Oncogenic Roles of Small Nucleolar RNA Host Gene 7 (SNHG7) Long Noncoding RNA in Human Cancers and Potentials

Long noncoding RNAs (lncRNAs) are a class of noncoding transcripts characterized with more than 200 nucleotides of length. Unlike their names, some short open reading frames are recognized for them encoding small proteins. LncRNAs are found to play regulatory roles in essential cellular processes such as cell growth and apoptosis. Therefore, an increasing number of lncRNAs are identified with dysregulation in a wide variety of human cancers. SNHG7 is an lncRNA with upregulation in cancer cells and tissues. It is frequently reported with potency of promoting malignant cell behaviors in vitro and in vivo. Like oncogenic/tumor suppressor lncRNAs, SNHG7 is found to exert its tumorigenic functions through interaction with other biological substances. These include sponging target miRNAs (various numbers are identified), regulation of several signaling pathways, transcription factors, and effector proteins. Importantly, clinical studies demonstrate association between high SNHG7 expression and clinicopathological features in cancerous patients, worse prognosis, and enhanced chemoresistance. In this review, we summarize recent studies in three eras of cell, animal, and human experiments to bold the prognostic, diagnostic, and therapeutic potentials.

Potential HNF1A-AS1/miR-214/INHBA signal regulation mechanism in colorectal cancer based on bioinformatics analysis and validation

Preceding studies have identified that noncoding RNA plays a significant role in the occurrence and development of tumors. Colorectal cancer (CRC) has attracted increasing attention due to its high incidence and mortality rate. Based on Cancer Genome Atlas (TCGA) database analysis, it was found that compared with normal tissues, HNF1A-AS1 and INHBA were highly expressed in CRC tissues; miR-214 was relatively low expressed, and it is predicted to specifically target the3' untranslated region (3'UTR region) of INHBA. Besides, the result was consistent with the quantitative reverse transcription PCR (RT-qPCR) verification results of 17 CRC cases and adjacent tissues collected clinically. Western Blot (WB) manifested that INHBA protein was highly expressed in CRC tissues, which was consistent with the results of CRC cell lines (HT29, SW480). Immunohistochemical (IHC) staining demonstrated that INHBA protein was brownish yellow, overwhelming majority of INHBA protein were located in the cytoplasm, and expression level was significantly higher than that in adjacent tissues. Based on previous studies, the biological process of INHBA-mediated TGF-β/Smad signaling pathway inducing the proliferation and invasion of CRC has been partially confirmed, but the upstream signaling molecules and mechanisms which regulating INHBA remain unclear. Herein, benefiting from bioinformatics, preliminary experimental results and previous research, they provide basis for the follow-up study on the regulation of HNF1A-AS1/miR-214/INHBA signal axis in CRC.

Long Noncoding RNA LIFR-AS1: A New Player in Human Cancers

Emerging evidence has indicated that aberrantly expressed long noncoding RNAs (lncRNAs) play a vital role in various biological processes associated with tumorigenesis. Leukemia inhibitory factor receptor antisense RNA1 (LIFR-AS1) is a recently identified lncRNA transcribed in an antisense manner from the LIFR gene located on human chromosome 5p13.1. LIFR-AS1 regulates tumor proliferation, migration, invasion, apoptosis, and drug resistance through different mechanisms. Its expression level is related to the clinicopathological characteristics of tumors and plays a key role in tumor occurrence and development. In this review, we summarize the role of LIFR-AS1 in the development and progression of different cancers and highlight the potential for LIFR-AS1 to serve as a biomarker and therapeutic target for a variety of human cancers.

DANSR: A Tool for the Detection of Annotated and Novel Small RNAs

Existing small noncoding RNA analysis tools are optimized for processing short sequencing reads (17–35 nucleotides) to monitor microRNA expression. However, these strategies under-represent many biologically relevant classes of small noncoding RNAs in the 36–200 nucleotides length range (tRNAs, snoRNAs, etc.). To address this, we developed DANSR, a tool for the detection of annotated and novel small RNAs using sequencing reads with variable lengths (ranging from 17–200 nt). While DANSR is broadly applicable to any small RNA dataset, we applied it to a cohort of matched normal, primary, and distant metastatic colorectal cancer specimens to demonstrate its ability to quantify annotated small RNAs, discover novel genes, and calculate differential expression. DANSR is available as an open source tool.

Reciprocal modulation of long noncoding RNA EMS and p53 regulates tumorigenesis

p53 plays a central role in tumor suppression. Emerging evidence suggests long noncoding RNA (lncRNA) as an important class of regulatory molecules that control the p53 signaling. Here, we report that the oncogenic lncRNA E2F1 messenger RNA (mRNA) stabilizing factor (EMS) and p53 mutually repress each other’s expression. EMS is negatively regulated by p53. As a direct transcriptional repression target of p53, EMS is surprisingly shown to inhibit p53 expression. EMS associates with cytoplasmic polyadenylation element-binding protein 2 (CPEB2) and thus, disrupts the CPEB2–p53 mRNA interaction. This disassociation attenuates CPEB2-mediated p53 mRNA polyadenylation and suppresses p53 translation. Functionally, EMS is able to exert its oncogenic activities, at least partially, via the CPEB2–p53 axis. Together, these findings reveal a double-negative feedback loop between p53 and EMS, through which p53 is finely controlled. Our study also demonstrates a critical role for EMS in promoting tumorigenesis via the negative regulation of p53.

Long noncoding RNA FAM225A promotes the malignant progression of gastric cancer through the miR-326/PADI2 axis

Gastric cancer (GC) is a global health problem and further studies of its molecular mechanisms are needed to identify effective therapeutic targets. Although some long noncoding RNAs (lncRNAs) have been found to be involved in the progression of GC, the molecular mechanisms of many GC-related lncRNAs remain unclear. In this study, a series of in vivo and in vitro assays were performed to study the relationship between FAM225A and GC, which showed that FAM225A levels were correlated with poor prognosis in GC. Higher FAM225A expression tended to be correlated with a more profound lymphatic metastasis rate, larger tumor size, and more advanced tumor stage. FAM225A also promoted gastric cell proliferation, invasion, and migration. Further mechanistic investigation showed that FAM225A acted as a miR-326 sponge to upregulate its direct target PADI2 in GC. Overall, our findings indicated that FAM225A promoted GC development and progression via a competitive endogenous RNA network of FAM225A/miR-326/PADI2 in GC, providing insight into possible therapeutic targets and prognosis of GC.