• AcTMX3
• Arma chinensis
• antioxidant defence
• diapause
• protein disulphide isomerase

• Animals
• Diapause, Insect
• Insect Proteins/metabolism
• Insect Proteins/genetics
• Antioxidants/metabolism
• Moths/genetics
• Moths/metabolism
• Moths/growth & development
• Thioredoxins/metabolism
• Thioredoxins/genetics
• Amino Acid Sequence
• Membrane Proteins/metabolism
• Membrane Proteins/genetics
• Phylogeny
• Sequence Alignment

• 2024XM07 Major Projects of China National Tobacco Corporation Guizhou Province
• 2023YFD1400600 National Key R&D Program of China
• CAAS-ZDRW202203 National Key R&D Program of China
• International Science and Technology Innovation Program of Chinese Academy of Agricultural Sciences

• BLCA
• bladder cancer
• machine learning
• neoantigen
• neoantigen‐related genes

• Humans
• Urinary Bladder Neoplasms/genetics
• Algorithms
• Drug Evaluation, Preclinical
• DNA-Binding Proteins
• Nuclear Proteins
• Transcription Factors

• cancer disparities
• candidate protein targets
• cardio-metabolic disparities
• innate immune variants
• pleiotropic actions
• population-enriched variants

• Male
• Humans
• Diabetes Mellitus, Type 2/genetics
• Prostatic Neoplasms
• Ethnicity
• Non-alcoholic Fatty Liver Disease
• Immunity, Innate/genetics

• R01 MD017405 NIMHD NIH HHS
• U54 MD007602 NIMHD NIH HHS
• National Institutes of Health

• endometrial cancer

• Female
• Humans
• MicroRNAs/metabolism
• TRPM Cation Channels/genetics
• Transforming Growth Factor beta/metabolism
• Cell Line, Tumor
• Cell Proliferation/genetics
• Endometrial Neoplasms/pathology
• Protein Disulfide-Isomerases/metabolism

• 81874105 National Natural Science Foundation of China (National Science Foundation of China)

• Bladder cancer
• Hub gene
• Prognosis

• Animals
• Mice
• Carcinoma, Transitional Cell
• DNA Copy Number Variations
• Prognosis
• Tumor Microenvironment
• Urinary Bladder
• Urinary Bladder Neoplasms/drug therapy
• Humans

• drug sensitivity
• hepatocellular carcinoma
• immune microenvironment
• molecular subtypes
• unfolded protein response (UPR)

• TCGA
• bladder cancer
• chemotherapy
• immunotherapy
• unfolded protein response

Imatinib is a nontoxic tyrosine kinase inhibitor, used in the treatment of advanced renal cell carcinoma. However, some patients with renal cell carcinoma develop resistance to imatinib. Protein disulfide isomerase family 6 (PDIA6) was involved in the chemo-resistance of lung adenocarcinoma. In this study, the effect of PDIA6 on imatinib-resistance of renal cell carcinoma was investigated. First, PDIA6 was found to be up-regulated in the imatinib-resistant renal cell carcinoma tissues and cells. Functional assays showed that knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells to imatinib through decreasing the half-maximal inhibitory concentration (IC50) of imatinib-resistant renal cell carcinoma cells. Secondly, cell proliferation of imatinib-resistant renal cell carcinoma cells was suppressed by PDIA6 silencing, and the apoptosis was promoted with reduced Bcl-2, enhanced Bax and cleaved caspase-3. Moreover, the interference of PDIA6 increased phosphorylation of H2A histone family member X (γH2AX), while decreased Rad51 and phosphorylated DNA-dependent protein kinase (DNA-PK) (p-DNA-PK) in imatinib-resistant renal cell carcinoma cells. Lastly, protein expression levels of Wnt3a and Frizzled1 (FZD1) in imatinib-resistant renal cell carcinoma cells were down-regulated by silencing of PDIA6. Over-expression of FZD1 attenuated PDIA6 silencing-induced increase in cell apoptosis and decrease in cell proliferation in imatinib-resistant renal cell carcinoma cells. In conclusion, knockdown of PDIA6 sensitized imatinib-resistant renal cell carcinoma cells into imatinib through inactivation of Wnt3a-FZD1 axis.

