BARX1 repressed FOXF1 expression and activated Wnt/ß-catenin signaling pathway to drive lung adenocarcinoma.

BACKGROUND: Underlying molecular mechanisms of BARX homeobox 1 (BARX1) in lung adenocarcinoma (LUAD) remain elusive. METHODS: Abnormally expressed genes in LUAD tissues were analyzed by RNA-sequencing. CCK-8, colony formation, transwell, and wound healing assays examined proliferation, colony formation, invasion, and migration of LUAD cells, respectively. Electrophoretic mobility shift assay and chromatin immunoprecipitation assay examined the interaction between BARX1 and Forkhead Box F1 (FOXF1). Xenograft mouse model of LUAD was constructed to monitor the growth and metastasis of tumor. RESULTS: BARX1 was upregulated, FOXF1 was downregulated in LUAD tissues and cells. There was a negative correlation between BARX1 and FOXF1 expression. BARX1 deficiency limited malignant phenotypes of LUAD cells, including proliferation, invasion, migration and EMT. In vivo, BARX1 knockdown suppressed tumor growth and metastasis in A549-drove xenograft mouse model. BARX1 interacted with FOXF1 promoter and repressed FOXF1 expression. Upregulation of BARX1 promoted the expression of Wnt5a, ß-catenin, and phosphorylated-glycogen synthase kinase-3 beta (p-GSK3ß), whereas inhibited FOXF1, p-ß-catenin, and GSK3ß in LUAD cells. BARX1 knockdown caused an opposite result. Rescue assays uncovered that FOXF1 reversed the impact of BARX1 on malignant phenotypes and Wnt/ß-catenin of LUAD cells. CONCLUSION: BARX1 repressed FOXF1 expression and activated Wnt/ß-catenin signaling pathway to drive lung adenocarcinoma.

Novel ADCs and combination therapy in urothelial carcinoma: latest updates from the 2023 ASCO-GU Cancers Symposium.

Antibody-drug conjugates (ADCs) combine the cytotoxicity of small-molecule drugs with antibody targeting. Due to their precise and powerful effect, they have become a new hotspot and an important trend in the research and development of anti-tumor antibody drugs. Every year, exciting new developments and innovations in the treatment of urological tumors are introduced at the American Society of Clinical Oncology-Genitourinary (ASCO-GU) Cancers Symposium. In this article, we summarize some of the most impressive advances in new clinical trials and clinical data on ADCs in the 2023 ASCO-GU Cancers Symposium for the treatment of urothelial carcinoma.

Whole-exome sequencing and bioinformatics analysis of a case of non-alpha-fetoprotein-elevated lung hepatoid adenocarcinoma.

Hepatoid adenocarcinoma of the lung (HAL) is an exceptionally rare malignant tumor with prominent hepatocellular carcinoma (HCC)-like characteristics in organs or tissues outside the liver, while there is no tumor in the liver. Most HAL cases have various degrees of serum alpha-fetoprotein (AFP) levels and exhibit a similar origin and clonal evolution process to HCC. We studied a case of HAL without elevating the AFP level by performing whole-exome sequencing (WES) and bioinformatics analyses after surgical resection. Our results showed mutations in two driver genes, NLRP3 and PBX1, and we identified HNRNPR, TP73, CFAP57, COL11A1, RUSC1, SLC6A9, DISC1, NBPF26, and OR10K1 as potential driver mutation genes in HAL. In addition, 76 significantly mutated genes (SMG) were identified after the statistical test of each mutation type on genes.

Development of a Prognostic Alternative Splicing Signature Associated With Tumor Microenvironment Immune Profiles in Lung Adenocarcinoma.

