDAR (promoter of CDKN1A antisense DNA damage activated RNA) is a novel long non-coding RNA that acts as a potential biomarker and involves in development of multiple cancers. However, the clinical significance and molecular mechanism of PANDAR in bladder cancer is still unknown. In this study, we aimed to figure out the role of PANDAR in bladder cancer. Methods The relative expression level of lncRNA PANDAR was determined by Real-Time qPCR in a total of 55 patients with urothelial bladder cancer and in different bladder cancer cell lines. We inhibited PANDAR expression by transfecting PANDAR specific siRNA and enhanced PANDAR expression by transfecting a PANDAR expression vector (pcDNA3.1-PANDAR). Cell proliferation was determined by using both CCK-8 assay and Edu assay. Cell apoptosis was determined by using ELISA assay, Hoechst 33342 staining and Flow cytometry. Cell migration was determined by using transwell assay. All experimental data from three independent experiments were analyzed by χ 2 test or Student’s t -test and results were expressed as mean ± standard deviation. Results We found that PANDAR was significantly up-regulated in bladder cancer tissues compared with paired-adjacent nontumorous tissues in a cohort of 55 bladder cancer patients. Moreover, increased PANDAR expression was positively correlated with higher histological grade ( P < 0.05) and advanced TNM stage ( P < 0.05). Further experiments demonstrated that inhibited cell proliferation/migration and induced apoptosis by silencing PANDAR were also observed in bladder cancer cells. Furthermore, over expression of PANDAR in bladder cancer cells promoted the proliferation/migration and suppressed apoptosis. Conclusions These findings demonstrate that PANDAR plays oncogenic roles in bladder cancer and PANDAR may serve as a potential prognostic biomarker and therapeutic target of bladder cancer.