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  • Glioma Progression influenced by Long Non-Coding RNAs

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Glioma Progression influenced by Long Non-Coding RNAs
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Glioma Progression influenced by Long Non-Coding RNAs

bioxone July 30, 2021July 29, 2021

Shayan Ahmed, Jamia Millia Islamia, New Delhi

What is Glioma?

A glioma is a form of brain tumour that arises from glial cells. It can be divided into subgroups based on shape and histology, such as astrocytoma and glioblastoma. The World Health Organization (WHO) has classified glioma into four categories. Rapid cell growth and a bad prognosis characterize Grade-IV glioblastoma. In recent years, the role of long non-coding RNAs (lncRNAs) in the genesis and progression of malignancies has been validated and shown, particularly in glioma. 

Role of lncRNA in Glioma Progression

AFAP1-AS1 is a lncRNA that promotes cell invasion and is linked to a bad prognosis in glioma patients. Currently, the most common treatments for glioma include surgery, chemotherapy, and radiation, and nanotechnology is progressively being used to diagnose and cure glioma. A growing number of lncRNAs have been investigated and analyzed using molecular genetics, and are consequently being evaluated as possible therapeutic biomarkers. There is ample evidence that lncRNAs function as functional RNA molecules without the capacity to encode protein.

LncRNAs with abnormal expression have been shown to have a role in the genesis and progression of tumours and malignancies, including glioma. Many studies, including one on glioblastoma, have conducted an integrated study of the lncRNA-microRNA (miRNA)- mRNA competing endogenous RNA (ceRNA) network in cancer formation. In a recent study, researchers investigated PSMA3-AS1 expression in glioma cells and how aberrant expression impacts glioma cell biological activities such as cell proliferation and apoptosis. They used the ceRNA method to investigate the regulation mechanism of PSMA3-AS1, in the hopes of gaining a new understanding of glioma therapeutic options and therapy.

Results & Significance

PSMA3-AS1 was shown to be up-regulated in glioma cells in this research, and then loss-of-function experiments were performed to confirm the effects of PSMA3-AS1 on glioma cell proliferation and apoptosis. According to the findings, PSMA3-AS1 downregulation produced anti-proliferative and pro-apoptotic effects on glioma cells. The PSMA3-AS1/miR-411-3p/HOXA10 axis was established in this study after miR-411-3p was discovered as the target gene of PSMA3-AS1 and HOXA10 was identified as the downstream target of miR-411-3p. As a member of the homeobox (HOX) gene family, HOXA10 promotes tumour development in a variety of malignancies. Silencing HOXA10 inhibited glioma cell growth while triggering apoptosis, suggesting that HOXA10 acted as an oncogene in glioma. Therefore, PSMA3-AS1, which stimulates glioma progression via the miR-411-3p/HOXA10 pathway, may potentially act as a novel biomarker and therapeutic target for glioma treatment.

Also read: Transcriptome-wide study of Botrychium lunaria fern

Reference:

  1. Huang, T., Chen, Y., Zeng, Y. et al. Long non-coding RNA PSMA3-AS1 promotes glioma progression through modulating the miR-411-3p/HOXA10 pathway. BMC Cancer 21, 844 (2021). https://doi.org/10.1186/s12885-021-08465-5 
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About the Author:

Shayan Ahmed is currently pursuing a Master of Science degree in Microbiology from the Department of Biosciences, Jamia Millia Islamia, New Delhi. His area of research interest lies in antibiotic resistance and associated molecular mechanisms. His recent work was focused on understanding colistin resistance patterns in the environment, particularly in water bodies.

Other Publications by Author:

  1. https://bioxone.in/news/worldnews/airborne-pollen-hypothesized-as-ideal-covid-19-carrier/ 
  2. https://bioxone.in/news/worldnews/native-state-mass-spectrometry/
  3. https://bioxone.in/news/worldnews/bacterial-capsules-versus-horizontal-gene-transfer/ 

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Tagged Apoptosis Astrocytoma Brain Tumor cancer cANCER bIOLOGY glial cells Glioblastoma Glioma Long Non-Coding RNAs Micro RNAs

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