Increased Expression of RCN1P2, TPM3P9, and HSP90AB3P as Non-Coding RNA in Gastric Cancer Linked to Proliferative, Inflammatory and Metastatic Pathways through a Competing Endogenous RNAs Network
Abstract
Background: This study aimed to find pseudogenes with significant expression alterations in gastric cancer (GC) that could be implicated in the disease's development via the competing endogenous RNAs (ceRNAs) network.
Methods: Pseudogenes, mRNAs, and microRNAs, whose expression changes considerably in GC specimens, were identified using the Cancer Genome Atlas (TCGA) data from 2006 to 2017 (USA). The ceRNAs network was constructed using the miRWalk, miRTarBase, and DIANA-LncBase. The cox regression test was performed to assess the correlation between candidate genes and patient prognosis. Finally, using the RT-qPCR method, the in-silico results were evaluated using GC samples and adjacent normal. Samples were collected from Imam Khomeini Hospital in Tehran (Iran) between 2020 and 2021.
Results: In the cancer samples compared to the normal ones, there were 86 miRNAs, 1985 mRNAs, and 33 pseudogenes showing expression alterations, either more than or less than a twofold difference. Constructed ceRNA network demonstrated that pseudogenes such as RCN1P2, TPM3P9, and HSP90AB3P were most connected to changed mRNAs and microRNAs in GC. The analysis of the ceRNA network for each of the mentioned pseudogenes indicated that the associated mRNAs play roles in cell proliferation, inflammation, and metastatic pathways. Furthermore, elevated expression of several mRNAs linked to potential pseudogenes was linked to a poor prognosis. RT-qPCR revealed a significant increase in the expression levels of RCN1P2, TPM3P9, and HSP90AB3P in GC samples.
Conclusion: The expression of RCN1P2, TPM3P9, and HSP90AB3P is dramatically enhanced in GC. They can also influence the survival rate of GC patients by regulating pathways involved in cell proliferation, inflammation, and metastasis via the ceRNAs network.