Achieving High Activity and Long-Term Stability towards Oxygen Evolution in Acid by Phase Coupling between CeO2-Ir.

The development of efficient and stable catalysts with high mass activity is crucial for acidic oxygen evolution reaction (OER). In this study, CeO2-Ir heterojunctions supported on carbon nanotubes (CeO2-Ir/CNTs) are synthesized using a solvothermal method based on the heterostructure strategy. CeO2-Ir/CNTs demonstrate remarkable effectiveness as catalysts for acidic OER, achieving 10.0 mA cm-2 at a low overpotential of only 262.9 mV and maintaining stability over 60.0 h. Notably, despite using an Ir dosage 15.3 times lower than that of c-IrO2, CeO2-Ir/CNTs exhibit a very high mass activity (2542.3 A gIr-1@1.53 V), which is 58.8 times higher than that of c-IrO2. When applied to acidic water electrolyzes, CeO2-Ir/CNTs display a prosperous potential for application as anodic catalysts. X-ray photoelectron spectrometer (XPS) analysis reveals that the chemical environment of Ir nanoparticles (NP) can be effectively modulated through coupling with CeO2. This modulation is believed to be the key factor contributing to the excellent OER catalytic activity and stability observed in CeO2-Ir/CNTs.

EMP3 as a key downstream target of miR-663a regulation interferes with MAPK/ERK signaling pathway to inhibit gallbladder cancer progression.

Gallbladder carcinoma (GBC) is the most common malignancy of the biliary tract, and its molecular pathogenesis remains unclear. Here we explore the functional roles of epithelial membrane protein 3 (EMP3) in GBC progression, which is aberrantly expressed in various types of cancers. The results showed that the expression level of EMP3 was reduced in human GBC tissues compared with non-malignant tissues. Further, the low expression of EMP3 was associated with the poor prognosis of GBC patients by Kaplan-Meier analysis. The ectopic expression of EMP3 inhibited GBC cell proliferation, migration and invasion in vitro and in vivo. Conversely, the depletion of EMP3 promoted GBC cell growth and metastasis. In addition, we found that EMP3 was a target gene of miR-663a, and the downregulation of EMP3 in GBC was attributed to the overexpression of miR-663a. MiR-663a was also shown to be a tumor-promoting factor mediating GBC development. In this study, we demonstrate that downregulation of EMP3 activates MAPK/ERK signaling, which regulates GBC progression. These data reveal the mechanism by which EMP3 inhibits the progression of GBC, suggesting that the miR-663a/EMP3/MAPK/ERK axis may be a new therapeutic target for GBC treatment.

Candida vulturna Outbreak Caused by Cluster of Multidrug-Resistant Strains, China.

Candida vulturna belongs to the Candida haemulonii species complex and is phylogenetically related to C. auris. We report a C. vulturna outbreak among persons in Shanxi Province, China, during 2019-2022. Isolates were resistant to multiple antifungal drugs and exhibited enhanced adhesion and biofilm formation properties.

Boosting Catalytic Selectivity through a Precise Spatial Control of Catalysts at Pickering Droplet Interfaces.

Exploration of new methodologies to tune catalytic selectivity is a long-sought goal in catalytic community. In this work, oil-water interfaces of Pickering emulsions are developed to effectively regulate catalytic selectivity of hydrogenation reactions, which was achieved via a precise control of the spatial distribution of metal nanoparticles at the droplet interfaces. It was found that Pd nanoparticles located in the inner interfacial layer of Pickering droplets exhibited a significantly enhanced selectivity for p-chloroaniline (up to 99.6%) in the hydrogenation of p-chloronitrobenzene in comparison to those in the outer interfacial layer (63.6%) in pure water (68.5%) or in pure organic solvents (46.8%). Experimental and theoretical investigations indicated that such a remarkable interfacial microregion-dependent catalytic selectivity was attributed to the microenvironments of the coexistence of water and organic solvent at the droplet interfaces, which could provide unique interfacial hydrogen-bonding interactions and solvation effects so as to alter the adsorption patterns of p-chloronitrobenzene and p-chloroaniline on the Pd nanoparticles, thereby avoiding the unwanted contact of C-Cl bonds with the metal surfaces. Our strategy of precise spatial control of catalysts at liquid-liquid interfaces and the unprecedented interfacial effect reported here not only provide new insights into the liquid-liquid interfacial reactions but also open an avenue to boost catalytic selectivity.

Tri-templating Synthesis of Multilevel Mesoporous Silica Microspheres with a Complex Interior Structure for Efficient CO2 Capture and Catalysis.

