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PubMed2007

Transcriptional and proteomic profiles of group B Streptococcus type V reveal potential adherence proteins associated with high-level invasion.

Group B Streptococcus (GBS) is an opportunistic organism that can harmlessly colonize the human gut, vagina, and rectum but can also cause pneumonia, sepsis, and meningitis in neonates born to colonized mothers. We have shown previously that growth rate and oxygen level regulate the ability of GBS to invade eukaryotic cells in vitro. Herein we extend and expand on these observations to show that GBS type V, an emergent serotype, grown in a chemostat at a cell mass-doubling time (t(d)) of 1.8 h with oxygen invaded human ME-180 cervical epithelial cells in large numbers compared with those grown at the same t(d) without oxygen or at a slower t(d) of 11.0 h. The fact that several GBS type V cell wall-associated and membrane proteins were expressed exclusively under the invasive growth condition prompted an investigation, using genomics and proteomics, of all upregulated genes and proteins. Several proteins with potential roles in adherence were identified, including an undefined surface antigen (SAG1350), a lipoprotein (SAG0971), penicillin-binding protein 2b (SAG0765), glyceraldehyde-3-phosphate dehydrogenase (SAG0823), and an iron-binding protein (SAG1007). Mouse antisera to these five proteins inhibited binding of GBS type V to ME-180 cells by > or =85%. Recombinant undefined surface antigen (SAG1350), lipoprotein (SAG0971), and penicillin-binding protein 2b (SAG0765) each bound to ME-180 cells in a dose-dependent fashion, confirming their ability to act as ligands. Collectively, these data increase the number of potential GBS adherence factors and also suggest a role for these surface-associated proteins in initial pathogenic events.

Bacterial Adhesion↗
PubMed2026

Serum Proteomic Profiling Implicates a Dysregulated Neurohormonal-Inflammatory Axis in Post-Fontan Sinus Tachycardia.

BACKGROUND: Postoperative sinus tachycardia is a poorly understood complication following the Fontan procedure. The molecular signaling cascades triggering acute tachycardia remain uncharacterized, limiting therapeutic innovation. Here, we present a retrospective study leveraging serum proteomics and machine learning to identify the molecular drivers of postoperative Fontan sinus tachycardia. METHODS: We integrated a clinically relevant ovine Fontan model with continuous telemetric heart rate monitoring and human patient data. Serum proteomics coupled with least absolute shrinkage and selection operator and Boruta machine learning algorithms were used to identify protein panels predictive of postoperative sinus tachycardia. Cross-species validation was performed by comparing proteomic signatures from sheep and pediatric patients undergoing Glenn or Fontan surgery. RESULTS: Ovine Fontan animals demonstrated significant heart rate elevation beginning on postoperative day 1, peaking at postoperative day 3 (159.4±11.7 bpm versus preoperative, 105.3±10.5 bpm; P=0.0002), before trending toward baseline by postoperative day 10. This pattern was mirrored in human patients with a more modest magnitude. Surgical controls did not exhibit tachycardia. The principal component most correlated with heart rate (principal component 1: r=0.78, P=2.2×10-4) was enriched for inflammatory and neural pathways. The Boruta algorithm identified an 11-protein panel with strong predictive power (area under the receiver operating characteristic curve, 0.963). Cross-species comparison demonstrated that angiotensinogen, angiotensin-converting enzyme, and pentraxin 3 were similarly dysregulated in both species postoperatively. CONCLUSIONS: This study provides molecular evidence implicating a dysregulated neurohormonal-inflammatory axis in acute postoperative Fontan sinus tachycardia and establishes a foundation for developing targeted diagnostics and therapeutics for this complication.

Animals↗
PubMed2026

Coral color morphs exhibit distinct microbial and proteomic profiles linked to stress and immune mechanisms in a changing ocean.

