Integrative bioinformatics analysis reveals ECM and nicotine-related genes in both LUAD and LUSC, but different lung fibrosis-related genes are involved in LUAD and LUSC.

There are several bioinformatics studies related to lung cancer, but most of them have mainly focused on either microarray data or RNA-Seq data alone. In this study, we have combined both types of data to identify differentially expressed genes (DEGs) specific to lung cancer subtypes. We obtained six microarray datasets from the GEO and also the expression matrix of LUSC and LUAD from TCGA, which were analyzed by GEO2R tool and GEPIA2, respectively. Enrichment analyses of DEGs were performed using the Enrichr database. Protein module identification was done by MCODE plugin in cytoscape software. We identified 30 LUAD-specific, 17 LUSC-specific, and 17 DEGs shared between LUAD and LUSC. Enrichment analyses revealed that LUSC-specific DEGs are involved in lung fibrosis. In addition, DEGs shared between LUAD and LUSC are involved in extracellular matrix (ECM), nicotine metabolism, and lung fibrosis. We identified lung fibrosis-related genes, including SPP1, MMP9, and CXCL2, involved in both LUAD and LUSC, but SERPINA1 and PLAU genes involved only in LUSC. We also found an important module separately for LUAD-specific, LUSC-specific, and shared DEGs between LUSC and LUAD. S100P, GOLM, AGR2, AK1, TMEM125, SLC2A1, COL1A1, and GHR genes were significantly associated with survival. Our findings suggest that different lung fibrosis-related genes may play roles in LUSC and LUAD. Additionally, nicotine metabolism and ECM remodeling were found to be associated with both LUSC and LUAD, regardless of subtype, emphasizing the role of smoking in the development of lung cancer and ECM in the high aggressiveness and mortality of lung cancer.

Identification of autophagy and angiogenesis modulators in colorectal cancer based on bioinformatics analysis.

Colorectal cancer (CRC) is the third most common cancer and the fourth leading cause of cancer-related death worldwide. The purpose of this study was to discover novel molecular pathways and potential prognosis biomarkers. To achieve this, we acquired five microarray datasets from the Gene Expression Omnibus (GEO) database. We identified differentially expressed genes between CRC and adjacent normal tissue samples and further validated them using The Cancer Genome Atlas (TCGA) database. Using various analytical approaches, including the construction of a competing endogenous RNA (ceRNA) network, Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway analyses, as well as survival analysis, we identified key genes and pathways associated with the diagnosis and prognosis of CRC. We obtained a total of 185 differentially expressed genes, comprising 17 lncRNAs, 30 miRNAs, and 138 mRNAs. The ceRNA network consisted of 17 lncRNAs, 25 miRNAs, and 7 mRNAs. Among the 7 mRNAs involved in the ceRNA network, SLC7A5 and KRT80 were found to be upregulated, while ADIPOQ, CCBE1, KCNB1, CADM2, and CHRDL1 were downregulated in CRC. Further analysis revealed that ADIPOQ and SLC7A5 are involved in the AMPK and mTOR signaling pathway, respectively. In addition, survival analysis demonstrated a statistically significant relationship between ADIPOQ, SLC7A5, and overall survival rates in CRC patients. In conclusion, our findings suggest that downregulation of ADIPOQ and upregulation of SLC7A5 in tumor cells lead to increased mTORC1 activity, reduced autophagy, enhanced angiogenesis, and ultimately contribute to cancer progression and decreased survival in CRC patients.

Types of Cell Death from a Molecular Perspective.

The former conventional belief was that cell death resulted from either apoptosis or necrosis; however, in recent years, different pathways through which a cell can undergo cell death have been discovered. Various types of cell death are distinguished by specific morphological alterations in the cell's structure, coupled with numerous biological activation processes. Various diseases, such as cancers, can occur due to the accumulation of damaged cells in the body caused by the dysregulation and failure of cell death. Thus, comprehending these cell death pathways is crucial for formulating effective therapeutic strategies. We focused on providing a comprehensive overview of the existing literature pertaining to various forms of cell death, encompassing apoptosis, anoikis, pyroptosis, NETosis, ferroptosis, autophagy, entosis, methuosis, paraptosis, mitoptosis, parthanatos, necroptosis, and necrosis.

Effect of rs1058240 polymorphism in 3'-UTR of GATA3 gene on potential binding of miRNAs and its association with RRMS risk: bioinformatics analysis and case-control study.