Multilevel porous architectures with microscopic shape control and tailor-made complex structures offer great potential for various innovative applications, but their elaborate design and synthesis have remained a scientific and technological challenge. Herein, we report a simple and effective tri-templating method, in which microscale Pickering droplets, nanoscale polystyrene colloids (PS), and molecular cetyltrimethylammonium chloride micelles are synchronously employed, for the fabrication of such micro-nanohierarchical mesoporous silica microspheres. In this protocol, Pickering droplet-directed interfacial sol-gel growth and its spatially confined surfactant assembly-directed sol-gel coating on PS suspensions are coupled together, enabling the successful formation of structured mesoporous silica that consists of numerous nanocompartments enclosed by a permeable shell. By varying the quantity of PS colloidal templates, rational regulation of the complex interior structure is achieved. Also, ascribed to the multilevel arrangement, this peculiar architecture not only shows desirable fast mass transport of external molecules but also possesses easy handling ability. After loading with tetraethylenepentamine or enzyme species, the yielded microspherical CO2 sorbents or immobilized biocatalysts, respectively, exhibit enhanced CO2 capture capacity and enzymatic catalysis efficiency. Notably, taking advantage of their microscopic characteristics, the immobilized biocatalysts could be ideally packed in a fixed-bed reactor for long-term continuous-flow enzymatic reactions. This tri-templating strategy provides a new synthetic route to access other multilevel microscopic materials with fascinating complex structures and paves a way to promote their practical applications.

Early Prediction Model of Acute Aortic Syndrome Mortality in Emergency Departments.

Purpose: Acute aortic syndrome is a constellation of life-threatening medical conditions for which rapid assessment and targeted intervention are important for the prognosis of patients who are at high risk of in-hospital death. The current study aims to develop and externally validate an early prediction mortality model that can be used to identify high-risk patients with acute aortic syndrome in the emergency department. Patients and Methods: This retrospective multi-center observational study enrolled 1088 patients with acute aortic syndrome admitted to the emergency departments of two hospitals in China between January 2017 and March 2021 for model development. A total of 210 patients with acute aortic syndrome admitted to the emergency departments of Peking University Third Hospital between January 2007 and December 2021 was enrolled for model validation. Demographics and clinical factors were collected at the time of emergency department admission. The predictive variables were determined by referring to the results of previous studies and the baseline analysis of this study. The study's endpoint was in-hospital death. To assess internal validity, we used a fivefold cross-validation method. Model performance was validated internally and externally by evaluating model discrimination using the area under the receiver-operating characteristic curve (AUC). A nomogram was developed based on the binary regression results. Results: In the development cohort, 1088 patients with acute aortic syndromes were included, and 88 (8.1%) patients died during hospitalization. In the validation cohort, 210 patients were included, and 20 (9.5%) patients died during hospitalization. The final model included the following variables: digestive system symptoms (OR=2.25; P=0.024), any pulse deficit (OR=7.78; P<0.001), creatinine (µmol/L)(OR=1.00; P=0.018), lesion extension to iliac vessels (OR=4.49; P<0.001), pericardial effusion (OR=2.67; P=0.008), and Stanford type A (OR=10.46; P<0.001). The model's AUC was 0.838 (95% CI 0.784-0.892) in the development cohort and 0.821 (95% CI 0.750-0.891) in the validation cohort, and the Hosmer-Lemeshow test showed p=0.597. The fivefold cross-validation demonstrated a mean accuracy of 0.94, a mean precision of 0.67, and a mean recall of 0.13. Conclusion: This risk prediction tool uses simple variables to provide robust prediction of the risk of in-hospital death from acute aortic syndrome and validated well in an independent cohort. The tool can help emergency clinicians quickly identify high-risk acute aortic syndrome patients, although further studies are needed for verifying the prospective data and the results of our study.

m6A mRNA modification maintains colonic epithelial cell homeostasis via NF-κB-mediated antiapoptotic pathway.