BACKGROUND: Coral phenotypic plasticity facilitates acclimation and adaptation to environmental variability. Coral species often display a variety of color morphs, yet key biological and ecological implications of such phenotypic variation remain underexplored. Here, we present the first proteomic and untargeted lipidomic and metabolomic survey to explore the biological characteristics and potential ecological significance of different color morphs (pink and brown) of healthy Pocillopora verrucosa sampled along a latitudinal gradient. RESULTS: Our multi-omic approach elucidated distinct mechanisms associated with these dominant color morphs. We discovered bacterial indicators specific to each morph: putative pathogens such as Salmonella, Escherichia-Shigella, and carotenoid-producing Gemmatimonas were notably associated with the pink morph, whereas the brown morph was associated with potentially beneficial bacteria, such as Lysobacter, Acinetobacter, and Endozoicomonas. Despite these microbiome differences, the lipidome and metabolome of P. verrucosa were surprisingly homogeneous across colors and locations, suggesting similar metabolic performances during summer conditions. Key polar and apolar lipid classes, such as fatty acids, glycerophosphocholines, and retinoids, were prevalent. Notably, our proteomic analysis revealed morph-specific expressions, with pink morphs exhibiting enhanced levels of GFP-like proteins, Ankyrin, and the enzyme pullulanase, suggesting novel putative protective roles. In contrast, the brown morphs showed a higher abundance of heat shock proteins, indicating putative differential stress response capabilities. CONCLUSION: This comprehensive study provides the first proteomic survey of P. verrucosa and identifies key physiological pathways and trade-offs linked to color morphs, which can further contribute to enhancing our understanding of coral resilience in the face of climate change. SIGNIFICANCE STATEMENT: Understanding the phenotypic plasticity of corals is crucial for uncovering mechanisms of resilience in warming oceans, yet the biological significance of coral color morphs still needs to be explored. Using an innovative multi-omic approach (proteomics, lipidomics, and metabolomics), we provide the first comprehensive analysis of differences between pink and brown morphs of Pocillopora verrucosa. Our data reveal key taxa, potentially pathogenic or beneficial, associated with each morph, and suggest different strategies for each color morph to cope with heat stress, either expressing proteins involved in UV protection and heterotrophic activity or enhanced levels of heat stress resilience and DNA repair. These findings offer insights into the phenotypic plasticity of coral color morphs and their differential responses to climate change. Video Abstract.

Anthozoa↗
PubMed2026

Proteomic profiling of the aqueous extract from the antennal gland of the Pacific white shrimp, Litopenaeus vannamei.

The antennal gland (AnG) of decapod crustaceans has been proposed as a potential source of bioactive molecules involved in chemical communication; however, its protein composition remains largely unexplored. Here, we present the first reference proteomic map of the aqueous extract from the antennal gland of the Pacific white shrimp Litopenaeus vannamei. Protein extracts from immature and mature females were analyzed using an integrated workflow combining one-dimensional SDS-PAGE, reverse-phase high-performance liquid chromatography (RP-HPLC), and nanoLC-tandem mass spectrometry. Electrophoretic and chromatographic analyses revealed a high degree of qualitative similarity between reproductive stages. SDS-PAGE resolved six major protein bands (∼227, 166, 77, 42, 35, and 17 kDa), most comprising multiple co-migrating proteins as revealed by LC-MS/MS. Hemocyanin was identified as the predominant protein and was detected across several electrophoretic bands. Additional proteins were associated with innate immunity, including β-1,3-glucan-binding protein and coagulable hemolymph protein; reproductive processes, including vitellogenin, spermatogonial stem-cell renewal factor, farnesoic acid O-methyltransferase, estrogen sulfotransferase, and prostaglandin reductase 1; as well as energy metabolism, protein homeostasis, cytoskeletal organization, and intracellular trafficking. Because several identified proteins are widely distributed or known hemolymph components, their detection cannot be assumed to reflect AnG-specific expression or function. Collectively, these findings establish a molecular reference for the L. vannamei AnG and reveal protein components associated with multiple physiological processes. This dataset provides a proteomic framework for future comparative and functional studies aimed at elucidating antennal gland physiology and experimentally evaluating the potential involvement of proteinaceous or peptide-based molecules in chemical communication in decapod crustaceans.

Animals↗
PubMed2002

Targeted proteomic profiling of renal Na(+) transporter and channel abundances in angiotensin II type 1a receptor knockout mice.