Background: Alternative splicing (AS), a pivotal post-transcriptional process across more than 95% of human transcripts, is involved in transcript structural variations and protein complexity. Clinical implications of AS events and their interaction with tumor immunity were systematically analyzed in lung adenocarcinoma (LUAD). Methods: Transcriptome profiling as well as AS data of LUAD were retrospectively curated. Then, the network of the overall survival (OS)-relevant AS events with splicing factors was established. After screening OS-relevant AS events, a LASSO prognostic model was conducted and evaluated with ROC curves. A nomogram that integrated independent prognostic indicators was created. Immune response and immune cell infiltration were estimated with ESTIMATE, CIBERSORT, and ssGSEA algorithms. Drug sensitivity was inferred with pRRophetic package. Results: In total, 2415 OS-relevant AS events were identified across LUAD patients. The interaction network of splicing factors with OS-relevant AS events uncovered the underlying regulatory mechanisms of AS events in LUAD. Thereafter, a prognostic model containing 12 AS events was developed, which acted as a reliable and independent prognostic indicator following verification. A nomogram that constituted stage and risk score displayed great effectiveness in evaluating the survival likelihood. Moreover, the AS-based prognostic model was in relation to immune response and immune cell infiltration. Patients with a high-risk score displayed therapeutic superiority to cisplatin, erlotinib, gefitinib, and gemcitabine. Finally, three AS-relevant genes (CDKN2A, TTC39C, and PKIB) were identified as prognostic markers. Conclusion: Collectively, our findings developed an AS event signature with powerful prognostic predictive efficacy in LUAD.

A Germline Mutation in ATR Is Associated With Lung Adenocarcinoma in Asian Patients.

Background: Familial lung cancer (FLC) accounts for 8% of lung adenocarcinoma. It is known that a few germline mutations are associated with risk increasing and may provide new screening and treatment option. The goal of this study is to identify an FLC gene among three members of an FLC family. Methods: To uncover somatic and embryonic mutations linked with familial lung cancer, whole exome sequencing was done on surgical tissues and peripheral blood from three sisters in a family diagnosed with pulmonary lung adenocarcinoma (LUAD). At the same time, single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing data in public databases were enrolled to identify specific gene expression level. Results: Ataxia Telangiectasia and Rad3-Related Protein (ATR) gene C.7667C >G (p.T2556S) mutation were found in 3 patients with familial lung cancer. Whole-genome sequencing revealed that the three sisters exhibited similar somatic mutation patterns. Besides ATR mutations, common mutated genes (BRCA1, EGFR, and ROS1) that characterize LUAD were also found in 5 tumor samples. Analysis for the ATR expression in LUAD patients by single-cell sequencing data, we found ATR expression of tumor patients at high level in immune cells when compared with normal patients, but the expression of ATR in stromal cells has the opposite result. Conclusion: We found a germline mutation in the ATR gene in three sisters of a Chinese family affected by familial lung cancer, which may be a genetic factor for lung cancer susceptibility.

Comprehensive Analysis of the Function, Immune Profiles, and Clinical Implication of m1A Regulators in Lung Adenocarcinoma.

Background: Previous studies have demonstrated that transcriptional RNA methyladenosine modification significantly affects tumor initiation and progression. However, clinical implications of N1-methyladenosine (m1A) regulators and their effect on tumor immunity in lung adenocarcinoma (LUAD) are still poorly elucidated. Methods: Herein, the characteristics of somatic mutation, copy number variation (CNV), DNA methylation, and expression levels of m1A regulators were thoroughly analyzed. We classified 955 lung adenocarcinoma patients into different m1A modification patterns based on an unsupervised consensus clustering algorithm. We then calculated the differences in gene expression, prognosis outcomes, and immune profiles among different m1A clusters. Subsequently, we screened differently expressed genes (DEGs) related to prognosis among different m1A clusters. We identified m1A related gene clusters according to the prognosis-related different expressed genes. We further constructed a scoring standard named the m1A score and comprehensively analyzed the survival outcomes, clinical-pathological features, immune microenvironment, treatment responses of immunotherapy, and drug susceptibility in different m1A score groups. Results: In total, three different m1A modification patterns were identified, which contained cluster A, B, and C. Among them, cluster A processed the poorest clinical outcomes, the lowest immune cell infiltration rate, and the highest tumor purity score. Then, three m1A gene clusters (gene cluster A, B, C) were speculated. Subsequently, we combined m1A modification patterns and m1A gene cluster to classify lung adenocarcinoma patients into high and low m1A score groups. The low m1A score group was accompanied by higher mortality, higher tumor mutation burden (TMB) and genome mutation frequency, and lower programmed cell death-Ligand 1 (PD-L1) expression and tumor immune dysfunction and exclusion (TIDE) expression. Moreover, the m1A score exhibited positive correlation with almost all immune cells. Finally, common chemotherapeutic and targeted therapy agents exhibited obvious differences in drug susceptibility in different m1A score groups. Conclusions: Collectively, we explored the potential value of m1A regulators in the prognosis and treatment of lung adenocarcinoma in multiple dimensions and provided some preliminary basis for the follow-up study of m1A regulators in lung adenocarcinoma.

