Nomogram based on multimodal magnetic resonance combined with B7-H3mRNA for preoperative lymph node prediction in esophagus cancer.

BACKGROUND: Accurate preoperative prediction of lymph node metastasis (LNM) in esophageal cancer (EC) patients is of crucial clinical significance for treatment planning and prognosis. AIM: To develop a clinical radiomics nomogram that can predict the preoperative lymph node (LN) status in EC patients. METHODS: A total of 32 EC patients confirmed by clinical pathology (who underwent surgical treatment) were included. Real-time fluorescent quantitative reverse transcription-polymerase chain reaction was used to detect the expression of B7-H3 mRNA in EC tissue obtained during preoperative gastroscopy, and its correlation with LNM was analyzed. Radiomics features were extracted from multi-modal magnetic resonance imaging of EC using Pyradiomics in Python. Feature extraction, data dimensionality reduction, and feature selection were performed using XGBoost model and leave-one-out cross-validation. Multivariable logistic regression analysis was used to establish the prediction model, which included radiomics features, LN status from computed tomography (CT) reports, and B7-H3 mRNA expression, represented by a radiomics nomogram. Receiver operating characteristic area under the curve (AUC) and decision curve analysis (DCA) were used to evaluate the predictive performance and clinical application value of the model. RESULTS: The relative expression of B7-H3 mRNA in EC patients with LNM was higher than in those without metastasis, and the difference was statistically significant (P < 0.05). The AUC value in the receiver operating characteristic (ROC) curve was 0.718 (95%CI: 0.528-0.907), with a sensitivity of 0.733 and specificity of 0.706, indicating good diagnostic performance. The individualized clinical prediction nomogram included radiomics features, LN status from CT reports, and B7-H3 mRNA expression. The ROC curve demonstrated good diagnostic value, with an AUC value of 0.765 (95%CI: 0.598-0.931), sensitivity of 0.800, and specificity of 0.706. DCA indicated the practical value of the radiomics nomogram in clinical practice. CONCLUSION: This study developed a radiomics nomogram that includes radiomics features, LN status from CT reports, and B7-H3 mRNA expression, enabling convenient preoperative individualized prediction of LNM in EC patients.

LINC01133 regulates MARCKS expression via sponging miR-30d-5p to promote the development of lung squamous cell carcinoma.

LncRNAs are vital regulators for lung squamous cell carcinoma (LUSC). However, the detailed role that LINC01133 plays in LUSC is unclear. This work sought to explore the potential function of LINC01133.Levels of LINC01133, miR-30d-5p, and MARCKS were separately tested in both tissues and cells using qRT-PCR. Proliferation was assessed through MTT experiment and apoptosis was detected upon flow cytometry. Transwell experiments were implemented to evaluate migratory and invasive abilities. The interaction between two genes was affirmed through luciferase reporter assay and RNA pull-down experiment. Western blotting measured the protein level of MARCKS. Animal models were established and tissues were taken for IHC analysis of MARCKS and Ki67.LINC01133 was elevated in LUSC and its downregulation could suppress proliferation, migration and invasion but induced apoptosis. LINC01133 interacted with and regulated the binding of miR-30d-5p to MARCKS. LINC01133/miR-30d-5p axis mediated proliferation, apoptosis, migration and invasion in LUSC cells, as well as modulated tumor growth in animal models. LINC01133 interacted with miR-30d-5p to modulate MARCKS expression, contributes to promoted cell proliferation, migration, invasion, and inhibited cell apoptosis in vitro, and promoted tumor growth in vivo. These findings could provide possible therapeutic targets in view of LUSC treatment in the future.

[Retracted] MACC­1 antibody target therapy suppresses growth and migration of non­small cell lung cancer.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the control data in Fig. 2B and C on p. 7332, showing immunofluorescence and migration assay experiments respectively, were strikingly similar to data appearing in different form in another article which was written by different authors at different research institutes [Tian L, Shen D, Li X, Shan X, Wang X, Yan Q and Liu J: Ginsenoside Rg3 inhibits epithelial­mesenchymal transition (EMT) and invasion of lung cancer by down­regulating FUT4. Oncotarget 7: 1619­1632, 2016]. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 7329­7336, 2017; DOI: 10.3892/mmr.2017.7517].