The renal tubule transporters responsible for Na(+) and water transport along the nephron have been identified and cloned, permitting comprehensive analysis of transporter protein abundance changes in complex physiological models by using a "targeted proteomics" approach. Here, we apply this approach to screen renal homogenates from mice in which the gene for the angiotensin II type 1a (AT(1a)) receptor has been deleted (versus wild-type mice) to determine which sodium transporters and channels are regulated by the AT(1a) receptor at the protein abundance level. In mice maintained on a low NaCl diet (<0.02% NaCl), (1) the abundances of 2 aldosterone-regulated transporters were markedly decreased in knockout versus wild-type mice, namely, the thiazide-sensitive cotransporter and the alpha-subunit of the amiloride-sensitive Na(+) channel (alpha-ENaC); (2) the abundances of beta-ENaC and gamma-ENaC were markedly increased; and (3) there were no significant changes in the abundances of the proximal tubule Na+-H(+) exchanger or the Na(+)-K(+)-2Cl(-) cotransporter of the thick ascending limb. When the experiment was repeated on higher NaCl diets (0.4% or 6% NaCl), the decrease in alpha-ENaC abundance persisted, whereas the other changes were abolished. Analysis of serum aldosterone concentration in AT(1a) knockout mice and wild-type mice on the low NaCl diet revealed the absence of a decrease with AT(1a) gene deletion (11.8 +/- 2.3 nmol/L for knockout mice and 5.7 +/- 0.8 nmol/L for wild-type mice [significantly increased]). These results reveal that the AT(1a) receptor plays an important role in regulation of Na(+) transporter and channel proteins in the "post-macula densa" region of the renal tubule via a mechanism that is not dependent on altered circulating aldosterone concentrations.

Angiotensin II↗
PubMed2006

Proteomic profiling of hepatocellular carcinoma in Chinese cohort reveals heat-shock proteins (Hsp27, Hsp70, GRP78) up-regulation and their associated prognostic values.

To facilitate the identification of candidate molecular biomarkers that are linked to the pathogenesis of hepatocellular carcinoma (HCC), we investigated protein-expression profiles of 146 tissue specimens including 67 pairs of tumors and adjacent non-tumors resected from HCC patients as well as 12 normal livers by 2-DE. Among the 1800 spots displayed in the liver proteome, a total of 90 protein species were found to be significantly different between the three groups (P < 0.05). Three of the top candidate markers up-regulated in HCC, with high receiver operating characteristic (ROC) curves, were identified by MS/MS analysis and belonged to the chaperone members: heat-shock protein (Hsp)27, Hsp70 and glucose-regulated protein (GRP)78. Over-expression of these chaperone proteins in HCC tissues was confirmed by Western blotting and immunohistochemistry. In correlation with clinico-pathological parameters, expression of Hsp27 was linked to alpha-fetoprotein level (P = 0.007) whereas up-regulation of GRP78 was associated with tumor venous infiltration (P = 0.035). No significant association of Hsp70 with any pathologic features was observed. The present HCC proteome analysis revealed that in response to the stressful cancerous microenvironment, tumor cells strived to increase the expression of chaperone proteins for cyto-protective function and to enhance tumor growth and metastasis.

Adolescent↗
PubMed2006

Proteome profiling in the rat Harderian gland.

The Harderian gland is an orbital gland located behind the ocular bulb in most terrestrial vertebrates probably functioning for production of lipid secretion to protect the eye. We herein present a protein reference database of the rat Harderian gland that may serve as analytical tool for future proteomic work, report lipid and porphyrin handling cascades, address sequence conflicts and report structures that have not been so far described by proteomics methods.

Amino Acid Sequence↗
PubMed2025

Plasma inflammatory proteome profiles identify MASLD among children with overweight or obesity.

BACKGROUND & AIMS: Pediatric metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly prevalent among children with overweight or obesity, yet its early diagnosis remains a major clinical challenge. This study aimed to identify circulating inflammatory proteins associated with MASLD and to develop a proteomic risk score (ProScore) to improve diagnostic accuracy. METHODS: In this cross-sectional study of 161 children (median age 8.5&#xa0;years) with overweight or obesity, MASLD was assessed by vibration-controlled transient elastography, with 42 cases identified. Plasma concentrations of 92 inflammation-related proteins were quantified using a high-throughput proximity extension assay. The ProScore was compared with eleven conventional anthropometric/metabolic indices (WHtR, METS-IR, SPISE, PNFI, VAI, LAP, TyG, TyG-ALT, TyG-WC, TyG-WHtR, and TyG-BMI) and a genetic risk score (GRS). Six machine learning algorithms were employed and diagnostic performance was assessed using area under the curve (AUC) with fivefold cross-validation. RESULTS: Fifteen proteins were significantly associated with MASLD. A six-protein panel (FGF-21, CDCP1, CD244, OPG, Flt3L, MCP-1) achieved the highest diagnostic accuracy (AUC&#x2009;=&#x2009;0.84), exceeding that of all conventional indices (AUC&#x2009;=&#x2009;0.65-0.78; all P&#x2009;<&#x2009;0.05). ProScore performance remained robust in school-based validation (AUC&#x2009;=&#x2009;0.83), with no substantial improvement when combined with conventional indices. Diagnostic accuracy was higher in children with lower GRS (AUC&#x2009;=&#x2009;0.92) than in those with higher GRS (AUC&#x2009;=&#x2009;0.80; P&#x2009;=&#x2009;0.003). CONCLUSIONS: A proteomic signature of systemic inflammation provides accurate, non-invasive identification of MASLD in at-risk children, outperforming conventional metabolic and genetic tools, and may have utility in clinical and public health settings.

