Abstract
Gastric cancer (GC) represents a notable amount of morbidity and mortality worldwide. Understanding the molecular basis of CG will offer insight into its pathogenesis in an attempt to identify new molecular biomarkers to early diagnose this disease. Therefore, studies involving small non-coding RNAs have been widely explored. Among these, PIWI-interacting RNAs (piRNAs) are an emergent class that can play important roles in carcinogenesis. In this study, small-RNA sequencing was used to identify the global piRNAs expression profile (piRNome) of gastric cancer patients. We found 698 piRNAs in gastric tissues, 14 of which were differentially expressed (DE) between gastric cancer (GC), adjacent to gastric cancer (ADJ), and non-cancer tissues (NC). Moreover, three of these DE piRNAs (piR-48966*, piR-49145, piR-31335*) were differently expressed in both GC and ADJ samples in comparison to NC samples, indicating that the tumor-adjacent tissue was molecularly altered and should not be considered as a normal control. These three piRNAs are potential risk biomarkers for GC, especially piR-48966* and piR-31335*. Furthermore, an in-silico search for mRNAs targeted by the differentially expressed piRNAs revealed that these piRNAs may regulate genes that participate in cancer-related pathways, suggesting that these small non-coding RNAs may be directly and indirectly involved in gastric carcinogenesis.
Highlights
Gastric cancer (GC) is the fifth most common malignancy in the world and the third leading cause of cancer-related death worldwide [1]
PIWI-interacting RNAs are known to be related to the maintenance of genomic integrity, and, for a long time, their expression was associated with restriction to the stem cells [24,25,27,44] and reproductive cells in mammals [33,45,46]
An increased number of studies have demonstrated that PIWI-interacting RNAs (piRNAs) are found in somatic cells and cancer, regulating gene expression at transcriptional and post-transcriptional levels by epigenetic mechanisms [23,38,47,48]
Summary
Gastric cancer (GC) is the fifth most common malignancy in the world and the third leading cause of cancer-related death worldwide [1]. The molecular mechanism of gastric cancer formation and progression has not been completely elucidated [4,5]. GC exhibits a wide range of molecular alterations, including pathways involved in mitosis, immune signaling, cell adhesion, and migration [6,7] These alterations have been described both in genetic and epigenetic levels [8,9] and many studies have deeply investigated these epigenetic alterations [10,11]. The function of non-coding RNAs (ncRNAs) in cancer development and progression [12,13,14], mostly the role of miRNAs in post-transcriptional regulation, has been very well characterized [12,15,16]
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