Colonic mucosal barrier dysfunction is one of the major causes of inflammatory bowel disease (IBD). However, the mechanisms underlying mucosal barrier dysfunction are poorly understood. N6-methyladenosine (m6A) mRNA modification is an important modulator of epitranscriptional regulation of gene expression, participating in multiple physiological and pathological processes. However, the function of m6A modification in colonic epithelial cells and stem cells is unknown. Here, we show that m6A modification is essential for maintaining the homeostatic self-renewal in colonic stem cells. Specific deletion of the methyltransferase 14 (Mettl14) gene in mouse colon resulted in colonic stem cell apoptosis, causing mucosal barrier dysfunction and severe colitis. Mechanistically, we revealed that Mettl14 restricted colonic epithelial cell death by regulating the stability of Nfkbia mRNA and modulating the NF-κB pathway. Our results identified a previously unidentified role for m6A modification in colonic epithelial cells and stem cells, suggesting that m6A modification may be a potential therapeutic target for IBD.

Metal-Nanoparticles-Loaded Ultrathin g-C3N4 Nanosheets at Liquid-Liquid Interfaces for Enhanced Biphasic Catalysis.

Exploiting new interface-active solid catalysts is crucial to construct efficient Pickering emulsion systems for biphasic catalysis. In this work, ultrathin g-C3N4 nanosheets (g-C3N4-NSs) were developed as a new solid emulsifier to directly position catalytic sites at oil-water interfaces for improving the reaction efficiency of a biphasic reaction. Exemplified by a metal-involved biphasic reaction of nitroarenes reduction, the developed Pd/g-C3N4-NSs catalyst with Pd nanoparticles loaded on the surface of g-C3N4-NSs exhibited excellent activity with a catalytic efficiency of 1220 h-1. Such activity was 4.2 and 17.9 times higher than those of Pd/g-C3N4-bulk and the ordinary Pd/C8-SiO2 catalyst, respectively. Also, in the biphasic oxidation reaction of alcohols, Pd/g-C3N4-NSs achieved a 2.3-fold activity enhancement. It was found by analyzing the solidified emulsion droplets that the Pd/g-C3N4-NSs catalyst was parallelly assembled at the oil-water interfaces. Because of the ultrathin thickness of g-C3N4-NSs, such a unique interfacial assembly behavior allowed precise positioning of Pd nanoparticles at the oil-water interfaces. As a result, the oil-soluble reactant could directly react with the water-soluble reactant at the oil-water interface hosting the Pd nanoparticles. Our elaborately designed reaction interface was believed to substantially avoid the diffusion barrier between oil-soluble and water-soluble reactants and then to significantly enhance the reactivity of biphasic reactions. This work highlights the importance of the interfacial location of catalytic sites in biphasic catalysis.

Caught in Phase Transition: Snapshot of the Metallofullerene Sc3N@C70 Rotation in the Crystal.

The molecular structure of Sc3N@C2v(7854)-C70 was determined by single-crystal X-ray diffraction. Variable-temperature X-ray diffraction analysis unraveled the details of the phase transition caused by the temperature-driven jumplike rotation of the fullerene cage between two orientations. Whereas in the lower-temperature P21/c phase the fullerene predominantly occupies one orientation, two orientations become equally occupied in the higher-temperature C2/m phase. This work provides a rare example of the well-defined order-disorder transition in metallofullerene crystals and thus gives important insight into the problem of disorder impeding metallofullerene crystallography.

Long noncoding RNA lncGALM increases risk of liver metastasis in gallbladder cancer through facilitating N-cadherin and IL-1ß-dependent liver arrest and tumor extravasation.

BACKGROUND: Long noncoding RNAs (lncRNA) represent significant factors of the mammalian transcriptome that mediates varied biological and pathological processes. The liver is the most common site for gallbladder cancer (GBC) distant metastasis and contributes to the majority of GBC-related death. How lncRNA affects GBC metastasis is not completely understood. RESULTS: A novel lncRNA termed lncGALM (lncRNA in GBC associated with liver metastasis) was discovered to be highly expressed in cancer patients and xenografted tumors with liver metastasis. Elevated lncGALM in GBC patients also correlated to decreased survival. Invasion and migration of GBC cells were enhanced through lncGALM, both in vitro and in vivo. lncGALM functioned as sponges by competitively binding to and inactivating miR-200 family members, which increase epithelial-mesenchymal transition-associated transcription factor ZEB1 and ZEB2, leading to a fibroblastic phenotype and increased expression of N-cadherin. In addition, lncGALM bound to IL-1ß mRNA and stabilized the IL-1ß gene that mediates liver sinusoidal endothelial cell (LSECs) apoptosis. lncGALM-expressing LiM2-NOZ cells acquired a strong ability to migrate and adhere to LSECs, promoting LSECs apoptosis and therefore facilitating tumor cell extravasation and dissemination. CONCLUSIONS: lncGALM promotes GBC liver metastasis by facilitating GBC cell migration, invasion, liver arrest, and extravasation via the invasion-metastasis cascade. Targeting lncGALM may be protective against the development of liver metastasis in GBC patients.