Humans↗
PubMed2001

Proteomic profiling of the cancer microenvironment by antibody arrays.

Critical changes in protein expression that enable tumors to initiate and progress originate in the local tissue microenvironment, and there are increasing indications that these microenvironmental alterations in protein expression play critical roles in shaping and directing this process. As a model to better understand how patterns of protein expression shape the tissue microenvironment, we analyzed protein expression in tissue derived from squamous cell carcinoma of the oral cavity through an antibody microarray approach for high-throughput proteomic analysis. Utilizing laser capture microdissection to procure total protein from specific microscopic cellular populations, we demonstrate that quantitative, and potentially qualitative, differences in expression patterns of multiple proteins within epithelial cells reproducibly correlate with oral cavity tumor progression. Furthermore, differential expression of multiple proteins was also found in stromal cells surrounding and adjacent to regions of diseased epithelium that directly correlated with tumor progression of the epithelium. Most of the proteins identified in both cell types are involved in signal transduction pathways, thus we hypothesize that extensive molecular communication involving complex cellular signaling between epithelium and stroma play a key role in driving oral cavity cancer progression.

Antibodies, Neoplasm↗
PubMed2004

Screening for disease-markers and investigating drug effects by proteome profiling: can it meet expectations?

Drugs exert their functions mainly by affecting proteins. Therefore, it seems straightforward to focus on proteins in order to investigate drug effects. Unfortunately, proteins are of very high complexity, rendering it much more difficult to screen for protein alterations as compared to gene regulation. However, the efficiency and applicability of proteome analysis has been dramatically increased recently. We are on the way to be able to comprehensively assess disease-related proteome alterations, which may become an essential source of information for knowledge-based drug design. This review will provide an overview of current techniques in proteome analysis, focusing on screening technologies for biomedical research. An outlook at the future potential of proteomics supported by modern bioinformatics will highlight why proteomics is worth the effort.

Amino Acid Sequence↗
PubMed2006

Proteomic profiling distinguishes astrocytomas and identifies differential tumor markers.

Methods to permit more precise delineation of astrocytomas of different grades may have therapeutic utility. The authors selectively microdissected pure populations of cells from normal brain and astrocytomas. They performed two-dimensional protein gel electrophoresis (2DGE) followed by protein sequencing. Differential expression was confirmed immunohistochemically. 2DGE identified proteomic patterns and proteins that differentiated normal brain from tumor and distinguished astrocytomas of increasing grade.

Astrocytoma↗
PubMed2026

Targeted Modulation of Abundant Proteins Enhances Proteomic Profiling of Ovarian Cancer Ascites: A Pilot Technical Workflow Comparison.

Ascites from ovarian cancer patients are increasingly recognized as a valuable biofluid for cancer research, as its protein composition reflects the disease state and may reveal biomarkers of treatment sensitivity and response. However, the detection of low-abundance proteins is hindered by the presence of highly abundant proteins such as albumin. In this study, we evaluated five protein preparation methods for their effectiveness in depleting high-abundance or enriching low-abundance proteins in ovarian cancer ascites. The Norgen (Nor), Minutes (Min), and Perchloric acid (PerCA) methods were based on abundant protein depletion, while the Urine (Uri) and Nanomics (Nano) kits focused on low-abundance protein enrichment. Processed samples were analyzed using label-free quantitative bottom-up proteomics by LC-MS/MS, followed by a bioinformatics assessment. Compared with undepleted ascites (UnD), Min, Nor, Nano, and PerCA increased protein identifications, whereas Uri produced profiles similar to those of UnD. Notably, PerCA and Nano enabled the identification of distinct protein subsets associated with cancer-related pathways, including immune responses and autophagy. PerCA enriched transmembrane and secreted immunomodulatory glycoproteins, whereas Nano enrichment primarily captured secreted, nuclear, and cytoplasmic soluble proteins. Overall, our results show that both high-abundance protein depletion and low-abundance enrichment improve ascites proteome coverage, each offering distinct advantages in identifying biologically relevant low-abundance proteins.

