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Published on: March 28, 2021
Targeting BC200/miR218-5p Signaling Axis for Overcoming Temozolomide Resistance and Suppressing Glioma Stemness
Yu-Kai Su1,2,3,4, Jia Wei Lin1,2,3,4, Jing-Wen Shih5,6
1Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei City 11031, Taiwan.
Abstract:
Background: Glioblastoma (GB) is one of the most common (~30%) and lethal cancers of the central nervous system. Although new therapies are emerging, chemoresistance to treatment is one of the major challenges in cancer treatment. Brain cytoplasmic 200 (BC200) RNA, also known as BCYRN1, is a long noncoding RNA (lncRNA) that has recently emerged as one of the crucial members of the lncRNA family. BC200 atypical expression is observed in many human cancers. BC200 expression is higher in invasive cancers than in benign tumors. However, the clinical significance of BC200 and its effect on GB multiforme is still unexplored and remains unclear. Methods: BC200 expression in GB patients and cell lines were investigated through RT-qPCR, immunoblotting, and immunohistochemistry analysis. The biological importance of BC200 was investigated in vitro and in vivo through knockdown and overexpression. Bioinformatic analysis was performed to determine miRNAs associated with BC200 RNA. Results: Our findings revealed that in GB patients, BC200 RNA expression was higher in blood and tumor tissues than in normal tissues. BC200 RNA expression have a statistically significant difference between the IDH1 and P53 status. Moreover, the BC200 RNA expression was higher than both p53, a prognostic marker of glioma, and Ki-67, a reliable indicator of tumor cell proliferation activity. Overexpression and silencing of BC200 RNA both in vitro and in vivo significantly modulated the proliferation, self-renewal, pluripotency, and temozolomide (TMZ) chemo-resistance of GB cells. It was found that the expressions of BC200 were up-regulated and that of miR-218-5p were down-regulated in GB tissues and cells. miR-218-5p inhibited the expression of BC200. Conclusions: This study is the first to show that the molecular mechanism of BC200 promotes GB oncogenicity and TMZ resistance through miR-218-5p expression modulation. Thus, the noncoding RNA BC200/miR-218-5p signaling circuit is a potential clinical biomarker or therapeutic target for GB.
Insights
Brain cytoplasmic 200 (BC200) RNA promotes glioblastoma growth and temozolomide resistance by downregulating miR-218-5p. This BC200/miR-218-5p pathway presents a potential therapeutic target for glioblastoma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Glioblastoma (GB) is a lethal central nervous system cancer with significant chemoresistance challenges.
- Brain cytoplasmic 200 (BC200) RNA, a long noncoding RNA (lncRNA), shows atypical expression in various cancers, but its role in GB is unclear.
- Understanding BC200's clinical significance is crucial for developing new GB treatment strategies.
Purpose of the Study:
- To investigate the clinical significance and biological role of BC200 RNA in glioblastoma multiforme.
- To explore the molecular mechanism underlying BC200's influence on GB oncogenicity and chemoresistance.
- To identify potential biomarkers and therapeutic targets for glioblastoma.
Main Methods:
- BC200 expression analysis in GB patients and cell lines using RT-qPCR, immunoblotting, and immunohistochemistry.
- In vitro and in vivo functional studies involving BC200 knockdown and overexpression.
- Bioinformatic analysis to identify microRNAs (miRNAs) interacting with BC200 RNA, specifically focusing on miR-218-5p.
Main Results:
- BC200 RNA was significantly upregulated in GB tissues and blood compared to normal tissues, correlating with IDH1/P53 status and higher than p53 and Ki-67 markers.
- Modulation of BC200 expression (overexpression or knockdown) affected GB cell proliferation, self-renewal, pluripotency, and temozolomide (TMZ) chemo-resistance in vitro and in vivo.
- BC200 expression was inversely correlated with miR-218-5p expression in GB, with miR-218-5p inhibiting BC200.
Conclusions:
- The BC200/miR-218-5p signaling circuit plays a critical role in promoting glioblastoma oncogenicity and TMZ resistance.
- BC200 facilitates GB progression and chemoresistance by modulating miR-218-5p expression.
- The BC200/miR-218-5p axis represents a promising novel biomarker and therapeutic target for glioblastoma treatment.
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