Clinicopathological and immunological characterization of RNA m6A methylation regulators in ovarian cancer
Background N6‐methyladenosine (m6A) modification is one of the critical gene regulatory mechanisms implicated in cancer biology. However, the roles of m6A regulators in ovarian cancer are still poorly understood. Methods We integrated multiple databases including Gene Expression Omnibus (GEO), ROC P...
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Published in | Molecular genetics & genomic medicine Vol. 9; no. 1 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Bognor Regis
John Wiley & Sons, Inc
01.01.2021
John Wiley and Sons Inc Wiley |
Subjects | |
Online Access | Get full text |
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Summary: | Background
N6‐methyladenosine (m6A) modification is one of the critical gene regulatory mechanisms implicated in cancer biology. However, the roles of m6A regulators in ovarian cancer are still poorly understood.
Methods
We integrated multiple databases including Gene Expression Omnibus (GEO), ROC Plotter, Kaplan‐Meier Plotter, and Tumor Immune Estimation Resource (TIMER) to explore clinicopathological significance of m6A regulators in ovarian cancer.
Results
We showed that alterations in the expression of m6A regulators were related to the malignancy and poor prognosis of ovarian cancer. We found decreased YTHDC1 and increased RBM15 expressions were associated with ovarian cancer cell metastases and HNRNPC was a predictor of paclitaxel resistance. Moreover, dysregulated m6A regulators were enriched in the activation of cancer‐related pathways. Our results further demonstrated that the level of immune cell infiltration and the expression of various immune gene markers were closely associated with the expressions of specific m6A regulators (RBM15B, ZC3H13, YTHDF1, and IGF2BP1).
Conclusions
Our study establishes a new prognostic profile of ovarian cancer patients based on m6A regulators, and highlights the potential roles of m6A regulators in ovarian cancer development.
m6A regulators play important roles in ovarian cancer cell biology. |
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Bibliography: | Qingying Wang and Qinyi Zhang contributed equally. |
ISSN: | 2324-9269 2324-9269 |
DOI: | 10.1002/mgg3.1547 |