Pancancer analysis of the correlations of HS6ST2 with prognosis, tumor immunity, and drug resistance.

HS6ST2 has ability to encodes a member of the heparan sulfate (HS) sulfotransferase gene family, which catalyze the transfer of sulfate to HS and a crucial regulator of cell growth, differentiation, adhesion, and migration. Although mounting evidence supports a vital role for HS6ST2 in tumorigenesis of some cancers, no pan-cancer analysis of HS6ST2 has been reported. Therefore, we aimed to explore the prognostic value of HS6ST2 in 33 cancer types and investigate its potential immune function. Based on data from The Cancer Genome Atlas, Cancer Cell Lines Encyclopedia, Genotype Tissue Expression, and GSCA, we used a range of bioinformatics approaches to explore the potential carcinogenic role of HS6ST2, analysis of HS6ST2 and prognosis, DNA methylation, RNA methylation, microsatellite instability (MSI), tumor mutation burden (TMB), and immune cell infiltration in different tumors. The results show that HS6ST2 was highly expressed in most cancers but lower in Breast invasive carcinoma, Kidney Chromophobe, Kidney renal clear cell carcinoma, Kidney renal papillary cell carcinoma, and Uterine Corpus Endometrial Carcinoma. Moreover, HS6ST2 is positively or negatively associated with prognosis in different cancers. HS6ST2 expression was not only associated with MSI in 5 cancer types and associated with TMB in 10 cancer types, and it's significantly correlated with DNA methylation in 13 types of cancer, but it's correlated with RNA methylation related genes in most cancer. HS6ST2 expression was correlated with immune cell infiltration, immune-related genes, tumor immune microenvironment, and drug resistance in various cancers. Eventually, HS6ST2 was validated in human lung adenocarcinoma tissues. Our study reveals that HS6ST2 can function as a prognostic marker in various malignant tumors because of its role in tumorigenesis and tumor immunity.

Estrogen Sulfotransferase SULT1E1 Expression Levels and Regulated Factors in Malignant Tumours.

Estrogen plays a key role in the development and progression of many malignant tumours, and the regulation of estrogen levels involves several metabolic pathways. Among these pathways, estrogen sulfotransferase (SULT1E1) is the enzyme with the most affinity for estrogen and is primarily responsible for catalysing the metabolic reaction of estrogen sulphation. Relevant studies have shown significant differences in the expression of SULT1E1 in different malignant tumours, suggesting that SULT1E1 plays a dual role in malignant tumours, both inhibiting the growth of malignant tumours and promoting their development. In addition, the expression level of SULT1E1 may be regulated by a variety of factors, which in turn affect the growth and therapeutic effects of malignant tumours. The aim of this paper is to review the mechanism of action of SULT1E1 in malignant tumours and the mechanisms that are regulated, in order to provide potential targets for the treatment of malignant tumour patients in the future and theoretical support for the realisation of more personalised and effective therapeutic regimens.

Progress of magnetic resonance imaging radiomics in preoperative lymph node diagnosis of esophageal cancer.

Esophageal cancer, also referred to as esophagus cancer, is a prevalent disease in the cardiothoracic field and is a leading cause of cancer-related mortality in China. Accurately determining the status of lymph nodes is crucial for developing treatment plans, defining the scope of intraoperative lymph node dissection, and ascertaining the prognosis of patients with esophageal cancer. Recent advances in diffusion-weighted imaging and dynamic contrast-enhanced magnetic resonance imaging (MRI) have improved the effectiveness of MRI for assessing lymph node involvement, making it a beneficial tool for guiding personalized treatment plans for patients with esophageal cancer in a clinical setting. Radiomics is a recently developed imaging technique that transforms radiological image data from regions of interest into high-dimensional feature data that can be analyzed. The features, such as shape, texture, and waveform, are associated with the cancer phenotype and tumor microenvironment. When these features correlate with the clinical disease outcomes, they form the basis for specific and reliable clinical evidence. This study aimed to review the potential clinical applications of MRI-based radiomics in studying the lymph nodes affected by esophageal cancer. The combination of MRI and radiomics is a powerful tool for diagnosing and treating esophageal cancer, enabling a more personalized and effectual approach.

