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miR-133b Promotes Esophageal Squamous Cell Carcinoma Metastasis.

Authors :
Huang, Cong-Gai
Liu, Qing
Zheng, Shu-Tao
Liu, Tao
Tan, Yi-Yi
Peng, Tian-Yuan
Chen, Jiao
Lu, Xiao-Mei
Source :
Clinical Medicine Insights: Oncology; 12/22/2023, p1-5, 5p
Publication Year :
2023

Abstract

Background: Evaluation of biological changes at the molecular level has important clinical implications for improving the survival rate of esophageal squamous cell carcinoma (ESCC). Therefore, we plan to analyze and elucidate the expression of microRNA-133b (miR-133b), M2 pyruvate kinase (PKM2), and signal transducer and activator of transcription 3 (STAT3) in ESCC and their associated clinicopathological significance. Methods: The 72 patients with ESCC were selected as the experimental study group. Normal adjacent tissues (NAT) were matched as the control group. In this study, in situ hybridization was used to detect the expression of miR-133b in ESCC, and tissue expressions of PKM2 and STAT3 were detected by immunohistochemistry, and literature review was conducted. Results: Studies had shown that the positive expression of miR-133b in NAT was significantly higher than that in ESCC (χ<superscript>2</superscript> = 9.007, P =.003). PKM2 and STAT3 in ESCC had a significantly higher positive expression levels than those of NAT (χ<superscript>2</superscript> = 56.523, P =.000; χ<superscript>2</superscript> = 72.939, P =.000). From correlation analysis, there was a negative correlation between miR-133b and PKM2(r = −0.515, P <.001), a negative correlation between miR-133b and STAT3(r = −0.314, P =.007), and a positive correlation between PKM2 and STAT3(r = 0.771, P <.001). Conclusions: In ESCC, our study demonstrated that downregulation of miR-133b and upregulation of PKM2 and STAT3. We predict that miR-133b may inhibit the STAT3 pathway by downregulating PKM2. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
11795549
Database :
Complementary Index
Journal :
Clinical Medicine Insights: Oncology
Publication Type :
Academic Journal
Accession number :
174422643
Full Text :
https://doi.org/10.1177/11795549231219502