AIM: Multiple sclerosis is believed to be an autoimmune disease that is influenced by T helper (Th) cell differentiation. GATA3 plays an important role in reducing the development and severity of MS by shifting the differentiation of Th cells to Th2 and regulatory T cells while inhibiting the differentiation of Th1 and Th17 cells. Considering the functional role of rs1058240 SNP in the 3'-UTR of GATA3 mRNA, the association of target SNP with the risk of RRMS was examined. METHODS: Genomic DNA was extracted from whole blood samples of 200 RRMS patients and 226 healthy individuals as a control group. Different genotypes of rs1058240 SNP were determined using the RFLP-PCR technique. Statistical analysis was performed using SPSS software and χ2 and logistic regression tests. The stability of GATA3 mRNA secondary structures and the binding patterns of GATA3-miRNAs with different alleles were evaluated using RNAfold and RNAhybrid programs, respectively. RESULTS: The results indicated that the GATA3 rs1058240 G allele (p value = 0.010, OR = 1.45, CI = 1.09-1.93) and GG genotype (adjusted p value = 0.017, OR = 2.27, 95%CI = 1.16-4.44) increased the risk of RRMS, particularly in women (adjusted p value = 0.006, OR = 2.99, 95%CI = 1.37-6.52). Bioinformatics analysis revealed that although the allelic variation of this polymorphism had only a slight effect on mRNA stability (-177 to -177.20), the G allele significantly increased miRNA binding strength and miRNA-mRNA thermodynamic stability for hsa-miR-337-5p, hsa-miR-4445-3p, hsa-miR-4485-3p, hsa-miR-95-3p (ΔMFE > 0) compared to the A allele. CONCLUSION: The G allele and GG genotype of rs1058240 in GATA3 mRNA 3'-UTR were found to be risk factors for increasing the susceptibility to RRMS.

Identification of novel nuclear pore complex associated proteins in esophageal carcinoma by an integrated bioinformatics analysis.

Nucleoporins (NUPs) are components of the nuclear pore complex (NPC) that participate in the nucleocytoplasmic transport of macromolecules as well as in many essential processes that may be led to carcinogenesis. We selected three expression profile microarray datasets from GEO and as well as TCGA data to identify differentially expressed NUPs genes in esophageal carcinoma. Our findings indicated that NUP133, NUP37, NUP43, NUP50, GLE1 and NDC1 are overexpressed in esophageal carcinoma, among which NUP50 and GLE1genes are reported for the first time in esophageal carcinoma. All identified NUPs were also associated with distant metastasis.Communicated by Ramaswamy H. Sarma.

Differential expression of KCNQ1 and ATP4A genes according to the sex and age in the stomach.

We compared the expression of six genes in stomach tissue samples between healthy men and women in different age groups to study sexually dimorphic gene expression. Real-Time RT-PCR was used to compare gene expression between men and women. Our results showed that the expression of KCNQ1 (p = 0.01) was significantly higher in non-menopausal women compared to post-menopausal women. In addition, the expression level of the ATP4A gene in men under 35 years was significantly higher than in men above 50 (p = 0.026). Sexually and age dimorphic gene expression in some genes throughout life may affect gastric function.

Association of Val660Leu, progesterone receptor polymorphic variant, with susceptibility to RRMS disease.

BACKGROUND: Multiple sclerosis is an inflammatory, autoimmune, and progressive neurodegenerative disease of the central nervous system with an unknown etiology. Based on the gender differences in epidemiological, clinical, and pathological features of multiple sclerosis, the role of sex hormones and their receptors in this disease has been considered. A single nucleotide polymorphism located in the exon 4 of progesterone receptor, rs1042838 (G/T -Val660Leu), was associated with reduced progesterone receptor activity. We aimed to investigate the association of this polymorphism with the risk of multiple sclerosis. METHOD: A total of 426 individuals were included in the present study, including 200 patients and 226 age and sex adjusted healthy controls in Iranian population. The target SNP was genotyped using PCR-RFLP, and statistical analysis was performed using SPSS 21.0 and by ꭓ2 and logistic regression tests. RESULTS: The results showed that the allele T acts as a risk allele, so that the genotypes TG and TT significantly increase RRMS susceptibility compared to the genotype GG. CONCLUSION: Our data suggest that Val660Leu polymorphism might be a risk factor for the development of RRMS.

Significant Association of DNASE1 Variable Number Tandem Repeats and Single Nucleotide Polymorphisms With Gastric Cancer.