Prognostic role of vitamin D receptor in digestive system tumours: A systematic review and preliminary meta-analysis.

The prognostic value of vitamin D receptor (VDR) in a variety of digestive system tumours remains controversial. In view of this, we conducted a meta-analysis. Published studies (as of Mar 30, 2023) assessing the prognostic role of VDR in digestive system tumours were retrieved. Pooled analyses were conducted based on the hazard ratios (HRs) of high VDR expression extracted from the included studies. If heterogeneity was detected, the random-effects model was used; otherwise, the fixed-effects model was used. Subgroup analysis, sensitivity analysis and meta-regression were performed to explore the sources of heterogeneity. Eight studies with 3,109 patients were included. The pooled results indicated that patients with high VDR expression generally had better overall survival (OS) (pooled HR = 0.67; 95% CI = 0.53-0.85; P = 0.001). Subgroup analyses showed that tumour type was the variable affecting the association between VDR expression and OS. VDR expression in colorectal cancer was not associated with OS (pooled HR = 0.84; 95% CI = 0.68-1.03; P = 0.086). We eliminated publication bias using the "trim and fill" method and found that high VDR expression remained an indicator of good OS (P = 0.001). Only a few studies explored the relationship between VDR expression and cancer-specific survival (CSS) or progression-free survival (PFS), and the pooled results indicated no association between them (P>0.05). VDR expression is a prognostic indicator in digestive system tumours and may also be used as a reference for vitamin D supplementation. Detection of VDR expression not only helps to evaluate prognosis but also to formulate more precise treatment plans for patients with digestive system tumours.

Over-expression of USP15/MMP3 predict poor prognosis and promote growth, migration in non-small cell lung cancer cells.

Aberrant ubiquitin modifications caused by an imbalance in the activities of ubiquitinases and de-ubiquitinases are emerging as important mechanisms underlying non-small cell lung cancer (NSCLC) progression. The deubiquitinating enzyme ubiquitin-specific peptidase 15 (USP15) has been identified as an important factor in oncogenesis and a potential therapeutic target. However, the expression profile and function of USP15 in NSCLC remain elusive. In the present study, we investigated the expression pattern and the potential biological functions of USP15 in NSCLC both in cells and animal models. Our data revealed that USP15 was highly expressed in NSCLC tissues and cells compared with normal counterpart. We subsequently knocked down USP15 expression in two NSCLC cell lines, which significantly suppressed cell proliferation. In addition, knocking down USP15 expression reduced NSCLC cell migration and invasion according to the results from Matrigel-Transwell analysis. NSCLC animal model results showed that USP15 knockdown also reduced NSCLC size. Biochemical analysis revealed that USP15 knockdown inhibited matrix metalloproteinase (MMP)3 and MMP9 expression. Furthermore, high levels of USP15 and MMP3 expression were associated with poor prognosis in NSCLC. In conclusion, the results from the present study suggest that the high expression of USP15 promotes NSCLC tumorigenesis. Therefore, it is proposed that USP15 and MMPs may represent novel biomarkers for NSCLC progression and prognosis.

Effect of different surgical approaches on the prognosis of patients with postoperative radiotherapy for stage IIB-IVA esophageal squamous cancer.