NOP2/Sun RNA methyltransferase 2 promotes tumor progression via its interacting partner RPL6 in gallbladder carcinoma.

NOP2/Sun domain family, member 2 (NSUN2) is a nuclear RNA methyl-transferase catalyzing 5-methylcytosine formation. Evidence shows that NSUN2 is correlated with cell unlimited proliferation. However, its functional role in gallbladder carcinoma (GBC), which is the most common biliary tract malignancy and has a poor prognosis, remains to be determined. Here we found that NSUN2 was highly expressed in GBC tissues as well as cell lines. NSUN2 silencing repressed GBC cell proliferation and tumorigenesis both in vitro and in vivo. Conversely, upregulation of NSUN2 enhanced GBC cell growth and colony formation. We further discovered that RPL6 was a closely interacting partner with NSUN2. Silencing RPL6 resulted in insufficient NSUN2 translational level and accumulative NSUN2 transcriptional level. Exogenous expression of NSUN2 partially rescued the effect of RPL6 in gallbladder cancer progression. Taken together, our data provided novel mechanic insights into the function of NSUN2 in GBC, thus pointing to NSUN2 as a potential and effective therapeutic approach to GBC treatment.

Ho2O@C84: Crystallographic Evidence Showing Linear Metallic Oxide Cluster Encapsulated in IPR Fullerene Cage of D2d(51591)-C84.

Fullerene C84 is the third-most-abundant species after C60 and C70. In the past decade, a variety of C84-based clusterfullerenes have been well-studied experimentally, which otherwise do not include oxide clusterfullerenes (OCFs). In this work, we report a comprehensive inspection of Ho2O@C84, including its mass, spectroscopic, crystallographic, electrochemical (EC), and density functional theory (DFT) studies. Importantly, crystallographic data reveal an IPR cage of D2d(51591)-C84 with a linear endohedral Ho-O-Ho cluster, indicating that the compression effect of the C84 cage is less pronounced compared to that of a smaller cage. The experimentally observed structure is confirmed by DFT computations, which also verify its superior stability. Further studies suggest that Ho2O@C84 has reduced EC and HOMO-LUMO gaps compared to those of empty species, again demonstrating the effect of cluster encapsulation.

Trapping Metallic Oxide Clusters inside Fullerene Cages.

The sub-nanometer sized void inside a fullerene cage permits the accommodation of a single atom, atomic cluster, or even small molecule, resulting in the formation of endohedral fullerenes. Particularly, clusterfullerenes can be formed by encapsulating multiple metallic ions in most cases along with nonmetal ions (i.e., N3-, C22-, S2-, O2-) inside the fullerene cage. Such an association makes clusterfullerene more functional than empty fullerenes and conventional mono-metallofullerenes. To date, a variety of clusterfullerenes have been reported, including metal nitrides, carbides, oxides, sulfides, cyanides, and so on. Among them, oxide clusterfullerenes (OCFs) can contain variable oxide clusters (i.e., M4O2, M4O3, M3O, and M2O; M = Sc or other metal), yielding one of the most versatile families. Thus, OCFs may provide a more convenient platform for developing new functional molecules and for studying previously less-explored topics such as formation mechanisms of clusterfullerenes. In this Account, we review recent progress in the field of OCFs, including their synthesis, isolation, and structural and electrochemical studies as well as the preliminary exploration into their potential functions and applications. Thanks to the concrete crystallographic results of an OCF series, we can track the transition of endohedral cluster and fullerene cage. It is suggested that the configuration and internal dynamics of the oxide cluster are highly dependent on not only the cage size but also cage structure. On the other hand, based on the experimental observations, two competitive transformation pathways are established for the majority of OCFs, verifying the bottom-up or top-down formation mechanism. It is also found that the redox behaviors of OCFs are more or less comparable to their isoelectronic species with common cage structure and similar cluster geometry but varied greatly with the cluster variety (i.e., Sc2O vs Sc4O2-3). The mechanism behind such phenomena has been discussed. In addition, the potential of Dy-based OCFs as single molecular magnets (SMMs) is presented theoretically. Nevertheless, experimental advance remains to be achieved.

Ho2O@C74: Ho2O Cluster Expands within a Small Non-IPR Fullerene Cage of C2(13333)-C74.