Introduction: Defects in the apoptotic process are among the most important events involved in carcinogenesis, and defects in DNASE1, as one of the apoptotic machinery components, plays a role in various types of cancer. Previous studies have indicated significant differences in the DNASE1 polymorphisms in different populations. We hypothesized an association of two polymorphic sites in the exon 8 and the intron 4 of the DNASE1 gene with the risk of gastric cancer. Materials and Methods: The study was carried out on 120 gastric cancer patients and 120 age and sex adjusted controls using PCR and RFLP-PCR. Results: The genotype GG (rs1053874) in exon 8 of DNASE1 (odds ratio [95% confidence interval]) 4.65 [2.10-10.29], p < 0.001) and genotype 2/3 of variable number tandem repeat (VNTR) in the intron 4 (3.75 [1.56-9.01], p = 0.003) are both linked to gastric cancer. Conclusion: We propose that both polymorphic sites have a part to play in gastric cancer, and so may be useful diagnosis markers.

Significant Association of Variable Number Tandem Repeat Polymorphism rs58335419 in the MIR137 Gene With the Risk of Gastric and Colon Cancers.

The purpose of the article: The MIR137 gene acts as a tumor-suppressor gene in colon and gastric cancers. The aim of this study was to investigate the association of functional variable number tandem repeat (VNTR) polymorphism rs58335419 locating in the upstream of the MIR137 gene with the risk of colon and gastric cancers. Materials and methods: Totally, 429 individuals were contributed in the study, including 154 colon and 120 gastric cancer patients and 155 healthy controls. The target VNTR was genotyped using PCR and electrophoresis for all samples. Statistical analysis was performed using SPSS 21.0 software and by T, χ2 and logistic regression tests. Results: Excluding the rare genotypes, our results showed that genotype 3/5 (95% CI = 1.08-3.73, OR = 2.01, p = 0.026) significantly increased the risk of colon cancer but not gastric cancer (95% CI = 0.88-3.30, OR = 1.70, p = 0.114). Also, in the stratification analysis for VNTRs and sex, genotypes 3/4 (95% CI = 1.00-6.07, OR = 2.46, p = 0.049) and 3/5 (95% CI = 1.25-7.18, OR = 2.99, p = 0.014) significantly increased the risk of colon cancer in men but not in women. In addition, all genotypes including the rare genotypes as a group, significantly increase the risk of gastric (95% CI = 1.14-3.00, OR = 1.85, p = 0.012) and colon (95% CI = 1.38-3.43, OR = 2.17, p = 0.001) cancers compared to the genotype 3/3 as a reference. Conclusion: The results show that increasing the copy of VNTR in the MIR137 gene, increases the risk of colon and gastric cancers and can serve as a marker for susceptibility to colon and gastric cancers.

Significant Association of rs77493513 Polymorphism in 3'-UTR of the NRG1 Gene with the Risk of Multiple Sclerosis Disease.

Multiple sclerosis (MS) is a chronic inflammatory and autoimmune disease characterized by demyelination of the central nervous system (CNS). Neuregulin 1 (NRG1) is a signaling protein that plays an important role in a variety of biological processes, including potentiate oligodendrocyte differentiation and myelination in the CNS, immune response regulation, and inflammation. Single nucleotide polymorphism (SNP) rs77493513 is located in the untranslated region of the 3' mRNA (3'-UTR) of the NRG1 gene, which is predicted to be the binding site of several microRNAs and may play an important role in post-transcriptional regulation. Study aimed to investigate the association of SNP rs77493513 in the NRG1 gene with the risk of MS disease. In this study, genomic DNA was extracted from whole blood samples of 182 patients with relapsing-remitting multiple sclerosis (RRMS) and 198 controls. Different genotypes of rs77493513 polymorphism were determined using RFLP-PCR technique. Statistical analysis was performed using SPSS 21.0 software and by t, χ2 and logistic regression tests. Our data showed that genotypes AC (OR=3.63, CI= 1.93-6.81, p<0.001) and CC (OR=7.90, CI= 4.13-15.11, p<0.001) significantly increased the risk of MS disease and C allele is risk allele. Also, AC (OR=0.16, CI= 0.04-0.63, p= 0.009) and CC (OR=0.14, CI= 0.03-0.53, p=0.04) genotypes significantly decrease the age of onset of the disease. The results show that allele C of rs77493513 polymorphism in the NRG1 gene can be a risk factor for MS.