Molecular subtyping of small cell lung cancer.

Small cell lung cancer (SCLC), originating from lung neuroendocrine stem cells, is a common pulmonary malignant tumor. SCLC, with poor prognoses, accounts for approximately 13-15% of all lung cancer cases. Due to the slow progress of clinical treatment, the 5-year survival rate of SCLC has remained below 7% for many years. In recent years, with the development and popularity of gene sequencing technologies, we were able to better grasp patterns of gene mutations and tumor evolution in SCLC. Thus, appropriate molecular subtyping strategies have been established to help predict patients' prognoses and develop the treatment regimen for SCLC more accurately. In this narrative review, we aim to summarize the evolution of mutation-based molecular subtyping of SCLC, as well as the trends in molecular targeting and immunotherapeutic for SCLC. Based on the latest sequencing data for SCLC, thereafter, we discuss therapeutic opinions of SCLC from basic to clinic. This review may provide a basis for guiding the development of subsequent individualized precision-targeted therapy for SCLC patients to improve their clinical prognoses.

Evolution of small cell lung cancer tumor mutation: from molecular mechanisms to novel viewpoints.

Small cell lung cancer (SCLC) is a clinically common malignant tumor originating from the lung neuroendocrine stem cells, which has a poor prognosis and accounts for approximately 15% of all lung cancer cases. However, research on its treatment has been slow, and the 5-year survival rate of patients with SCLC has been < 5% for many years. In recent years, the development and popularization of gene sequencing technology have facilitated the understanding of the gene mutation landscape and tumor evolution of SCLC, thereby leading to a more accurate prediction of the prognosis of SCLC and the development of individualized treatment. In this review, we aimed to discuss the mutation evolution of SCLC from the perspective of a tumor evolution theory and described the sequence of mutation evolution in the occurrence and development of SCLC. In addition, we summarized the existing whole-exome sequencing (WES) data of SCLC cases at our center along with relevant publications on sequencing. Thereafter, we discuss the role of different mutated pathways in the occurrence of SCLC to predict its prognosis more accurately and summarized individualized treatment strategies.

Immunological Classification of Tumor Types and Advances in Precision Combination Immunotherapy.

Immunity is an important physiological function acquired throughout evolution as a defense system against the invasion of pathogenic microorganisms. The immune system also eliminates senescent cells and maintains homeostasis, monitoring cell mutations and preventing tumor development via the action of the immune cells and molecules. Immunotherapy often relies on the interaction of immune cells with the tumor microenvironment (TME). Based on the distribution of the number of lymphocytes (CD3 and CD8) in the center and edge of the tumor and the expression level of B7-H1/PD-L1, tumors are divided into hot tumors, cold tumors, and intermediate tumors (including immune-suppressed and isolated). This review focuses on the advances in precision combination immunotherapy, which has been widely explored in recent years, and its application in different tumor types.

p33ING1b regulates acetylation of p53 in oral squamous cell carcinoma via SIR2.

