한빛사논문
- 조회665
Ji-Hoon Jeong1,5, Seung-Ho Park1,5, Hyunhee Kim1, Hae Yun Nam2, Sung-Hak Kim3, Minseok Jeong1, Min-Jeong Kong1, Jihyun Son1, Ji-Eun Jeong1, Ji-Hye Song4, Seong Who Kim2,6 and Kyung-Chul Choi1,6
1Department of Biomedical Sciences, AAMIST, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
2Department of Biochemistry and Molecular Biology, AMIST, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
3Department of Animal Science, Chonnam National University, Gwangju, Korea.
4Korea Food Research Institute, Wanju-gun 55365, Korea.
5These authors contributed equally: Ji-Hoon Jeong, Seung-Ho Park.
6These authors jointly supervised this work: Seong Who Kim, Kyung-Chul Choi.
Corresponding authors :Correspondence to Seong Who Kim or Kyung-Chul Choi.
Abstract
Glioblastoma multiforme (GBM), the most aggressive and malignant glioma, has a poor prognosis. Although patients with GBM are treated with surgery, chemotherapy, and radiation therapy, GBM is highly resistant to treatment, making it difficult and expensive to treat. In this study, we analyzed the Gene Expression Profiling Interactive Analysis dataset, the Cancer Genome Atlas dataset, and Gene Expression Omnibus array data. ZBTB7A (also called FBI1/POKEMON/LRF) was found to be highly expressed in low-grade glioma but significantly downregulated in patients with GBM. ZBTB7A is a transcription factor that plays an important role in many developmental stages, including cell proliferation. The activation of epithelial-mesenchymal transition (EMT) is a key process in cancer progression and metastasis. Erythrocyte membrane protein band 4.1 like 5 (EPB41L5) is an essential protein for EMT progression and metastasis in various types of cancer. We found that ZBTB7A depletion in U87 cells induced GBM progression and metastasis. Based on RNA sequencing data, ZBTB7A directly binds to the promoter of the EPB41L5 gene, reducing its expression and inhibiting GBM progression. We demonstrated that ZBTB7A dramatically inhibits GBM tumor growth through transcriptional repression of EPB41L5. Thus, both ZBTB7A and EPB41L5 may be potential biomarkers and novel therapeutic targets for GBM treatment. Overall, we discovered the role of a novel tumor suppressor that directly inhibits GBM progression (ZBTB7A) and identified EPB41L5 as a therapeutic target protein for patients with GBM.
논문정보
- Research article
- 2023년 01월 (BRIC 등록일 2023-01-10)
- 국내 연구진
- 생명과학 > 세포생물학
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