Association study of polymorphism in Thrombomodulin gene [rs1042579] with cardiovascular disease.

BACKGROUND AND AIM: Thrombomodulin (THBD) gene plays an important role in activation and control of protein C. Regulation protein C levels as an important risk factor for cardiovascular disease. Mutations in this gene can affect Thrombomodulin levels. In this study, we aimed to investigate the role of single nucleotide polymorphism (SNP) in rs1042579 THBD gene in patients with cardiovascular disease. METHODS: The samples of this case-control study consisted of 105 Iranian patients with cardiovascular disease and 95 healthy controls who enrolled from March 2017 to December 2018 in this study.  Demographic data, medical history, and para-clinical were measured, and Sanger sequencing was used for allelic discrimination. Control samples were identified and then selected for genotyping of other ARMS-PCR technique. RESULTS: Data analysis revealed that the rs1042579 polymorphism of the THBD gene was associated with a risk of coronary heart disease. Sequencing results confirmed the existence of CC homozygous, heterozygous TC and TT homozygous genotypes. TT genotype is a risk factor in patients compared to healthy controls. CONCLUSION: The results of this study showed that the rs1042579 polymorphism was associated with an increased risk of cardiovascular disease.

PHLPP2 gene L1016S (rs61733127) and PIK3R1 gene Met326Ile (rs3730089) polymorphisms are associated with the risk of colon and breast cancers.

The PIK3R1 and PHLPP2 genes encode the p85 alpha subunit of PI3K and a phosphatase for AKT, respectively, which play a direct role in regulating the PI3K-AKT pathway that promotes cell survival, growth, and differentiation. While most attention is focused on the factors that positively affect this pathway, negative regulation is equally important. The aim of this study was to investigate the association of SNPs rs61733127 (L1016S) in PHLPP2 gene and rs3730089 (Met326Ile) in PIK3R1 gene with colon and breast cancer, respectively because both SNPs have been reported to play a functional role in corresponding encoded enzymes and both genes are negatively involved in regulating the PI3K-AKT pathway. 139 colon and 149 breast cancers patients and 279 healthy controls were included in the present study. The target SNPs were genotyped using tetra- ARMS-PCR. In addition, the genotypes of 10 samples for each SNP were confirmed by sequencing. Statistical analysis was performed using SPSS 21.0 and by Fisher exact, T, χ2 and logistic regression tests. As revealed, the genotype AG (OR = 2.18, p = 0.001, CI = 1.36-3.50) and allele G (OR = 1.92, p = 0.001, CI = 1.30-2.84) of rs61733127 in the PHLPP2 gene significantly increased the risk of colon cancer. In addition, genotype AA (OR = 0.2, p = 0.001, CI = 3.00-8.00) and allele A (OR = 0.5, p = 0.001, CI = 1.00-4.00) of rs3730089 in the PIK3R1 gene significantly decreased the risk of breast cancer. The results suggest that SNPs in genes involved in regulating of PI3K-AKT pathway can be used as a marker for susceptibility to colon and breast cancers.

ErbB4 3'-UTR Variant (c.*3622A>G) is Associated with ER/PR Negativity and Advanced Breast Cancer.

A genetic variant may alter a gene expression level and as a result be associated with pathological characteristics in breast cancer. In this research, the frequency and association of the ErbB4 3'-untranslated region (3'-UTR) variant, rs12471583 (c.*3622A>G) was studied in an Iranian breast cancer patients. In silico assessment was performed to predict the function of the rs12471583 variant located on the 3'-UTR of ErbB4. Furthermore, as a case-control study, this polymorphism was genotyped in 243 breast cancer patients and non-cancerous controls using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. The Armitage's trend test and regular association tests were performed to analyze a possible association between the rs12471583 and risk of breast cancer and its relevant pathological traits. The bioinformatics analysis predicted that the rs12471583 SNP is located on the four miRNA binding sites, including miR-511-5p, miR-4659a-5p, miR-4659b-5p, and miR-6830-3p. According to logistic regression tests, the G allele is negatively associated with ER- (OR = 0.20, 95% C.I. = 0.04-0.93, p = 0.026), PR- (OR = 0.31, 95% C.I. = 0.10-0.98, p = 0.039), ER-/PR- (OR = 0.20, 95% C.I. = 0.04-0.93, p = 0.026), and advanced breast cancer (OR = 0.40, 95% C.I. = 0.18-0.85, p = 0.016). It has been found that ErbB4 expression may be linked to unfavorable outcomes in breast cancer. Likewise, our results suggest that the G allele may strengthen miRNA-ErbB4 binding efficiency and as a result reduce expression of ErbB4. This is a possible explanation for the observed association.