BACKGROUND: Oral squamous cell carcinoma (OSCC), a form of head and neck squamous cell carcinoma (HNSCC) has a poor 5-year survival rate. OSCC patients are often treated with cisplatin but resistance to chemotherapy is often observed. This makes it important identification of alternative therapeutic targets which will result in more favorable outcome in OSCC patients. The plant homeodomain (PHD)-containing protein Inhibitor of Growth family of tumor suppressor proteins (p33ING1b) has been indicated as a tumor suppressor in different cancers including OSCC. This protein has been shown to function by modulating transcriptional activity of p53; however, the exact mechanism(s) are not well defined. METHODS: Expression of total and acetylated p53 and p33ING1b protein was determined in OSCC cell lines YD-9, YD-8, and YD-38 by immunoblot analysis. Effect of modulation of p33ING1b protein expression on acetylation of p53 and cell proliferation was determined by immunoblot and MTT assay. Effect of modulation of p33ING1b protein expression on transactivation of p53 was assessed by heterologous promoter-based reporter and chromatin immunoprecipitation. Effect of modulation of expression of p33ING1b on SIR2 mRNA and protein was determined by quantitative real-time PCR and immunoblot analyses. Impact of modulation of p33ING1b alone or in combination with SIR2 on chemosensitivity of YD-9 and YD-8 cells to cisplatin was determined in time and dose-dependent cell proliferation assays. RESULTS: Here, using a panel of OSCC cell lines with wild type or mutant p53, we show that p33ING1b expression is correlated to acetylation of p53 at lysine 382 residue. Increased acetylation of p53 following overexpression of p33ING1b was associated with increased expression of the pro-apoptotic proteins BAX, p21, and cleaved-Caspase 3, and decreased cell proliferation. Reporter assays with p21 and BAX promoters showed that p33ING1b expression levels directly correlated to promoter activity of these 2 genes. Chromatin immunoprecipitation assay showed that transcriptional regulation of p21 and BAX by acetylated p53 is dependent on expression level of p33ING1b. Differential acetylation of p53 following modulation of p33ING1b expression was indirect. Expression of p33ING1b was found to be inversely correlated to the NAD-dependent deacetylase silent information regulator 2 (SIR2). SIR2 was transcriptionally regulated by p33ING1b. Relative expression of p33ING1b was found to dictate chemosensitivity of OSCC cell lines to cisplatin treatment. Concomitant overexpression of p33ING1b and knockdown of SIR2 had a synergistic effect on chemosensitivity of OSCC cell lines to cisplatin, compared to either overexpression of p33ING1b or knockdown of SIR2 alone. CONCLUSIONS: The results from the current study thus elucidate that p33ING1b regulates p53 acetylation irrespective of p53 mutation and subsequent transactivation by transcriptional regulation of SIR2 expression. The results also indicate that p33ING1b and SIR2 are potentially attractive therapeutic targets.

White Matter Abnormalities of Auditory Neural Pathway in Sudden Sensorineural Hearing Loss Using Diffusion Spectrum Imaging: Different Findings From Tinnitus.

Sudden sensorineural hearing loss (SSNHL) is a complex and challenging emergency which requires evidence regarding its pathophysiological changes to guide the treatment. The aim of this study was to evaluate the white matter integrity of the auditory neural pathway in patients with unilateral SSNHL in acute stage by using diffusion spectrum imaging tractography. In the present study, 60 individuals with acute SSNHL (29 males, 50.7 ± 11.8 years) and 25 healthy controls (13 males, 45.2 ± 13.2 years) underwent diffusion spectrum imaging tractography and high resolution T1 structural examinations using a 3T magnetic resonance imaging system. The areas of the auditory neural pathway were defined as regions of interest (ROIs). The quantitative anisotropy (QA) and the generalized fractional anisotropy (GFA) were compared between the patients with unilateral SSNHL and controls in these ROIs. We further evaluated the correlation between the parameter values and hearing loss level. The mean pure tone audiometry of patients at the onset presentation was 63.2 ± 26.2 dB. The right-sided SSNHL was involved in 25 (41.7%) cases and the left-sided in 35 (58.3%) cases. The QA values in the contralateral medial geniculate body, the bilateral anterior corona radiata and the anterior limb of internal capsule were significantly reduced in SSNHL patients compared to controls. In addition, the decrease QA value of the contralateral medial geniculate body was related to the increase severity of disease, even after controlling potential confounding factors. The present study demonstrated that patients with SSNHL exhibited altered integrity of white matter in the auditory neural pathway. Furthermore, the decreased QA values in the contralateral medial geniculate body might predict the severity of this disease. In the present study, tinnitus has not been found to effect in brain area obviously.

Diagnostic model of combined ceRNA and DNA methylation related genes in esophageal carcinoma.

Esophageal cancer is a common malignant tumor in the world, and the aim of this study was to screen key genes related to the development of esophageal cancer using a variety of bioinformatics analysis tools and analyze their biological functions. The data of esophageal squamous cell carcinoma from the Gene Expression Omnibus (GEO) were selected as the research object, processed and analyzed to screen differentially expressed microRNAs (miRNAs) and differential methylation genes. The competing endogenous RNAs (ceRNAs) interaction network of differentially expressed genes was constructed by bioinformatics tools DAVID, String, and Cytoscape. Biofunctional enrichment analysis was performed using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). The expression of the screened genes and the survival of the patients were verified. By analyzing GSE59973 and GSE114110, we found three down-regulated and nine up-regulated miRNAs. The gene expression matrix of GSE120356 was calculated by Pearson correlation coefficient, and the 11696 pairs of ceRNA relation were determined. In the ceRNA network, 643 lncRNAs and 147 mRNAs showed methylation difference. Functional enrichment analysis showed that these differentially expressed genes were mainly concentrated in the FoxO signaling pathway and were involved in the corresponding cascade of calcineurin. By analyzing the clinical data in The Cancer Genome Atlas (TCGA) database, it was found that four lncRNAs had an important impact on the survival and prognosis of esophageal carcinoma patients. QRT-PCR was also conducted to identify the expression of the key lncRNAs (RNF217-AS1, HCP5, ZFPM2-AS1 and HCG22) in ESCC samples. The selected key genes can provide theoretical guidance for further research on the molecular mechanism of esophageal carcinoma and the screening of molecular markers.

