Esophageal cancer is one of the leading malignancies globally and long non-coding RNAs (lncRNAs) have been proved to have an important role in different malignancies including esophageal cancer. However their role in disease progression is still not clear. The objective of the study was to investigate the expression and role of LINC01234 in progression of esophageal cancer cells. LncRNA LINC01234 was found to be upregulated in esophageal cancer cells by chip sequencing. The expression level of LINC01234 was detected from different esophageal cancer cell lines by qRT-PCR. After this, the LINC01234 knockdown effects on cell proliferation, migration, invasion, and apoptosis were evaluated by cell proliferation assay, wound healing assay, invasion assay, and flow cytometric analysis in vitro. Expression of lncRNA LINC01234 was found to be markedly upregulated in the CEC2 cell line. Furthermore, cell proliferation, migration and invasion were significantly (P < 0.05) suppressed as compared to negative control while apoptotic rate was also found increased as a result of the knockdown of LINC01234. Significantly upregulated expression of LINC01234 in CEC2 cells and downregulated expression after knockdown is observed. The impact of LINC01234 knockdown on cell migration, invasion, proliferation and apoptosis indicated that LINC01234 may represent a new marker and a potential therapeutic target for esophageal cancer.
Background: Esophageal cancer is one of the most common malignant tumours in humans. A series of esophageal cancer cell lines are accompanied by human papilloma virus (HPV) infection, but the mechanism behind HPV in cancer malignancy is not clear.Methods: This research was conducted in different generations of HPV E6E7 gene-induced human foetal esophageal epithelial immortalised cells (Shantou Human Embryonic Esophageal Epithelial cell line; SHEE); the RNA sequencing transcriptomic analysis was performed to explore the mechanism of HPV infection in these cell lines. Results:The results showed that there are 9,990 differential genes in late-stage cells compared with HPV18 E6E7-infected early foetal esophageal epithelial immortalised cells. Among these, 4,882 genes are upregulated, and 5,108 genes are downregulated. We used bioinformatics to analyze the expression and function of aberrantly expressed lncRNA, miRNA, mRNA and construct the competing endogenous RNA (ceRNA) network and protein protein interaction (PPI) network.Conclusions: we predicted TP53TG1 promotes to malignant transformation of SHEEs by acting as a ceRNA to competitively bind to miR-6835 and regulate IGF2 expression. We also predicted IL6 serve as prognostic biomarkers and therapy target. With these results maybe provides new insights into the mechanisms of HPV carcinogenesis in esophageal cancer.
Objective The incidence of the upper gastrointestinal tumor has increased rapidly during recent decades. The relationship between local water pollution and the tumor is still not much clear, so this study was conducted to further investigate the local water pollution and its influence on the malignant cell transformation. Prevalence of human papillomavirus (HPV) in local esophageal cancer (EC) patients was also analyzed in Shenqiu County for the first time. Methods Two-step cell transformation was used to study different sources of water in the malignant cell transformation, and the existence of 3-methylcholanthrene (3-MC) in water was analyzed from the river and shallow and deep wells. HPV DNA in tissue samples of EC patients was detected by polymerase chain reaction (PCR) and HPV diagnostic kit. Results The river water has higher cytotoxicity than the shallow well water and induced significant cell malignant transformation, while deep well water has not shown the malignant cell transformation. In Huaihe River water, the 3-MC concentration was found higher than shallow and deep wells. An HPV infection rate was found high in patients with esophageal cancer. Conclusion Long-term consumption of polluted water can induce malignant cell transformation, and the presence of HPV may be an important cause of cancer.
The development of esophageal cancer accompanied by the presence of human papillomavirus (HPV) DNA into the host genome. By evaluating the expression of this virus for tumor cell origin and also their cell grows and migrations, we examined esophageal cancer clonality in the context of intra-tumor heterogeneity. In this research, we have checked the expression of HPV18 E6 and E7 in different single cell clones by the manual cell picking method in the HPV positive esophageal cancer (EC109), EC109 cell line used as a negative control, and Hela cell line used as the positive control. Quantitative real-time PCR (QRT-PCR) was run to detect the expression levels of HPV E6 and E7, Cell Counting Kit-8 (CCK-8) assay was used to examine cell proliferation, invasion assays performed using Costar chambers and wounding assay to study cell migrations in vitro. We investigated the intra-tumor heterogeneity of HPV E6 and E7 in esophageal cancer and the evaluation of the growth and migrations at the clonal level, using 10 single cell clones. In particular clones, C7 & C10 displayed a highly variable expression in both HPV E6 and E7 and weak in four clones (C1, C3, C4, and C9) consequently, the cell invasion, proliferation, and migration increase with increasing the level of HPV expression and inverse. In conclusion, the resulting based on single cell cloning showed the relationship between HPV and cell growth and migration in esophageal cancer. Future study in HPV DNA integration needed to explore the mains specific integration site of HPV DNA in esophageal cancer and molecular monitoring of the HPV for future prevention researches and also effective therapeutic strategies.
Human papillomavirus (HPV) infection was associated with some carcinomas, especially malignant tumors in upper digestive tract, upper respiratory tract, and genitourinary system. The mechanism of the viral transformation of normal cells is still not very clear. To investigate the tumorigenesis of epithelial cells, E6/E7‐induced malignant transformation model cells were used for expression profiling analysis by performing RNA expression microarray detection. Bioinformatics analysis was applied to investigate the cellular process changes along with the E6/E7 expression in SHEE cells. The differentially expressed genes were further grouped and uploaded for Search Tool for the Retrieval of Interacting Genes analysis. The protein‐protein interaction results were visualized. The hub genes and their first‐neighbors genes were selected, followed by gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis. The obtained results demonstrated that tumor‐related biological processes began to emerge during the carcinogenesis process from 48th passage to 76th passage of SHEE cells after E6/E7 expression. Ten hub genes were identified and analyzed during the E6/E7‐induced tumorigenesis. This study explores the gene expression network in the progressive transformation of immortalized esophageal epithelial cells induced by E6/E7 expression. Understanding the biological processes and hub genes that first appear during the transformation will provide some clues to the mechanism of E6/E7‐induced carcinogenesis of esophageal epithelial cells.
Cancers are multifactorial but the advancement in research in the recent decades have drawn attention towards lncRNAs as they are proven to play important function as biological regulators. LINC01234, CASC9 are important long non coding RNAs (lncRNAs). They are not extensively studied therefore, their role in esophageal cancer as well as in other cancers is still not clear. There are few studies about LINC01234 and CASC9 for their role in esophageal cancer. The objective of the study was to investigate the expression of LINC01234 and CASC9 in different cell lines. Our lab cultured and maintained model esophageal cancer cells which were obtained after transformation of human embryonic esophageal epithelial cells into malignant cells by HPV18 E6E7. After this, elevated expression of LINC01234 was found in Gene Chip showing that it may have some role in causing esophageal cancer. For further verification, qRT-PCR was used for the detection of expression level of LINC01234 in different cell lines. Furthermore, expression of CASC9 was also investigated by qRT-PCR in different cell lines. Expression of LINC01234 and CASC9 was markedly high in esophageal cancer cell lines as compared to other cell lines while high expression of LINC01234 was also found in one lung cancer cell line. These lncRNAs may be used as biomarker and potential therapeutic target for esophageal cancer intervention by further exploration of their functions.
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