{"title":"The miR-192-EGR1/HOXB9 Loop Regulates Glioma Cell Stemness and Malignant Phenotypes by Promoting Their Mesenchymal Transition","authors":"Guo-Wei Li, Yan-Ping Jin, Min-Feng Sheng","doi":"10.1111/jcmm.70842","DOIUrl":null,"url":null,"abstract":"<p>To clarify the regulatory effects of miR-192 on the malignant phenotypes of glioma cells. We used PCR, WB and immunofluorescence to detect regulatory factors in glioma samples. Then, we chose lentiviral plasmid transfection to construct cell models. We used CCK-8 and colony formation to evaluate the proliferation ability of these cells and used Transwell/scratch tests to evaluate their invasion ability. CD133-expressing GSCs were observed under a microscope, and their stemness properties were evaluated. We constructed a tumour-bearing model via subcutaneous inoculation. Tumour growth curves and tumour weights were determined subsequently. The proteins involved in the miR-192-EGR1/HOXB9 loop were evaluated via IHC staining. MiR-192 was significantly reduced in glioma samples, and this factor downregulated EGR1 and HOXB9 via targeted binding, thus forming a semi-open loop. Moreover, the proliferation, invasion and migration of glioma cells overexpressing miR-192 were significantly decreased. These malignant phenotypes were abrogated completely with EGR1 or HOXB9 overexpression. Similarly, these changes were essentially consistent with MT marker expression and the stem-like properties in glioma cells. Meanwhile, miR-192 inhibits the tumorigenesis of glioma cells via the EGR1-HOXB9 loop. MiR-192 could inhibit MT in glioma cells through the EGR1-HOXB9 loop. Thus, it reduces their stemness and abrogates their malignant phenotypes.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 17","pages":""},"PeriodicalIF":4.2000,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70842","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/jcmm.70842","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
To clarify the regulatory effects of miR-192 on the malignant phenotypes of glioma cells. We used PCR, WB and immunofluorescence to detect regulatory factors in glioma samples. Then, we chose lentiviral plasmid transfection to construct cell models. We used CCK-8 and colony formation to evaluate the proliferation ability of these cells and used Transwell/scratch tests to evaluate their invasion ability. CD133-expressing GSCs were observed under a microscope, and their stemness properties were evaluated. We constructed a tumour-bearing model via subcutaneous inoculation. Tumour growth curves and tumour weights were determined subsequently. The proteins involved in the miR-192-EGR1/HOXB9 loop were evaluated via IHC staining. MiR-192 was significantly reduced in glioma samples, and this factor downregulated EGR1 and HOXB9 via targeted binding, thus forming a semi-open loop. Moreover, the proliferation, invasion and migration of glioma cells overexpressing miR-192 were significantly decreased. These malignant phenotypes were abrogated completely with EGR1 or HOXB9 overexpression. Similarly, these changes were essentially consistent with MT marker expression and the stem-like properties in glioma cells. Meanwhile, miR-192 inhibits the tumorigenesis of glioma cells via the EGR1-HOXB9 loop. MiR-192 could inhibit MT in glioma cells through the EGR1-HOXB9 loop. Thus, it reduces their stemness and abrogates their malignant phenotypes.
期刊介绍:
The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries.
It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.