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Year : 2020  |  Volume : 3  |  Issue : 3  |  Page : 135-142

Comprehensive RNAseq analysis reveals PIK3CD promotes glioblastoma tumorigenesis by mediating PI3K-Akt signaling pathway

1 Department of Health Technology and Informatics, Hong Kong Polytechnic University, Hong Kong Special Administrative Region, China
2 Cardiovascular Research Institute, Xiamen Cardiovascular Hospital, Xiamen University, Xiamen, Fujian Province, China
3 Department of Anatomical Pathology, Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
4 Department of Neurosurgery/Neuro-Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong Province, China

Correspondence Address:
Dr. Shing-shun Tony To
Department of Health Technology and Informatics, Hong Kong Polytechnic University, Hong Kong Special Administrative Region
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/glioma.glioma_23_20

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Background and Aim: Glioblastoma (GBM) is the most common and aggressive form of primary malignant brain tumors. Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta (PIK3CD), which is overexpressed in GBM, is involved in GBM pathogenesis and drug resistance. However, the molecular mechanism by which PIK3CD drives its transcriptional program toward GBM favors remains elusive. Materials and Methods: Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) and CRISPR-associated 9 technology was used to knock-out (KO) PIK3CD gene, and comprehensive RNAseq analysis was performed to investigate the underlying role of PIK3CD in GBM. Results: To minimize the off-target effects, two KO cell clones were used, and our data showed that PIK3CD KO altered the expression 306 genes in both KO cell clones compared with the parent U87 cell line. Gene set enrichment analysis revealed that genes involved in epithelial-mesenchymal (MES) transition-related biological processes were highly depressed in both KO cell clones in a similar fashion, suggesting PIK3CD's involvement in MES transformation/transition in GBM. Comprehensive pathway analysis by three different platforms confirmed that PIK3CD exerted its oncogenic function in GBM through phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway. In addition, other signaling pathways (integrin, cadherin, Wnt, and inflammation mediated by chemokine and cytokine signaling pathways) were found decreased in the KO cell clones. Further, The Cancer Genomic Atlas (TCGA) analysis of our PI3K-Akt pathway-related genes showed a similar pattern of expression. Conclusion: PIK3CD is involved in GBM pathogenesis, and this action probably mediated through the PI3K-Akt signaling pathway.

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