Abstract
To study the problem in esophageal cancer, the function of SOX2 and miR-126 has not been completely explored. The objective of this study was to find out how SOX2 and miR-126 act in esophageal cancer and their relation to the clinical and prognostic features. The expression of SOX2 and miR-126 was properly assessed in the carcinoma of the esophagus, and the nearby healthy tissues surgically excised from 35 included patients. SOX2 was elevated in esophageal cancer relative to normal tissues contrary to the miR-126 levels. This inverse relationship was linked to adverse clinical features. SOX2 has been involved as an oncogene in various types of malignant tumors; microRNA-126 (miR-126) is extensively expressed in vascular endothelial cells, which control angiogenesis. Furthermore, many published reports reasonably concluded that based on the prime characteristic of malignant cells, miR-126 may act appropriately as a promotor or a suppressor for the malignant growth. In esophageal cancer, SOX2 works as an oncogene, whereas miR-126 acts as a tumor suppressor gene. SOX2 overexpression and miR-126 downregulation were shown to be linked to a poor prognosis.
Highlights
Carcinoma of the esophagus (CE) is generally rated as the eighth most significant type of cancer and the sixth most common cause of cancer-related deaths [1]
The quantitative real time PCR was used to evaluate the mRNA levels of SOX2 and miR-126 in CE and nearby healthy tissues (NT) obtained from thirty-five patients
SOX2 was significantly elevated relative to normal tissues
Summary
Carcinoma of the esophagus (CE) is generally rated as the eighth most significant type of cancer and the sixth most common cause of cancer-related deaths [1]. MicroRNAs (miRNAs) are small non-coding areas consisted of 20–22 nucleotides in the RNAs; it optimally performs a significant role in mammals by adequately regulating an essential verity of molecular processes [4, 5]. Disturbed regulation of one or a limited number of miRNAs has been appropriately recognized to naturally produce a profound impact on the proper mode of expression of hundreds of mRNAs that pushes resolutely the cells to transform [6, 7]. Several published reports scientifically prove that over 50% of the miRNAs genes are in cancer-associated genomic locations or unstable sites [8, 9]. Genomic expression analysis from an extensive range of malignant tissues/cells showed that the active presence of aberrant miRNA undoubtedly continues to remain a fundamental principle rather than an event [10, 11]
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