• PDIA6
• Wnt3a-Fzd1
• imatinib-resistant
• renal cell carcinoma cells

• CSN5
• PDIA6
• Pancreatic cancer
• β-catenin signaling pathway

• Adult
• Aged
• Aged, 80 and over
• Animals
• B7-H1 Antigen/genetics
• B7-H1 Antigen/metabolism
• COP9 Signalosome Complex/biosynthesis
• COP9 Signalosome Complex/genetics
• Deubiquitinating Enzymes/genetics
• Deubiquitinating Enzymes/metabolism
• Disease Progression
• Female
• Humans
• Intracellular Signaling Peptides and Proteins/biosynthesis
• Intracellular Signaling Peptides and Proteins/genetics
• Male
• Mice, Inbred BALB C
• Mice, Nude
• Middle Aged
• Neoplasm Grading/methods
• Pancreatic Neoplasms/genetics
• Pancreatic Neoplasms/immunology
• Pancreatic Neoplasms/metabolism
• Peptide Hydrolases/biosynthesis
• Peptide Hydrolases/genetics
• Protein Disulfide-Isomerases/biosynthesis
• Protein Disulfide-Isomerases/genetics
• Tumor Escape/physiology
• beta Catenin/genetics
• beta Catenin/metabolism
• Mice

Bioinformatics approaches have proven useful in understanding biological responses to spaceflight. Spaceflight experiments remain resource intensive and rare. One outstanding issue is how to maximize scientific output from a limited number of omics datasets from traditional animal models including nematodes, fruitfly, and rodents. The utility of omics data from invertebrate models in anticipating mammalian responses to spaceflight has not been fully explored. Hence, we performed comparative analyses of transcriptomes of soleus and extensor digitorum longus (EDL) in mice that underwent 37 days of spaceflight. Results indicate shared stress responses and altered circadian rhythm. EDL showed more robust growth signals and Pde2a downregulation, possibly underlying its resistance to atrophy versus soleus. Spaceflight and hindlimb unloading mice shared differential regulation of proliferation, circadian, and neuronal signaling. Shared gene regulation in muscles of humans on bedrest and space flown rodents suggest targets for mitigating muscle atrophy in space and on Earth. Spaceflight responses of C. elegans were more similar to EDL. Discrete life stages of D. melanogaster have distinct utility in anticipating EDL and soleus responses. In summary, spaceflight leads to shared and discrete molecular responses between muscle types and invertebrate models may augment mechanistic knowledge gained from rodent spaceflight and ground-based studies.

• animal models
• bedrest
• cross-species comparison
• hindlimb unloading
• microgravity
• muscle
• spaceflight
• transcriptomics

• Animals
• Caenorhabditis elegans
• Circadian Rhythm/physiology
• Databases, Genetic
• Drosophila melanogaster
• Extraterrestrial Environment
• Gene Expression/genetics
• Gene Expression Profiling/methods
• Hindlimb Suspension
• Mice
• Models, Animal
• Muscle, Skeletal/pathology
• Muscular Atrophy/pathology
• Space Flight
• Stress, Physiological/physiology
• Transcriptome/genetics
• Weightlessness/adverse effects

Although long non-coding (lnc)RNAs have been reported to be involved in the pathological development of bladder cancer, the functions of lncRNA prostate cancer-associated transcript 6 (PCAT6) and its underlying mechanism of action in bladder cancer remain unknown. The present study aimed to investigate the effect of PCAT6 in bladder cancer progression and explore its potential application as a novel treatment target. The expression of PCAT6 and miR-143-3p in bladder cancer tissues, adjacent normal tissues and cell lines was measured using reverse transcription-quantitative PCR. Fluorescence in situ hybridization assay was used to detect the subcellular localization of PCAT6. MTT, EdU, Transwell and wound healing assays were conducted to assess the biological function of PCAT6 on cell proliferation, migration and invasion. Putative binding sites between miR-143-3p and PCAT6 or PDIA6 were predicted using starBase, Lncbase and TargetScan analyzes. Dual-luciferase reporter assay was also used to confirm the potential binding between PCAT6 and miR-143-3p. RNA immunoprecipitation assay was performed to verify the possible interaction between PCAT6 and miR-143-3p. Western blotting was used to measure the expression of PDIA6. The results demonstrated that the expression levels of PCAT6 were upregulated in bladder cancer tissues relative to those in adjacent normal bladder tissues. Knockdown of PCAT6 served a role in suppressing the proliferation, migration and invasion of T24T and EJ bladder cancer cells. PCAT6 knockdown contributed to a reduction of PDIA6 expression at the mRNA and protein levels compared with that in negative control-transfected cells, whilst the miR-143-3p inhibitor partially mitigated this reduction effect. In addition, rescue experiments revealed that the miR-143-3p inhibitors reversed the effects of PCAT6 silencing on the malignant phenotypes of bladder cancer. Collectively, the results of the present study demonstrated that PCAT6 may serve an oncogenic role in bladder cancer via the miR-143-3p/PDIA6 axis. These results may provide a potential therapeutic target for the treatment of bladder cancer.