A genetic variant in the flanking region of miR-182 could decrease the susceptibility to the breast cancer risk in the iranian population.

Breast cancer is one of the most malignant tumors in the world. It is, in fact, the second leading cause of cancer death in women. Recent research has identified the role of miR-182 in this disease as an oncogene agent. In this study, the association of rs4541843 in the flanking region of the miR-182 sequence with the susceptibility to breast cancer risk has been studied in the Iranian population. By using the PCR_RFLP, the genotype rs4541843 was determined in 161 patients and 164 control subjects. The genotypes of the individuals were analyzed statistically to find the association between rs4541843 and the breast cancer incidence and its pathological characteristics. The results revealed that due to the dominance of the G allele, the frequency of GG + AG genotypes, as compared with AA, had a significant correlation with the incidence of this disease in controls and cases (P = 0.022; OR = 0.523). Moreover, the genotypes AG and AA could significantly decrease the susceptibility to the breast cancer risk; also in the presence of the A allele (OR, 0.565; P = 0.015), the incidence of the disease could be decreased. Our results indicated that this SNP was associated with the breast cancer risk of the Iranian population. We suppose that rs4541843 may influence the processing of the mature miRNA by affecting the cleavage of Drosha. Therefore, this SNP can be considered as a candidate genetic marker for the susceptibility to breast cancer in the Iranian women.

Evaluating the Immune Response of Recombinant H1N1 Hemagglutinin with MF59 Adjuvant in Animal Model as a Novel Alternative to the Influenza Vaccine.

The H1N1 influenza virus is known as a serious pandemic threat across the globe. Vaccination is one of the most effective methods of protection against this virus and the way to reduce the seasonal pandemic risk. The commercial vaccine does not adequately respond to pandemic strains. This study examines the potential function of formulated H1N1 hemagglutinin with MF59 adjuvant against A/PR/8/34 (H1N1). To this end, a recombinant hemagglutinin (rHA) gene of influenza A virus was designed and expressed in SF9 cell by the Baculovirus expression system. Four groups of mice were immunized by rHA in combination with MF59, Alum adjuvant, and virus split only. The immunized mice subsequently used for the humoral immune assay and the results compared with untreated mice (negative group). Besides, both treated and control mice groups were challenged with mouse-adapted influenza virus A/PR/8/34(H1N1) through the intranasal drop. Bodyweight, survival, temperature variation, and the medical conditions of the samples were assessed. Mice immunized with the recombinant protein demonstrated a humoral response to the influenza A virus. Upon virus challenging, co-administration of rHA with MF59 adjuvant could lead to 92% survival of the vaccinated mice within 10 days. The MF59-treated group showed slight weight loss and high-temperature body two weeks after infection. This group also displayed a higher hemagglutination inhibition (HI) antibody titer as compared to the group vaccinated with virus split, and Alum adjuvant. Altogether, the results showed that the recombinant protein with the MF59 adjuvant created better safety than the Alum adjuvant, thereby can be considered as a safe and reliable vaccine against the H1N1 virus for further investigations.

Sexual dimorphism in the expression of GKN2 and FOXA2 genes in the human stomach.

A large proportion of the transcriptome is sex biased in a wide range of taxa. Sexually dimorphic genes expression is highly tissue-dependent. Although gastric cancer exhibits sex bias to some extent, sexually dimorphic gene expression in the stomach is yet to be fully understood. The aim of the present study was to compare the expression levels of 12 genes in the gastric tissue between age-matched healthy men and women of different age groups. A total of 70 human antrum gastric tissue samples were obtained by endoscopy. The difference in expression levels of the 12 intended genes between two genders was investigated using quantitative Real-Time PCR, following total RNA extraction. The results indicated that the expression levels of both the GKN2 (7.2-fold, p < 0.001) and FOXA2 (3.7-fold, p = 0.003) were significantly higher in men compared to those in women. In addition, FOXA1 gene expression was age-dependent only in women. Interestingly, the expression level of FOXA1 was significantly higher in premenopausal women compared to postmenopausal women (2.53-fold, p = 0.016). The expression levels of some of the investigated genes in this study were sex-dependent in the stomach. This sexual dimorphism in gene expression might influence the differential susceptibility to the gastric cancer between the sexes.

