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.
Dysregulation of miR-203-3p and miR-21-5p has been identified in esophageal cancer (EC). The restoration of miR-203-3p and reduction of miR-21-5p were able to cause tumor suppression. Here, co-transfection of miR-203-3p mimics and miR-21-5p inhibitors led to an extraordinary increased expression of miR-203-3p and synergistically inhibited proliferation, migration, and invasion in EC cells. Moreover, we found that Ran GTPase (Ran) was dramatically inhibited in EC cells treated with the co-transfection of miR-203-3p mimics and miR-21-5p inhibitors. Finally, in-vivo studies showed that overexpression of miR-203-3p, combined with the suppression of miR-21-5p, significantly co-inhibited growth of tumors. The obtained data suggested that the development of miRNA-based combination therapeutics represents a promising cancer treatment strategy.
Esophageal carcinoma (EC) is the sixth most deadly of all cancers. It is among the most malignant cancers due to its highly aggressive nature and low survival rate. The incidence of EC is high in Asia, particularly in Southern areas including China, Iran and Japan. There is a large body of evidence to suggest an association between the melanoma antigen gene (MAGE) family and the initiation of cancer; however, there is no clear evidence to suggest an association between EC and MAGE. Discovery of the chemical and physiological processes relevant to the occurrence of EC is vital for clinicians to diagnose and treat this highly aggressive cancer. The present study focused on the association of EC with the expression of MAGE family member A6 (MAGEA6) at the mRNA and protein levels using gene chip, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry. The expression of MAGEA6 in human esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) tissue samples were compared with those in paracancerous tissue. The result of the gene chip assay revealed that as the generation grew, there was a significant increase in MAGEA6 transcription in the esophageal epithelial cell line, SHEE Different ESC cell lines also exhibited a significantly higher transcription of MAGEA6 compared with the HaCaT cell line, as determined via reverse transcription-quantitative PCR. An higher positive rate of MAGEA6 expression in ESCC and EAC tissues was also revealed when compared with paracancerous tissues, as determined via immunohistochemistry. The results indicated that MAGEA6 is highly transcribed and expressed in the development of EC and may therefore serve as a novel biomarker for the diagnosis or treatment of EC.
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.
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.
The aim of the research is to investigate the expression of the cell cycle relative proteins (P53, P16, Cyclin D1, and Ki67) in Esophageal Cancer (EC) patients of the Chaoshan area, China. In China, Chaoshan has the high incidence of EC. Different areas have shown different rate for expression of these proteins in EC. We investigated the expression of p53, p16, cyclinD1, and ki67 for the first time in Chaoshan. In this research, DNA was extracted from formalin fixed and paraffin embedded tissues of esophageal cancer (EC) patients. The expression level of proteins cycle was detected by using immunohistochemistry (IHC). And the data was checked by χ2 test or Fisher's exact test of SPSS17.0. The positive immunohistochemical staining of p53, p16, cyclinD1, and ki67 were observed in 65.7% 39.2%, 69.1%, and 83.5% specimens respectively. There was a positive correlation between p53 positive staining and p16, cyclinD1, ki67 staining at p < 0.05. CyclinD1 has the high correlation with ki67 at p < 0.05. A significant inverse correlation was considered between the expression of p16 and cyclinD1 and there was no correlation observed between p16 and ki67. In Conclusion, this study demonstrated the high expression of p53, Cyclin D1 and Ki67 and low expression of P16 and the association of these cell cycle relative proteins in esophageal cancer are new data in Chaoshan area of China. Geographical distribution of EC on the molecular basis is revealed in this research.
Thin sections of leaves of plants infected by tobacco etch potyvirus (TEV) or tobacco mosaic virus (TMV) were examined for the presence of ATPase activity by electron microscopy. ATPase activity was found as expected in mitochondria, chloroplasts and plasmalemma of both uninfected as well as cells infected by either TEV or TMV. In the TEV-infected cells, ATPase activity was localized to virus-induced vesicles, endoplasmic reticulum and in some cells, to ribosomes attached to the ER. In TMV-infected cells, ATPase activity was found in vesicles as well as in tubular membranes closely associated with the X-bodies.
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