Female↗
PubMedDate not supplied

Prediction of drug sensitivity and drug resistance in cancer by transcriptional and proteomic profiling.

The oncologist's challenges, particularly with advanced cancers, are (a) how to predict tumor response to a given drug or regimen; (b) how to predict which tumors of identical histology will remain indolent and which will be likely to progress; and (c) how to determine the appropriate timing of the emergence of drug-resistant cancer cells and hence switch to appropriate therapy. These issues are still unresolved; current clinical practice is hampered by the complexity and heterogeneity of anti-tumor drug resistance where multiple cellular, tumor microenvironment and host factors operate simultaneously. The rapid accumulation of genomic and proteomic databases for complex biological systems, such as cancer, together with advances in technology platforms, have paved the way to an increased molecular understanding and prediction of antitumor drug response. The complex phenotype of drug resistance can now be dissected and specific, clinically relevant markers pinpointed. Several microarray studies of genetic patterns from untreated and pre-treated cancers have provided "fingerprints" that can predict response to therapeutics. Nevertheless, such approaches require further validation in experimental models and in large clinical trials before their routine clinical use. Moreover, comparative transcriptional profiling alone is unlikely to predict drug sensitivity/resistance, a dynamic process where protein phosphorylation, protein trafficking, and protein-protein interactions with secondary effectors play key roles in the fate of cancer cells following therapeutic stress. Functional proteomics is potentially more predictive, but still faces technical challenges with regards to sampling, tumor heterogeneity, and lack of standardized methodologies. These obstacles are surmountable with current concerted research efforts and availability of powerful high-throughput genomic and proteomic instrumentations, and thus approaches to predict and overcome drug resistance could be rationalized.

Animals↗
PubMed2025

Proteome Profiling in Cerebrospinal Fluid Reveals Increased Levels of Peroxiredoxin 2 Discriminating Japanese Encephalitis Virus and Scrub Typhus Infection.

Japanese encephalitis virus (JEV) and scrub typhus (ST) are major etiological agents of acute encephalitis syndrome (AES) in India and South Asia. The pathophysiological changes at the molecular level caused by JEV and ST have yet to be studied in detail. The cerebrospinal fluid (CSF) proteomic landscape is a critical indicator of CNS pathology. Here, we conducted label-free quantitative proteomics on CSF from AES patients (n&#x2009;=&#x2009;15) to identify etiology-specific differentially expressed proteins (DEPs) linked to encephalitis. The key DEPs were validated via ELISA in CSF (n&#x2009;=&#x2009;49) and serum (n&#x2009;=&#x2009;33). Our findings revealed 50 proteins exhibited differential expression across JEV and ST groups, with a notable subset of three proteins, PRDX2, KLK6, and TTR. PRDX2 and KLK6 were markedly elevated in JEV CSF (AUC: 0.8933 and 0.9689) but not in ST or non-JEV AES, while TTR was reduced in JEV yet elevated in ST (AUC: 0.5619 vs. 0.8238). Further, PRDX2 upregulation was validated in JEV-infected mouse brains and cortical neurons. Overexpression of PRDX2 in human neuroblastoma cells correlated with enhanced antiviral gene expression, p-STAT1, p-AKT (ser473), and viral replication. Thus, our comprehensive proteomic analysis of CSF identifies PRDX2 as an important circulatory protein, differentially expressed between JEV and ST, with high specificity and enhancing viral propagation, underscoring its role in viral propagation and pathogenesis.

Humans↗
PubMed2026

Pilot study identifying distinct circulating proteomic profiles associated with longitudinal CT-defined fibrotic and inflammatory sarcoidosis.

