LINC00092

Colon Cancer (CC) incidence has sharply grown in recent years. Long non-coding RNAs (lncRNA) are produced by a group of non-protein-coding genes, and have important functions in controlling gene expression and impacting the biological features of various malignancies including CC.

Our research focused on examining the function of lncRNAs in the development of colon cancer. To this end, we selected and analyzed a dataset (GSE104836) from the GEO database, which contained information about the expression of mRNAs and lncRNAs in both colon cancer tissues and normal adjacent paired tumor tissues. The DESeq2 R package in Bioconductor was used to identify differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs) that showed differences in expression levels. Next, by literature review of previous studies, we chose two lncRNAs (FENDRR and LINC00092) for additional studies. To validate our findings, a series of tests were performed on a total of 31 tumor tissues and normal paired adjacent tumor tissues. The lncRNA expression levels were assessed in tumor tissues as well as in surrounding normal tumor tissues.

The data confirmed that just two particular lncRNAs, FENDRR and LINC00092, had considerably decreased expression levels throughout all stages of cancer. In addition, the survival assay was conducted using the GEPIA2 software, revealing that a reduced expression of FENDRR is correlated with a reduced overall survival. Furthermore, our investigation using receiver operating characteristic (ROC) methodology revealed that these two lncRNAs had significant discriminatory ability between colon cancer and normal tissues. To determine the cause of the decrease in the activity of these two long non-coding RNAs (lncRNAs), we used methylation-specific PCR (MSP) to examine the methylation pattern of their promoter regions. Our investigation revealed hypermethylation in the promoter regions of FENDRR and LINC00092 within tumor tissues compared to normal adjacent tumor tissues.

Taken together, our findings revealed the lncRNAs signatures as potential therapeutic targets and molecular diagnostic biomarkers in colon cancer. Furthermore, the evidence provided substantiates the important role of promoter methylation in regulating the expression levels for both of these lncRNAs.

LINC00092 is poorly expressed in Thyroid cancer (TC), while its role in TC tumorigenesis is still elusive. This study aimed to reveal the role and regulatory mechanism of LINC00092 in TC.RNA immunoprecipitation and dual luciferase reporter assays were employed to ascertain the relationships among lipoma preferred partner (LPP), miR-542-3p, and LINC00092. qRT-PCR analysis was performed to detect their expression levels in TC. LPP protein productions were evaluated via western blotting. CCK-8, transwell, and colony formation assays were done to estimate TC cells’ biological functions. A murine xenograft model was built to observe tumor formation in vivo.LINC00092 overexpression decreased the expression levels of miR-542-3p, and LPP was targeted by miR-542-3p. In TC cells and tissues, the elevation of miR-542-3p, and low amounts of LINC00092 and LPP can be observed. Both LINC00092 and SPAG6 were considered as the antineoplastic factors in TC since their overexpression dramatically repressed TC cells’ invasive and proliferative potentials, while miR-542-3p exerted the opposite functions in TC. The ectopic expression of LINC00092 also suppressed tumor growth in vivo. In addition, it revealed that miR-542-3p upregulation reversed LINC00092 overexpression-mediated effects on TC cells. At the same time, the enhanced influences of TC cells caused by miR-542-3p upregulation could be attenuated by the enforced LPP.This study innovatively reveals that LINC00092 acts as an antineoplastic lncRNA to restrain the development of TC via regulating miR-542-3p/LPP. The findings of this study may provide a prospective drug target on LINC00092/miR-542-3p/LPP axis for the treatment of TC.

Polycystic ovary syndrome (PCOS) is a perplexing condition in females of reproductive age. Dysplasia of ovarian granulosa cell (GC) is implicated in PCOS. Follicular fluid (FF)-extracellular vesicles (Evs) are important in cell-cell communication during follicular development. The current study elaborated on the function and mechanism of FF-Evs in the viability and apoptosis of GC cells in PCOS development. Human GC cells KGN were treated with dehydroepiandrosterone (DHEA) to mimic a PCOS-like condition in vitro, which were further co-cultured with the FF-derived Evs (FF-Evs). The FF-Evs treatment significantly reduced DHEA-induced apoptosis of KGN cells while promoting cell viability and migration. The lncRNA microarray analysis showed that FF-Evs mainly deliver LINC00092 into the KGN cells. Knockdown of LINC00092 negated the protective effect of FF-Evs against DHEA-induced damage on KGN cells. Moreover, by performing bioinformatics analyses and biotin-labeled RNA pull-down assay, we found that LINC00092 could bind to the RNA binding protein LIN28B and inhibit its binding to pre-microRNA-18-5p, which allowed biogenesis of pre-miR-18-5p and increased the expression of miR-18b-5p, a miRNA with known alleviating role in PCOS by suppressing the PTEN mRNA. Collectively, the present work demonstrates that FF-Evs can alleviate DHEA-induced GC damage by delivering LINC00092.