• bladder cancer
• long non-coding RNA
• microRNA-143-3p
• prostate cancer-associated transcript 6
• protein disulfide isomerase A6

• Apis cerana cerana
• Oxidative stress
• PDIA6
• RNA interference (RNAi)
• Site-directed mutagenesis
• Survival function

• Animals
• Antioxidants
• Bees/genetics
• Escherichia coli
• Hydrogen Peroxide
• Oxidation-Reduction
• Oxidative Stress

• ER quality control
• NMR
• P5
• SAXS
• calcium binding
• dimerization motif
• oxidative protein folding
• protein disulfide isomerase

Accumulated evidence has demonstrated that aerobic glycolysis serves as a regulator of tumor cell growth, invasion, and angiogenesis. Herein, we explored the role of protein disulfide isomerase family 6 (PDIA6) in the aerobic glycolysis and the progression of oral squamous cell carcinoma (OSCC).

The expression pattern of PDIA6 in OSCC tissues was determined by qPCR and western blotting. Lentivirus and small interfering RNAs (siRNAs) were introduced into cells to upregulate and downregulate PDIA6 expression. CCK-8, flow cytometry, transwell, and xenotransplantation models were applied to detect cell proliferation, apoptosis, migration, invasion, and tumorigenesis, respectively.

A high expression pattern of PDIA6 was observed in OSCC tissues, which was closely associated with lower overall survival and malignant clinical features in OSCC. Compared with the control group, overexpression of PDIA6 induced significant enhancements in cell growth, migration, invasiveness, and tumorigenesis and decreased cell apoptosis, while knockdown of PDIA6 caused opposite results. In addition, overexpression of PDIA6 increased glucose consumption, lactate production, and ATP level in OSCC cells.

This study demonstrated that PDIA6 expression was elevated in OSCC tissues, and overexpression of it promoted aerobic glycolysis and OSCC progression.

• Aerobic glycolysis
• Migration
• PDIA6
• Proliferation
• Tumorigenesis

Bladder cancer (BC) is a common malignancy worldwide that accounts for 3% of global cancer diagnoses. Chemotherapy resistance limits the therapeutic effect of chemotherapeutic agents in patients with BC. Prolyl 4-hydroxylase, beta polypeptide (P4HB) is an endoplasmic reticulum (ER) chaperone that is upregulated in bladder cancer tissues (The Cancer Genome Atlas, TCGA datasets). Knockdown or suppression of P4HB exerts anticancer activity and sensitizes cells to chemotherapy in various types of cancer.

We aimed to investigate whether the inhibition of P4HB enhances the anticancer efficacy of gemcitabine (GEM) in BC cells and to study the underlying molecular mechanisms.

The P4HB mRNA expression levels of 411 BC patients from the TCGA database and P4HB expression level of eighty BC paraffin-embedded samples detected by immunohistochemistry (IHC) staining were used for clinical feature and prognostic analyses. Bioinformatics analysis was utilized for the mechanistic investigation. Highly P4HB-expressed BC cell lines (T24 and 5637) treated with P4HB inhibitor (Bacitracin, BAC) were used to study the effects of BAC on the sensitivity of BC cells to GEM and the potential mechanism. P4HB inhibition experiments were performed in highly P4HB-expressed BC cells, and cell viability, colony formation, cell cycle, reactive oxygen species (ROS), apoptosis and pathway proteins were assessed in T24 and 5637 cells.