OBJECTIVE: To investigate the effect and clinical significance of different thoracic surgical approaches for patients with stage IIB-IVA esophageal squamous cell carcinoma on the survival and prognosis of postoperative radiotherapy patients. METHODS: One hundred thirty-two patients with stage IIB-IVA esophageal squamous cancer who received radiotherapy after surgery were screened for baseline characteristics and survival analysis. The Kaplan-Meier method was used to draw the survival curve for the follow-up data, and the log-rank test was used to compare the difference in survival rate between the two groups. The Cox regression model was used for multivariate survival analysis. RESULT: For stage IIB-IVA esophageal squamous cell carcinoma, the results of multivariate analysis showed that different surgical methods and clinical staging were independent factors affecting the survival and prognosis of patients after radiotherapy. The 1-, 3-, and 5-year survival rates of patients with advanced esophageal cancer through the left chest approach were 84.2%, 61.4%, and 36.8% respectively. The 1-, 3-, and 5-year survival rates of patients with advanced esophageal cancer through the right chest approach were 73.3%, 40.0%, and 21.3% respectively. There was no significant difference in the 1-year survival rate (P = 0.135) between the two surgical procedures. The 3-year survival rate (P < 0.05) and the 5-year survival rate (P < 0.05) were significantly different. CONCLUSION: For patients with stage IIB-IVA esophageal squamous cell carcinoma undergoing radiotherapy after surgery, the long-term survival prognosis of patients after the left thoracic approach is significantly higher than that of the right thoracic approach.

NUF2 Is a Potential Immunological and Prognostic Marker for Non-Small-Cell Lung Cancer.

Background: Globally, non-small-cell lung cancer (NSCLC) is one of the most prevalent tumors. Various studies have investigated its etiology, but the molecular mechanism of NSCLC has not been elucidated. Methods: The GSE19804, GSE118370, GSE19188, GSE27262, and GSE33532 microarray datasets were obtained from the Gene Expression Omnibus (GEO) database for the identification of genes involved in NSCLC development as well as progression. Then, the identified differentially expressed genes (DEGs) were subjected to functional enrichment analyses. The protein-protein interaction (PPI) network was built after which module analysis was conducted via the Search Tool for Retrieval of Interacting Genes/Proteins (STRING) and Cytoscape. There were 562 DEGs: 98 downregulated genes and 464 upregulated. These DEGs were established to be enriched in p53 signaling pathway, transendothelial leukocyte migration, cell adhesion molecules, contractions of vascular smooth muscles, coagulation and complement cascades, and axon guidance. Assessment of tumor immunity was performed to determine the roles of hub genes. Results: There were 562 dysregulated genes, while 12 genes were hub genes. NUF2 was established to be a candidate immunotherapeutic target with potential clinical implications. The 12 hub genes were highly enriched in the p53 signaling pathway, the cell cycle, progesterone-associated oocyte maturation, cellular senescence, and oocyte meiosis. Survival analysis showed that NUF2 is associated with NSCLC occurrence, invasion, and recurrence. Conclusion: The NUF2 gene discovered in this study helps us clarify the pathomechanisms of NSCLC occurrence as well as progression and provides a potential diagnostic and therapeutic target for NSCLC.

Aristolochic acid nephropathy: A scientometric analysis of literature published from 1971 to 2019.

BACKGROUND: Aristolochic acid nephropathy (AAN) is a type of drug-induced nephropathy that may result in acute kidney injury and is associated with a potentially progressive course of kidney fibrosis and upper tract urothelial carcinoma. Aristolochic acids (AAs) are a group of toxins commonly present in plants of the genera Aristolochia and Asarum, which are found worldwide. AAN still occurs in Asian and Balkan regions. The progressive lesions and mutational events initiated by AAs are irreversible, and no effective therapeutic regimen for AAN has been established. Furthermore, more people are at risk of this disease due to casual exposure to AAs. This study performed a scientometric analysis of global research literature focusing on AAN. METHODS: The Web of Science database was searched to identify all publications pertaining to "aristolochic acid nephropathy" or "Balkan endemic nephropathy" using these terms as key words to search the literature from 1971 to 2019. The collected data included the document type, author, journal, publication year, citation reports, and country of publication, and were analyzed using the VOSviewer software. RESULTS: A total of 1251 records were initially obtained. Publication types, including "meeting abstract," "letter," "editorial material," and "proceedings paper" were excluded, which left 1083 publications comprising 923 articles and 160 reviews. English was the predominant language of the publications. China had the most number of articles published with 217 (20.0%), followed by the USA with 186 articles (17.2%), and Germany with 138 articles (12.7%). Kidney International, Food and Chemical Toxicology, and Toxins were the 3 most active journals in publishing articles related to AAN. The total number of citations received by all publications was 39,970, with an average of 36.91 citations per article (range: 0-1769). The literature mainly focused on apoptosis, oxidative stress, and inflammation in AAN. CONCLUSION: This study indicated that AAN is a significant topic in nephrology research, as shown by the large number of publications. The literature has mainly focused on the mechanisms of AA-induced nephropathy.