INTRODUCTION: Pulmonary sarcoidosis exhibits heterogeneous clinical trajectories ranging from self-limited disease resolution to chronic progressive fibrosis, yet reliable biomarkers capable of distinguishing these disease patterns remain lacking. Whether longitudinal CT-defined sarcoidosis phenotypes are associated with distinct circulating molecular signatures remains unknown. METHODS: We performed high-throughput plasma proteomics (SomaScan 11K) in participants with pulmonary sarcoidosis classified into longitudinal chest CT-defined progressive fibrosis, progressive nodular inflammatory disease, or resolving disease trajectories, along with healthy controls. CT phenotypes were assigned based on predefined longitudinal changes in reticulation, traction bronchiectasis, nodular involvement, and mediastinal lymphadenopathy across serial CT scans. One plasma sample per participant was selected from the study visit corresponding to the CT time point at which criteria for the assigned longitudinal phenotype were met. Principal component analysis, hierarchical clustering, pathway enrichment, and correlation-based analyses linking protein expression to quantitative CT features were used to evaluate whether distinct longitudinal CT phenotypes were associated with divergent proteomic signatures. RESULTS: Principal component analysis and hierarchical clustering suggested partial segregation by CT-defined phenotype. Longitudinal CT phenotypes were associated with distinct pathway-level proteomic signatures, with progressive fibrosis enriched for epithelial-mesenchymal transition signaling, and progressive nodular inflammatory disease enriched for mTORC1, MYC, oxidative phosphorylation, adipogenesis, and fatty acid metabolism pathways. Correlation analyses showed coordinated protein-expression patterns associated with fibrotic CT features and mediastinal lymph node enlargement. DISCUSSION: These findings suggest that longitudinal CT-defined fibrotic and inflammatory sarcoidosis phenotypes are associated with distinct pathway-level proteomic signatures. This pilot study provides preliminary proof-of-concept evidence that integrating longitudinal CT imaging phenotypes with plasma proteomics may serve as a framework for future mechanistic studies and biomarker discovery in pulmonary sarcoidosis.

Humans↗
PubMed2006

Differential proteome profiles in E2F2-deficient T lymphocytes.

E2F transcription factors are important regulators of proliferation, differentiation and apoptosis. We have previously shown that E2F2-/- mice develop late-onset autoimmune features, similar to systemic lupus erythematosus. E2F2-deficient T lymphocytes exhibit enhanced T cell receptor (TCR)-stimulated proliferation, which is presumably responsible for causing autoimmunity in E2F2-deficient mice. The comparison of E2F2-/- and wild-type T lymphocyte expression profiles by 2-DE followed by MS identification has revealed a set of deregulated proteins involved in TCR-mediated signaling, cell survival and stress responses. The deregulation of these proteins may account for the hyperproliferative phenotype that characterizes E2F2-/- T cells. Our work shows that proteomic analysis of gene-knockout strains can be a useful methodology to study the functional role of specific genes.

Amino Acid Sequence↗
PubMed2005

Proteomic profiling for cancer progression: Differential display analysis for the expression of intracellular proteins between regressive and progressive cancer cell lines.

Tumor development and progression consist of a series of complex processes involving multiple changes in gene expression (Paolo et al. Physiol. Rev., 1993, 73, 161-195; Lance et al. Cell., 1991, 64, 327-336). Tumor cells acquire an invasive and metastatic phenotype that is the main cause of death for cancer patients. Therefore, for early diagnosis and effective therapeutic intervention, we need to detect the alterations associated with transition from benign to malignant tumor cells on a molecular basis. To unravel alterations concerned with tumor progression, the proteomic approach has attracted great attention because it can identify qualitative and quantitative changes in protein composition, including post-translational modifications. In this study, we performed proteomic differential display analysis for the expression of intracellular proteins in the regressive cancer cell line QR-32 and the inflammatory cell-promoting progressive cancer cell line QRsP-11 of murine fibrosarcoma by two-dimensional gel electrophoresis and mass spectrometry using an Agilent 1100 LC/MSD Trap XCT. We found 11 protein spots whose expression was different between QR-32 and QRsP-11 cells and identified nine proteins, seven of which, calreticulin precursor, tropomyosin 1 alpha chain, annexin A5, heat shock protein (HSP)90-alpha, HSP90-beta, PEBP, and Prx II, were over-expressed, and two, Anp32e and HDGF, which were down-regulated. The results suggest an important complementary role for proteomics in identification of molecular abnormalities in tumor progression.

Animals↗