Western blot analysis showed that P4HB expression was significantly higher in BC tissues than in paired normal tissues. IHC showed that patients with high P4HB expression had a poorer overall survival (OS) rate than those with low P4HB expression. Furthermore, increased P4HB expression was demonstrated to be an independent prognostic marker for BC. Functionally, P4HB inhibition by BAC decreased the cell proliferation ability in vitro. Moreover, BAC treatment sensitized BC cells to GEM. Molecular mechanism analysis indicated that inhibition of P4HB by BAC treatment enhanced the anticancer effects of GEM through increasing cellular ROS content and promoting cell apoptosis and PERK/eIF2α/ATF4/CHOP signaling.

High P4HB expression was significantly correlated with poor prognosis in BC patients. Inhibition of P4HB by BAC decreased the cell proliferation ability and sensitized BC cells to GEM by activating apoptosis and the PERK/eIF2α/ATF4/CHOP pathways.

• ER stress
• P4HB
• bacitracin
• bladder cancer
• gemcitabine

Increasing evidence from structural and functional studies has indicated that protein disulphide isomerase (PDI) has a critical role in the proliferation, survival and metastasis of several types of cancer. However, the molecular mechanisms through which PDI contributes to glioma remain unclear. Here, we aimed to investigate whether the differential expression of 17 PDI family members was closely related to the different clinicopathological features in gliomas from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas data sets. Additionally, four subgroups of gliomas (cluster 1/2/3/4) were identified based on consensus clustering of the PDI gene family. These findings not only demonstrated that a poorer prognosis, higher WHO grade, lower frequency of isocitrate dehydrogenase mutation and higher 1p/19q non‐codeletion status were significantly correlated with cluster 4 compared with the other clusters, but also indicated that the malignant progression of glioma was closely correlated with the expression of PDI family members. Moreover, we also constructed an independent prognostic marker that can predict the clinicopathological features of gliomas. Overall, the results indicated that PDI family members may serve as possible diagnostic markers in gliomas.

• glioma
• prognostic signature
• protein disulphide isomerase

The present study focused on the expression patterns, prognostic values and potential mechanism of the PDI family in gliomas. Most PDI family members’ mRNA expressions were observed significantly different between gliomas classified by clinical features. Construction of the PDI signature, cluster and risk score models of glioma was done using GSVA, consensus clustering analysis, and LASSO Cox regression analysis respectively. High values of PDI signature/ risk score and cluster 1 in gliomas were associated with malignant clinicopathological characteristics and poor prognosis. Analysis of the distinctive genomic alterations in gliomas revealed that many cases having high PDI signature and risk score were associated with genomic aberrations of driver oncogenes. GSVA analysis showed that PDI family was involved in many signaling pathways in ERAD, apoptosis, and MHC class I among many more. Prognostic nomogram revealed that the risk score was a good prognosis indicator for gliomas. The qRT-PCR and immunohistochemistry confirmed that P4HB, PDIA4 and PDIA5 were overexpressed in gliomas. In summary, this research highlighted the clinical importance of PDI family in tumorigenesis and progression in gliomas.

• GBM
• PDI
• PDI family
• glioma
• prognosis

• ERp72
• Endoplasmic reticulum stress response
• PDI family
• PDIA4
• Platelet
• Tumor

• RNA-binding proteins
• c-Myc
• interactomics
• proteomics

• Chromatin Immunoprecipitation
• Humans
• K562 Cells
• Mass Spectrometry/methods
• Protein Interaction Domains and Motifs
• Proto-Oncogene Proteins c-myc/metabolism
• RNA, Messenger/metabolism
• RNA-Binding Proteins/metabolism

• P41 RR002301 NCRR NIH HHS
• R01 CA193481 NCI NIH HHS
• T32 GM008505 NIGMS NIH HHS

Gastric cancer (GC) is a common tumor-associated lethal disease, and invasiveness and metastasis are primary challenges in its clinical treatment. Hypoxia microenvironment cannot be ignored in the process of metastasis. Hypoxia inducible factor-1α (HIF-1α) is the core component of the hypoxia signaling pathway. The aim of this study was to identify potential hub genes and signaling pathways associated with HIF-1α. We explored the invasiveness- and metastasis-associated phenotype of GC via bioinformatics analysis and molecular studies. Differentially expressed genes (DEGs) were identified in GC cells and HIF-1α-knockdown GC cells. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed, and a protein-protein interaction (PPI) network was constructed. Hub genes were identified via centrality analysis and Molecular Complex Detection (MCODE) module analysis. The findings suggested that prolyl 4-hydroxylase beta polypeptide (P4HB) has strong associations with HIF-1α. Further, we observed that HIF-1α and P4HB were upregulated in SGC-7901 and BGC-823 cells. In addition, inhibition of HIF-1α expression reduced invasion and metastasis in GC cells; this effect was partially reversed by P4HB overexpression. Our results confirm that P4HB plays a significant role in the regulatory network of HIF-1α. Therefore, HIF-1α and P4HB may be considered potential biomarkers of GC.