LINC00518 Promotes Cell Proliferation by Regulating the Cell Cycle of Lung Adenocarcinoma Through miR-185-3p Targeting MECP2.

Previous studies have shown that long intergenic non-protein coding RNA 00518 (LINC00518) are essential for the cell growth and metastasis of human cancer. However, the role of LINC00518 in lung adenocarcinoma (LUAD) is still unknown. This research put emphasis on the function of LINC00518 on the cell growth of LUAD. The lncRNA, miRNA and mRNA expression were measured by using qRT-PCR. Protein levels were measured by using Western blotting. CCK-8, colony formation assays and transwell assay were performed to evaluate the cell proliferation ability and invasion. Bioinformatic analysis and luciferase reporter assays were chosen to confirm the mechanism of LINC00518 in LUAD. We found that LINC00518 was highly expressed in LUAD specimens and the high-expression was negatively correlated with the overall survival rates. This finding was also proved in the LUAD cell lines. Through a series of in vitro and in vivo experiments, we proved that LICN00518 promoted the cell growth of LUAD by regulating the cell cycle. Moreover, LICN00518 upregulated the expression of MECP2 by mutagenesis of miR-185-3p. The results suggested that LICN00518 could be used as a survival indicator and potential therapeutic target for LUAD patients.

LncRNA MTX2-6 Suppresses Cell Proliferation by Acting as ceRNA of miR-574-5p to Accumulate SMAD4 in Esophageal Squamous Cell Carcinoma.

Esophageal squamous cell carcinoma (ESCC) has been one of the key causes of cancer deaths worldwide. It has been found that long non-coding RNA (lncRNA) is related to the generation and progression of various cancers (including ESCC). However, there are still many lncRNAs related to ESCC whose functions and molecular mechanisms have not been clearly elucidated. In this study, we first reported that lncRNA MTX2-6 was significantly downregulated in ESCC tissues and cell lines. The decreased expression of MTX2-6 is closely related to larger tumor and worse prognosis of ESCC patients. Through a series of functional experiments, we detected that overexpressed MTX2-6 inhibited cell proliferation and promoted cell apoptosis of ESCC in vitro and in vivo. Further studies showed that MTX2-6 exerts as a competing endogenous RNA (ceRNA) by binding miR-574-5p and elevates the expression of SMAD4 in ESCC. In summary, our results clarify the tumor suppressor roles of MTX2-6/miR-574-5p/SMAD4 axis in the progression of ESCC and provide emerging therapeutic targets for ESCC patients.

Downregulation of circRNA_100876 Inhibited Progression of NSCLC In Vitro via Targeting miR-636.

BACKGROUND: Non-small cell lung carcinoma (NSCLC) is a common malignant tumor with poor prognosis. CircRNA-100876 has been considered to be involved in NSCLC. However, the mechanism by which circRNA_100876 mediated the progression of NSCLC remains unclear. METHODS: CCK8 assay and immunofluorescence were used to detect cell proliferation. Flow cytometry and transwell assay were performed to analyze cell apoptosis, migration and invasion, respectively. Verification of possible target for circRNA_100876 and related miR-636 were done using luciferase assay. In addition, western blot was performed to detect the protein expressions in NSCLC cells. RESULTS: Silencing of circRNA_100876 notably inhibited the proliferation of NSCLC cells. Moreover, downregulation of circRNA_100876 significantly induce the apoptosis of NSCLC cells via mediation of apoptosis-related proteins. In addition, silencing of circRNA_100876 significantly inhibited migration and invasion of NSCLC cells. MiR-636 was the downstream target of circRNA_100876. Meanwhile, RET was the direct target of miR-636. Finally, circRNA_100876 shRNA2 notably suppressed the progression of NSCLC through PI3K/Akt signaling. CONCLUSION: CircRNA_100876 knockdown notably suppressed the progression of NSCLC through regulation of miR-636/RET axis, which may serve as a potential target for treatment of NSCLC.

