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.

Cells
|August 14, 2020
PubMed

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.

Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
8.5K
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
5.7K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.6K