• Cyanuric acid
• Liver toxicity
• Melamine
• Mouse
• Proteomics

• Animals
• Chemical and Drug Induced Liver Injury/genetics
• Gene Expression/drug effects
• Liver/drug effects
• Liver/metabolism
• Male
• Metabolic Networks and Pathways/drug effects
• Mice
• Proteomics
• Triazines/toxicity

• Apoptosis
• Autophagy
• MAP4K1
• NSCLC
• PDIA6

• Adult
• Aged
• Animals
• Antineoplastic Agents/pharmacology
• Apoptosis/drug effects
• Apoptosis/genetics
• Autophagy/drug effects
• Autophagy/genetics
• Biomarkers, Tumor
• Carcinoma, Non-Small-Cell Lung/genetics
• Carcinoma, Non-Small-Cell Lung/metabolism
• Carcinoma, Non-Small-Cell Lung/mortality
• Carcinoma, Non-Small-Cell Lung/pathology
• Caspases/metabolism
• Cell Line, Tumor
• Cell Proliferation
• Female
• Humans
• Immunohistochemistry
• JNK Mitogen-Activated Protein Kinases/metabolism
• Lung Neoplasms/genetics
• Lung Neoplasms/metabolism
• Lung Neoplasms/mortality
• Lung Neoplasms/pathology
• MAP Kinase Signaling System
• Male
• Mice
• Middle Aged
• Models, Biological
• Neoplasm Grading
• Neoplasm Staging
• Prognosis
• Protein Disulfide-Isomerases/genetics
• Protein Disulfide-Isomerases/metabolism
• Protein Serine-Threonine Kinases/metabolism

• Developmental toxicity
• Maternal transfer toxicity
• TDCIPP
• Zebrafish

• Animals
• Biological Products/metabolism
• Down-Regulation
• Female
• Larva/drug effects
• Male
• Maternal Exposure
• Organophosphates/metabolism
• Organophosphorus Compounds/toxicity
• Phosphates/metabolism
• Water Pollutants, Chemical/toxicity
• Zebrafish/metabolism
• Zebrafish/physiology

• beta catenin
• small molecule libraries
• urinary bladder diseases

• Animals
• Apoptosis/drug effects
• Cell Line, Tumor
• Cell Proliferation/drug effects
• Humans
• Mice
• Mice, Inbred BALB C
• Oils, Volatile/pharmacology
• Urinary Bladder Neoplasms/drug therapy
• Urinary Bladder Neoplasms/genetics
• Urinary Bladder Neoplasms/metabolism
• Wnt Proteins/metabolism
• Wnt Signaling Pathway/drug effects
• Xenograft Model Antitumor Assays/methods
• beta Catenin/metabolism

To investigate the relationship between hypoxia-inducible factor-1α (HIF-1α), prolyl 4-hydroxylase beta (P4HB) expression, and clinicopathologic parameters, as well as the prognostic value of these genes for patients with gastric cancer (GC).

Hypoxia is a critical factor that shapes the GC microenvironment. In previous reports, we have demonstrated that P4HB is a potential target of HIF-1α. In the present study, gene expression profiling interactive analysis (GEPIA) was used to analyze the relationship between P4HB and hypoxia-associated genes. To this end, 428 GC tissue samples were used to analyze the expression of HIF-1α and P4HB via immunohistochemical staining. Patient samples were classified as having weak-expression or over-expression both in terms of HIF-1α and P4HB. Correlations between biomarkers and clinicopathological factors were analyzed to predict survival.