Downregulation of miR-7-5p Inhibits the Tumorigenesis of Esophagus Cancer via Targeting KLF4.

BACKGROUND: Esophageal cancer (EC) is one of the aggressive gastrointestinal malignancies. It has been reported that microRNAs (miRNAs) play key roles during the tumorigenesis of EC. To identify novel potential targets for EC, differential expressed miRNAs (DEG) between EC and adjacent normal tissues were analyzed with bioinformatics tool. METHODS: The differential expression of miRNAs between EC and adjacent normal tissues was analyzed. CCK-8 and Ki67 staining were used to detect the cell proliferation. Flow cytometry was performed to test the cell apoptosis. The correlation between miR-7-5p and KLF4 was detected by dual-luciferase report assay. Gene and protein expression in EC cells or in tissues were measured by qRT-PCR and Western blot, respectively. Cell migration and invasion were detected with transwell assay. Xenograft mice model was established to investigate the role of miR-7-5p in EC tumorigenesis in vivo. RESULTS: MiR-7-5p was found to be negatively correlated with the survival rate of patient with EC. In addition, downregulation of miR-7-5p significantly inhibited the growth and invasion of EC cells. Meanwhile, miR-7-5p directly targeted KLF4 in EC cells. Moreover, downregulation of miR-7-5p inhibited the tumorigenesis of EC via inactivating MAPK signaling pathway in vivo. CONCLUSION: Downregulation of miR-7-5p notably suppressed the progression of EC via targeting KLF4. Thus, miR-7-5p might serve as a new target for the treatment of EC.

Silence of FOXD2-AS1 inhibited the proliferation and invasion of esophagus cells by regulating miR-145-5p/CDK6 axis.

This study aimed to investigate the function of long non-coding RNA FOXD2 adjacent opposite strand RNA 1 (lncRNA FOXD2-AS1) during the progression of esophagus cancer (EC) and explore its underlying molecular mechanisms. The level of FOXD2-AS1 in EC tissues and paracancerous tissues was detected by using RT-qPCR; ROC curve was used to evaluate the diagnostic value of FOXD2-AS1 for EC. In addition, CCK8 assay and immunofluorescence staining assay were used to detect the proliferation of Eca-109 and TE-1 cells. To investigate the function of FOXD2-AS1 on cell apoptosis and cell cycle, flow cytometry was performed. To detect the invasion ability of EC cells, transwell invasion assay was performed. Starbase3.0 and Targetscan were used to predict the target genes of FOXD2-AS1 and miR-145-5p, and protein expressions were detected with western blot. We found FOXD2-AS1 was significantly upregulated in EC tissues compared with adjacent normal tissues, which was positively correlated with clinicopathological parameters of patients with EC. Downregulation of FOXD2-AS1 inhibited the proliferation and invasion by inducing apoptosis of EC cells. Moreover, FOXD2-AS1 may regulate the expression of CDK6 by targeting miR-145-3p. Meanwhile, silencing of FOXD2-AS1 caused G1 phase arrest of EC cells by reducing the expression of CDK6. In conclusion, silening FOXD2-AS1 significantly inhibited the proliferation and invasion of EC cells by regulating the miR-145-5p/CDK6 axis. Therefore, FOXD2-AS1 might be used as diagnostic biomarker and therapeutic target for EC.

BLACAT1 predicts poor prognosis and serves as oncogenic lncRNA in small-cell lung cancer.