Steering the cluster configuration inside a fullerene cage has been one of most interesting topics in the field of fullerenes, since the physical property of a cluster fullerene may be modified accordingly. It has been well-recognized that the cluster configuration can be tuned via altering the cage size. Typically, the carbide cluster and the oxide cluster are experimentally seen to be curled up within a small fullerene cage whereas they are expanded in a large cage. In this work, a new oxide cluster fullerene Ho2O@ C2(13333)-C74 is prepared and isolated. The single-crystal X-ray diffraction (XRD) study reveals that the Ho2O cluster, however, expands within the small non-IPR cage of C2(13333)-C74 with a Ho-O-Ho angle of >170°, indicating that cluster configuration is highly related to the cage shape and cage structure as well. The DFT computation demonstrates that the cluster-to-cage electron-transfer obviously enhances the aromaticity of the motif containing the fused-pentagon pair and hence stabilizes the non-IPR cage of C2(13333)-C74. In addition, the electrochemical and magnetic properties of Ho2O@ C2(13333)-C74 are studied to further investigate the effect of endohedral Ho2O cluster.

Genomic ERBB2/ERBB3 mutations promote PD-L1-mediated immune escape in gallbladder cancer: a whole-exome sequencing analysis.

OBJECTIVES: Patients with gallbladder carcinoma (GBC) lack effective treatment methods largely due to the inadequacy of both molecular characterisation and potential therapeutic targets. We previously uncovered a spectrum of genomic alterations and identified recurrent mutations in the ErbB pathway in GBC. Here, we aimed to study recurrent mutations of genes and pathways in a larger cohort of patients with GBC and investigate the potential mechanisms and clinical significance of these mutations. DESIGN: We performed whole-exome sequencing (WES) in 157 patients with GBC. Functional experiments were applied in GBC cell lines to explore the oncogenic roles of ERBB2/ERBB3 hotspot mutations, their correlation with PD-L1 expression and the underlying mechanisms. ERBB inhibitors and a PD-L1 blocker were used to evaluate the anticancer activities in co-culture systems in vitro and in vivo. RESULTS: WES identified ERBB2 and ERBB3 mutations at a frequency of 7%-8% in the expanded cohort, and patients with ERBB2/ERBB3 mutations exhibited poorer prognoses. A set of in vitro and in vivo experiments revealed increased proliferation/migration on ERBB2/ERBB3 mutation. Ectopic expression of ERBB2/ERBB3 mutants upregulated PD-L1 expression in GBC cells, effectively suppressed normal T-cell-mediated cytotoxicity in vitro through activation of the PI3K/Akt signalling pathway and contributed to the growth and progression of GBC in vivo. Treatment with an ERBB2/ERBB3 inhibitor or a PD-L1 monoclonal antibody reversed these immunosuppressive effects, and combined therapy revealed promising therapeutic activities. CONCLUSIONS: ERBB2/ERBB3 mutations may serve as useful biomarkers in identifying patients who are sensitive to ERBB2/ERBB3 inhibitors and PD-L1 monoclonal antibody treatment. TRIAL REGISTRATION NUMBER: NCT02442414;Pre-results.

ZFX Promotes Proliferation and Metastasis of Pancreatic Cancer Cells via the MAPK Pathway.

BACKGROUND/AIMS: The role of ZFX in tumourigenesis is unclear. We aimed to study ZFX expression, regulation, and function and the clinical implications of this protein in human pancreatic cancer (PCa). METHODS: One hundred and twenty patients with histologically confirmed PCa who underwent surgery were recruited for this study. Tumour samples and PCa cell lines were used to examine ZFX. Various cell functions related to tumourigenesis were assessed. In vivo mouse tumour xenografts were used to confirm the in vitro results. RESULTS: Patients with ZFX-positive tumours had worse overall survival than patients with ZFX-negative tumours. The depletion of ZFX using lentiviral shRNAs significantly inhibited cell proliferation by inducing cell cycle arrest in G0/G1 phase and resulted in increased cell apoptosis and invasive repression. In vivo studies confirmed that ZFX promoted tumour growth. Mechanistically, MAPK pathway activation was involved in the oncogenic functions of ZFX. CONCLUSIONS: ZFX acts as a putative oncogene in PCa and could be a novel therapeutic target for this disease.

EMP3, which is regulated by miR-663a, suppresses gallbladder cancer progression via interference with the MAPK/ERK pathway.