P4HB demonstrated a positive correlation with hypoxia-associated genes (P < 0.05). HIF-1α and P4HB overexpression have a significant correlation with TNM staging (χ² = 23.32, P = 0.00; χ² = 65.64, P = 0.00) and peritoneum cavity metastasis (χ² = 12.67, P = 0.00; χ² = 39.29, P = 0.00). In univariate analysis, patients with a high HIF-1α expression trend had a shorter disease-free survival (DFS: 44.80 mo vs 22.06 mo) and overall survival (OS: 49.58 mo vs 39.92 mo). P4HB overexpression reflected similar results: patients with over-expression of P4HB had a shorter survival time than those with weak-expression (DFS: 48.03 mo vs 29.64 mo, OS: 52.48 mo vs 36.87 mo). Furthermore, HIF-1α is also a clinicopathological predictor of dismal prognosis according to multivariate analysis (DFS, 95%CI: 0.52-0.88, P < 0.00; OS, 95%CI: 0.50-0.85, P < 0.00). However, P4HB was meaningful in DFS (95%CI: 0.58-1.00, P < 0.05) but not in OS (95%CI: 0.72-1.23, P > 0.05).

Overexpression of HIF-1α and P4HB is associated with poor prognosis in patients with GC. Thus, these genes may be potential prognostic biomarker candidates in GC.

• Gastric cancer
• Hypoxia inducible factor-1α
• Prolyl 4-hydroxylase beta polypeptide
• Overall survival
• Clinicopathological predictors
• Disease free survival

• Adult
• Aged
• Aged, 80 and over
• Biomarkers, Tumor/metabolism
• Cell Hypoxia
• Disease-Free Survival
• Female
• Gene Expression Profiling/methods
• Humans
• Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
• Kaplan-Meier Estimate
• Male
• Middle Aged
• Neoplasm Staging
• Procollagen-Proline Dioxygenase/metabolism
• Prognosis
• Protein Disulfide-Isomerases/metabolism
• Retrospective Studies
• Stomach/pathology
• Stomach Neoplasms/mortality
• Stomach Neoplasms/pathology

Protein disulfide isomerase (PDI) is an oxidoreductase that is overexpressed in several cancers. PDI family members (PDIs) play a role in various diseases including cancer. Select PDIs were reported as useful markers in other cancers but their expression in ovarian cancer has not been thoroughly assessed. We sought to evaluate the expression of PDI, PDIA6, PDIR, ERp57, ERp72 and AGR3 in ovarian cancer patient samples and examine their prognostic significance.

TMA samples from 415 tissues collected from three cancer centers (UM, USC, and KCCRI) were used to assess the expression levels of PDI family proteins using IHC.

We observed significant increases in PDI (p = 9.16E-36), PDIA6 (p = 5.51E-33), PDIR (p = 1.81E-12), ERp57 (p = 9.13E-07), ERp72 (p = 3.65E-22), and AGR3 (p = 4.56E-24) expression in ovarian cancers compared to normal tissues. Expression of PDI family members also increases during disease progression (p <0.001). All PDI family members are overexpressed in serous ovarian cancer (p<0.001). However, PDI, PDIA6, PDIR, ERp72 and AGR3 are more significantly overexpressed (p<0.001) than ERp57 (p<0.05) in clear cell ovarian carcinoma. Importantly, overexpression of PDI family members is associated with poor survival in ovarian cancer (p = 0.045 for PDI, p = 0.047 for PDIR, p = 0.037 for ERp57, p = 0.046 for ERp72, p = 0.040 for AGR3) with the exception of PDIA6 (p = 0.381).

Our findings demonstrate that select PDI family members (PDI, PDIR, ERp72, ERp57 and AGR3) are potential prognostic markers for ovarian cancer.

• PDI family proteins
• clinical outcome
• ovarian cancer
• patient survival
• tissue microarray (TMA)

• COA1 (cytochrome C oxidase assembly factor 1 homolog)
• Giant cell tumor of bone
• PDIA6 (protein disulfide isomerase family A, member 6)
• miR-127-3p
• miR-376a-3p
• microRNA

• Animals
• Bone Neoplasms/genetics
• Bone Neoplasms/metabolism
• Bone Neoplasms/pathology
• Cell Line, Tumor
• Cell Proliferation/genetics
• Chick Embryo
• Electron Transport Complex IV/genetics
• Electron Transport Complex IV/metabolism
• Genes, Tumor Suppressor
• Giant Cell Tumor of Bone/genetics
• Giant Cell Tumor of Bone/metabolism
• Giant Cell Tumor of Bone/pathology
• Heterografts
• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Protein Disulfide-Isomerases/genetics
• Protein Disulfide-Isomerases/metabolism
• Transfection