C86Y: as a destructive homozygous mutation deteriorating Pex7p function causing rhizomelic chondrodysplasia punctata type I.

Rhizomelic Chondrodysplasia Punctata (RCDP) type 1 is a peroxisomal biogenesis disorder with a genetic abnormality in PEX7 gene. In the present study, mutational analysis was performed on two Iranian RCDP patients with distinct clinical phonotype. Mutation detection was carried out by sequencing of RT-PCR product consisting the whole length of PEX7 cDNA. Sequence data revealed the same missense homozygous mutation of G to A at nucleotide 257 in exon3 of PEX7 coding sequence in both patients. Moreover, genomic analysis of the PEX7 gene confirmed the RT-PCR data. This mutation caused one amino acid residue substitution of Cys to Tyr at codon 86 located on WD1 repeat domain region of Pex7p, which severely affected the functionality of PEX7 protein. Back-transfection of vector encoding mutant Pex7p did not restore the normal peroxisomal function in RCDP patient's fibroblast cells dissimilar to the native type of PEX7.

Esophageal cancer alters the expression of nuclear pore complex binding protein Hsc70 and eIF5A-1.

Nuclear pore complex (NPC) is the only corridor for macromolecules exchange between nucleus and cytoplasm. NPC and its components, nucleoporins, play important role in the diverse physiological processes including macromolecule exchange, chromosome segregation, apoptosis and gene expression. Recent reports also suggest involvement of nucleoporins in carcinogenesis. Applying proteomics, we analyzed expression pattern of the NPC components in a newly established esophageal cancer cell line from Persia (Iran), the high-risk region for esophageal cancer. Our results indicate overexpression of Hsc70 and downregulation of subunit alpha type-3 of proteasome, calpain small subunit 1, and eIF5A-1. Among these proteins, Hsc70 and eIF5A-1 are in direct interaction with NPC and involved in the nucleocytoplasmic exchange. Hsc70 plays a critical role as a chaperone in the formation of a cargo-receptor complex in nucleocytoplasmic transport. On the other hand, it is an NPC-associated protein that binds to nucleoporins and contributes in recycling of the nucleocytoplasmic transport receptors in mammals and affects transport of proteins between nucleus and cytoplasm. The other nuclear pore interacting protein: eIF5A-1 binds to the several nucleoporins and participates in nucleocytoplasmic transport. Altered expression of Hsc70 and eIF5A-1 may cause defects in nucleocytoplasmic transport and play a role in esophageal carcinogenesis.

Identification of a novel missense mutation of PEX7 gene in an Iranian patient with rhizomelic chondrodysplasia punctata type 1.

Deficiency in the PTS2 protein import pathway due to mutations in PEX7 gene results in the rhizomelic chondrodysplasia punctata (RCDP) type 1. In the present study, we have reported a novel missense mutation, W75R, in the PEX7 gene in an Iranian patient with the RCDP type 1. The inability of PEX7 protein to transport PTS2 containing proteins including peroxisomal 3-ketoacyl-CoA thiolase and PTS2-EGFP protein to the surface of the peroxisomes showed that the W75R mutation in PEX7 gene severely impaired the function of PEX7 protein and was responsible for RCDP type 1 in this patient.

Proteomics of a new esophageal cancer cell line established from Persian patient.

Although the highest incidence of esophageal squamous cell carcinoma (ESCC) has repeatedly been reported from Persia (Iran), nevertheless the so far proteomic published reports were limited to one study on tissue specimens. Here we report the proteome of a newly established cell line from Persian ESCC patients and compare it with the normal primary cell proteome. Among polypeptides, whose expression was different in cell line sixteen polypeptides were identified by MALDI/TOF/TOF spectrometry. S100-A8 protein, annexin A1, annexin A2, regulatory subunit of calpain, subunit alpha type-3 of proteasome and glutamate dehydrogenase 1 were proteins down-regulated in cell line while peroxiredoxin-5, non-muscle myosin light polypeptide 6, keratin 1, annexin A4, keratin 8, tropomyosin 3, stress-induced-phosphoprotein 1 and albumin were found to be subject of up-regulation in cell line compared to the primary normal cells. The proteomic results were further verified by western blotting and RT-PCR on annexin A1 and keratin 8. In addition, among the aforementioned proteins, glutamate dehydrogenase 1, regulatory subunit of calpain, subunit alpha of type-3 proteasome and annexin A4 are proteins whose deregulation in ESCC is reported for the first time by this study.