Gallbladder cancer (GBC) is the most common malignancy of the biliary tract and its molecular pathogenesis is poorly understood. Aberrant expression of epithelial membrane protein-3 (EMP3) was reported in different kinds of cancers. Our study aimed to explore the elusive functional roles and the underlying molecular mechanisms of EMP3 with respect to GBC progression. The results showed that human GBC tissues exhibited decreased levels of EMP3 compared with non-malignant tissues. Kaplan-Meier analysis indicated that low expression of EMP3 was associated with poor prognosis of GBC patients. Upregulation of EMP3 repressed GBC cell proliferation, migration and invasion both in vitro and in vivo. Conversely, EMP3 silencing promoted GBC cell growth and metastasis. Additionally, we found that EMP3 was a target gene of miR-663a, and downregulation of EMP3 in GBC was attributed to the overexpression of miR-663a. Furthermore, miR-663a was proven to be a tumor-promoting factor mediating GBC development. Finally, we demonstrated that downregulation of EMP3 activated MAPK/ERK signaling, which modulated GBC progression. These data showed the mechanism by which EMP3 suppresses GBC progression, suggesting that the miR-663a/EMP3/MAPK/ERK axis may be a novel therapeutic target for GBC treatment.

Asiatic acid inhibits proliferation, migration and induces apoptosis by regulating Pdcd4 via the PI3K/Akt/mTOR/p70S6K signaling pathway in human colon carcinoma cells.

Previous studies have demonstrated that asiatic acid (AA), the major component of Centella asiatica, is able to meditate cytotoxic and anticancer effects on various types of carcinoma cells. In order to investigate the molecular mechanism that underlies the antitumor effect of AA, the present study investigated the effects of AA on proliferation, migration and apoptosis of SW480 and HCT116 colon cancer cells. Viability and changes in cell morphology in the cells were assessed by MTT assay and transmission electron microscopy, respectively. Colony formation analysis was used to observe proliferation of the single cell, and migratory ability of the cells was assessed by performing Transwell migration assay. Hoechst 33342 nuclear staining and flow cytometry were used to assess apoptosis in colon carcinoma cells. The expression of proteins associated with the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/p70S6K signaling pathway and epithelial-mesenchymal transition (EMT) marker were analyzed by western blotting. The present study revealed that proliferation and migration of colon carcinoma cells were inhibited by AA in a dose-dependent and time-dependent manner. Numerous apoptotic bodies were observed, and G2/M and S phase progression were delayed in colon cancer cells treated with AA, but not in the control group. A number of phosphorylated proteins, including PI3K, Akt (Ser473), mTOR, ribosomal protein S6 kinase (p70S6K) downregulated, while the expression of Pdcd4 was upregulated following treatment with AA. Additionally, AA affects expression of EMT markers in a dose-dependent manner. On the basis of these results, it was concluded that AA inhibited proliferation, migration and induced apoptosis of colon cancer cells by regulating Pdcd4 via the PI3K/Akt/mTOR/p70S6K signaling pathway. These observations suggest that AA may be a potential therapeutic agent for the treatment of colon carcinoma.

MicroRNA-30a-5p inhibits gallbladder cancer cell proliferation, migration and metastasis by targeting E2F7.

Gallbladder carcinoma (GBC), the most common malignant tumour of the bile duct, is highly aggressive and has a poor prognosis. MicroRNA-30a-5p (miR-30a-5p) is an important tumour suppressor that participates in many aspects of carcinogenesis and cancer development. However, the role of miR-30a-5p in GBC development remains to be determined, as do the mechanisms underlying its effects in GBC. Using samples collected from 42 subjects with gallbladder carcinoma (GBC), we showed decreased miR-30a-5p expression in the primary lesions vs. non-tumour adjacent tissues (NATs). Decreased miR-30a-5p was associated with shorter disease-free survival (DFS) and overall survival (OS). Inhibiting miR-30a-5p expression in 2 representative GBC cell lines (GBC-SD and NOZ) increased cell proliferation, migration, invasiveness, as well as ß-catenin nuclear translocation, vice versa. In nude mice, NOZ cells transfected with miR-30a-5p mimics grew slower (vs. miR-NC) upon subcutaneous inoculation, and had lower rate of hepatic metastasis upon spleen inoculation. Dual luciferase assay confirmed that E2F transcription factor 7 (E2F7) was a direct target of miR-30a-5p and antagonized the effects induced by miR-30a-5p downregulation in GBC cells. MiR-30a-5p attenuates the EMT and metastasis in GBC cells by targeting E2F7, suggesting miR-30a-5p is a tumour suppressor that may serve as a novel potential prognostic biomarker or molecular therapeutic target for GBC.