[Exploration of the process of prenatal screening and diagnosis for women with advanced maternal age based on results of 351 cases of fetal chromosomal abnormalities].

OBJECTIVE: To explore the suitable process for prenatal screening and diagnosis for women with advanced maternal age. METHODS: From January 2014 to November 2017, the indications and distributions of prenatal diagnosis for women with advanced maternal age only or accompanying with positive maternal serum test screening and non-invasive prenatal testing (NIPT), abnormal fetal ultrasound, one harboring chromosomal abnormalities or anomalous reproductive history were analyzed. The rate of fetal chromosomal abnormalities was compared between different groups. RESULTS: The 351 pregnant women with fetal chromosomal abnormalities have included 196 cases with advanced maternal age, 26 with positive maternal serum test, 96 with high-risk by NIPT, 14 with abnormal fetal ultrasound, 15 with one partner harboring chromosomal abnormalities, and 4 with anomalous reproductive history. Assuming that all pregnant women had undergone maternal serum test screening or NIPT without amniocentesis, the detection rate of fetal chromosome abnormality would be 51.0% and 69.2%, respectively. However, should these women have received both tests, the detection rate would be as high as 84.6%. Should those with one partner harboring chromosomal abnormalities undergone maternal serum test screening or NIPT without amniocentesis, the detection rate of fetal chromosomal abnormality would only be 6.7%. CONCLUSION: Should pregnant women with advanced maternal age undergo both maternal serum test and NIPT, the detection rate of fetal chromosomal abnormality will be higher than those receiving only maternal serum test screening or NIPT. Couples with one partner harboring chromosomal abnormalities should undergo prenatal diagnosis by amniocentesis.

Overexpression of G9a and MCM7 in oesophageal squamous cell carcinoma is associated with poor prognosis.

AIMS: Histone methyltransferase G9a has been primarily understood as a co-repressor of gene expression, but it has been shown that G9a also positively regulates nuclear receptor-mediated transcription. MCM7, a critical component of the DNA replication licensing complex, is amplified and overexpressed in a variety of human malignancies. The objectives of the present study were to study the relationship between the expression of G9a and MCM7 and the pathological grade, clinical stage and prognosis of oesophageal squamous cell carcinoma (OSCC). METHODS AND RESULTS: We collected 139 formalin-fixed and paraffin-embedded tissues from patients with OSCC and surveyed them by tissue microarray-based immunohistochemical staining. Associations between the expression of MCM7 and G9a and clinicopathological parameters and prognosis of OSCC were examined. From tissue microarray immunohistochemistry staining results, we found that nuclear staining intensity for MCM7 and G9a was associated with histological grade (both P < 0.001), tumour depth (P = 0.050, 0.034), lymph node metastasis (P = 0.001, 0.009) and tumour stage (P < 0.001, =0.003). G9a expression was correlated with that of MCM7. G9a overexpression independently predicted poor cancer-specific survival in OSCC (hazard ratio 0.05, 95% confidence interval 0.006-0.417, P = 0.006) and MCM7 (hazard ratio 0.05, 95% confidence interval 0.013-0.441, P = 0.004). OSCC patients whose tumours showed double-positive expression of G9a and MCM7 (G9a(+) MCM7(+) ) had much shorter survival than those from either the G9a or MCM7 low expression groups (G9a(-) MCM7(-) , G9a(+) MCM7(-) , G9a(-) MCM7(+) ). CONCLUSIONS: MCM7 and G9a may serve as effective prognostic factors and could also be used as biomarkers for predicting various clinical outcomes of OSCCs in the Chinese population.

Aberrant expression of NEK2 and its clinical significance in non-small cell lung cancer.

