4.6 Article

H19-and hsa-miR-338-3p-mediated NRP1 expression is an independent predictor of poor prognosis in glioblastoma

Journal

PLOS ONE
Volume 16, Issue 11, Pages -

Publisher

PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0260103

Keywords

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Funding

  1. National Natural Science Foundation of China [81874081, 81672490]
  2. Foundation of Jiangsu Provincial Health Department [YG201514]
  3. Foundation of Xuzhou Medical University [2018KJ09]
  4. Xuzhou Science and Technology Plan Project [KC20139]
  5. National Demonstration Center for Experimental Basic Medical Science Education (Xuzhou Medical University)
  6. National Innovation and Entrepreneurship Training Program for College Students [201910313026, 201910313019Z]

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This study identified the regulatory pathway of H19 and hsa-miR-338-3P in regulating NRP1 expression in GBM, which plays an important role in the disease.
Glioblastoma multiforme (GBM) is the most common and also the most invasive brain cancer. GBM progression is rapid and its prognosis is poor. Therefore, finding molecular targets in GBM is a critical goal that could also play important roles in clinical diagnostics and treatments to improve patient prognosis. We jointly analyzed the GSE103227, GSE103229, and TCGA databases for differentially expressed RNA species, obtaining 52 long non-coding RNAs (lncRNAs), 31 microRNAs (miRNAs), and 186 mRNAs, which were used to build a competing endogenous RNA network. Kaplan-Meier and receiver operating characteristic (ROC) analyses revealed five survival-related lncRNAs: H19, LINC01574, LINC01614, RNF144A-AS1, and OSMR-AS1. With multiple optimization mRNAs, we found the H19hsa-miR-338-3P-NRP1 regulatory pathway. Additionally, we noted high NRP1 expression in GBM patients, and Kaplan-Meier and ROC analyses showed that NRP1 expression was associated with GBM prognosis. Cox analysis indicated that NRP1 is an independent prognostic factor in GBM patients. In conclusion, H19 and hsa-miR-338-3P regulate NRP1 expression, and this pathway plays an important role in GBM.

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