Bladder cancer-associated transcript 1 (BLACAT1) is a novel identified long noncoding RNA (lncRNA) in bladder cancer, and has been suggested to function as an oncogenic lncRNA in several types of human cancer. However, its involvement in the progression of small-cell lung cancer (SCLC) remained unknown. The aim of our study was to investigate the clinical value and biological function in SCLC. In our results, BLACAT1 expression was increased in SCLC tissues and cell lines compared with paired adjacent normal tissues and bronchial epithelial cell lines, respectively. In addition, BLACAT1 high-expression was obviously associated with advanced clinical stage, large tumor size, more lymph node metastasis, present distant metastasis, and poor prognosis. Furthermore, multivariate analysis indicated that high-expression of BLACAT1 acted as an independent poor prognostic factor for overall survival in SCLC cases. The loss-of-function studies suggested that of BLACAT1 suppressed SCLC cell proliferation, migration, and invasion, and induced G0/G1 phase arrest. In conclusion, BLACAT1 is associated with the malignant status and prognosis in patients with SCLC, and functions as an oncogenic lncRNA in regulating cell proliferation and motility, suggesting BLACAT1 may act as a potential target for SCLC prevention and treatment.

E2F transcription factor 8 promotes cell proliferation via CCND1/p21 in esophageal squamous cell carcinoma.

PURPOSE: E2F transcription factor 8 (E2F8) is a novel member of the E2F family, but its function in esophageal squamous cell carcinoma (ESCC) remains unclear. This study aimed to research the function of E2F8 in ESCC. MATERIALS AND METHODS: We used quantitative real-time PCR and Western blot analyses to detect the expression pattern of E2F8 in ESCC. The effects of E2F8 on proliferation were investigated by Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine, and colony formation assays. We also confirmed the function of E2F8 in vivo. RESULTS: E2F8 expression was upregulated in ESCC, and promoted cell proliferation and influenced the expression of CCND1/p21. Downregulation of E2F8 expression inhibited cell proliferation in vivo. CONCLUSION: E2F8 was identified as a new potential oncogene in ESCC.

Grim-19 expressed by recombinant adenovirus for esophageal neoplasm target therapy.

Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EA) are the two most common types of esophageal cancer, which is the sixth highest cause of cancer­associated mortality and the eighth most common cancer worldwide. Gene associated with retinoid­interferon (IFN)­induced mortality­19 (Grim­19) is reported to be a cell death activator that may be used to define mechanisms involved in IFN­ß­ and retinoic acid­induced cell death and apoptosis in a number of tumor cell lines. The present study constructed a recombinant adenovirus expressing Grim­19 (rAd­Grim­19) and investigated its therapeutic outcomes in ESCC cells and tumor­bearing mice. Grim­19 expression was detected in EC­109 (ESCC) cells by reverse transcription­quantitative polymerase chain reaction and western blot analysis. Tumor cell death and apoptosis induced by rAd­Grim­19 in EC­109 cells were analyzed by flow cytometry. The inhibitory effects of rAd­Grim­19 on EC­109 growth were determined by MTT assays. Furthermore, the therapeutic effects of rAd­Grim­19 were investigated in EC­109­bearing mice. The results demonstrated that Grim­19 mRNA and protein expression was downregulated in EC­109 esophageal carcinoma cells compared with Het­1A normal esophageal epithelial cells. In addition, EC­109 cells exhibited a significant reduction in tumor cell growth in the rAd­Grim­19 group compared with the control groups. Furthermore, rAd­Grim­19 increased EC­109 cell apoptosis compared with the control group. These results indicated that rAd-Grim-19 may regulate tumor cell growth and apoptosis. Additionally, the results demonstrated that rAd­Grim­19 led to beneficial outcomes and prolonged the survival of esophageal tumor­bearing mice. In conclusion, the present study demonstrated that rAd­Grim­19 may have potential as an antitumor agent for esophageal neoplasms and may therefore be beneficial for patients with esophageal neoplasms.