The purpose of the present study was to identify a potential biomarker that is more effective than those already available for the prognosis of non-small cell lung cancer (NSCLC) patients. The expression of never in mitosis gene A (NIMA)-related kinase 2 (NEK2), minichromosome maintenance complex component 7 (Mcm7) and Ki67 was evaluated in 270 NSCLC tissues using immunohistochemical and immunofluorescence techniques. Associations between protein expression and clinicopathological characters were assessed, and the impact on overall survival was analyzed. High levels of NEK2, Mcm7 and Ki67 expression were detected in 25.9, 35.2 and 24.4% of the NSCLC tissues. Overexpression of NEK2 was detected more frequently in cases with high T and N stages (P<0.0001 and P=0.011, respectively). Correlations were present between the expression of NEK2, Mcm7 and Ki67. Kaplan-Meier curves indicated that the patients with overexpressed NEK2, Mcm7 and Ki67 had a poorer overall survival time compared to those with low expression for all stages (P<0.0001). In particular, the patients with NEK2 overexpression had a poorer prognosis. Multivariate Cox regression analysis showed that NEK2, Mcm7 and Ki67 are independent prognostic indicators for NSCLC. In conclusion, the data indicate that compared with Mcm7 and Ki67, NEK2 may be a more effective tumor proliferation marker of poor prognosis for NSCLC patients, and that NEK2 may represent a novel potential target for NSCLC therapeutic intervention.

Examining Nek2 as a better proliferation marker in non-small cell lung cancer prognosis.

The purpose of this study is to identify a better potential biomarker for the prognosis of patients with non-small cell lung cancer (NSCLC). The expressions of Nek2, MCM7, and Ki-67 were evaluated in 270 NSCLC tissues using immunohistochemical and immunofluorescence techniques. Associations between protein expression and clinical pathologic characters were assessed, and the impact on overall survival was analyzed. We detected high levels of Nek2, MCM7, and Ki-67 expression in 25.9, 35.2, and 24.4 % of NSCLC tissues, respectively. Overexpressions of Nek2 were detected more frequently in high T-stage and N-stage cases (P = 0.000, 0.011). The expressions of Nek2, MCM7, and Ki-67 were correlated with each other. Kaplan-Meier curves indicated that patients with overexpression of Nek2, MCM7, and Ki-67 had a poorer overall survival rate compared to those with low expression for all stages (P = 0.000). In particular, the patients with Nek2 overexpression had the most negative prognosis. Multivariate Cox regression analysis showed that Nek2, MCM7, and Ki-67 are independent prognostic indicators for NSCLC. Our data suggest that among Nek2 kinase, MCM7, and Ki-67, it is Nek2 kinase that is the more effective tumor proliferation marker of poor prognosis for NSCLC patients. Thus, Nek2 may represent a new potential target for NSCLC therapeutic intervention.

Analysis of EHMT1 expression and its correlations with clinical significance in esophageal squamous cell cancer.

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy, requiring effective biomarkers for prognosis and therapeutic responsiveness. Histone H3K9 methyltransferases (EHMT1 and EHMT2) are global genome organizers, which are crucial for maintaining the balance state of cells in a tissue-specific manner. It was previously suggested that EHMT1 expression is a predictor of prognosis in several malignant tumors; however, the prognostic significance of EHMT1 expression in ESCC has not been determined. A cohort of 50 ESCC cases and 46 paired normal esophageal tissue samples were evaluated to assess the levels of EHMT1 expression by immunohistochemistry and reverse transcription-polymerase chain reaction. The SPSS software package was used for statistical data analysis. A significantly upregulated EHMT1 expression was observed in squamous preinvasive lesions and ESCC compared to the matched normal esophageal epithelia (52.0 vs. 21.7%, respectively). The expression of EHMT1 was correlated with tumor grade (G), depth of invasion (T) and lymph node metastasis (N) in ESCC. EHMT1 overexpression was found to be associated with poor cancer-specific survival in squamous cell carcinomas (χ2=3.922, P=0.048). The expression of EHMT1 was identified as an independent prognostic factor for overall survival in ESCC patients. In conclusion, EHMT1 expression is upregulated in ESCC and early preinvasive esophageal squamous lesions and the overexpression of EHMT1 is associated with poor prognosis in ESCC. Therefore, the expression of EHMT1 may be an effective prognostic biomarker for ESCC.