Project description:Gastric cancer (GC) remains one of the most prevalent tumor worldwide, and ranks third in cancer-related deaths globally. Long non-coding RNAs (lncRNAs) have been reported to play significant role in the progression and metastasis in gastric cancer (GC), however, the molecular mechanism are largely elusive. We aim to identify up-regulated lncRNA in gastric cancer peritoneal metastasis and study their function in promoting tumor progression and metastasis.
Project description:The long intergenic non-coding RNA linc01133 is reported to be oncogenic in various malignancies. However, the role and mechanism of linc01133 in regulating gastric cancer growth is still not clear. In the present study, we found that linc01133 was significantly up-regulated in gastric cancer tissues compared to non-tumorous gastric tissues. Linc01133 over-expression significantly correlated with tumor size and tumor differentiation in gastric cancer patients. The expression of linc01133 was regulated by c-Jun and c-Fos collaboratively. In both in vitro and in vivo studies, linc01133 was shown to promote gastric cancer cell growth. Linc01133 localized in the cytoplasm and functioned as an endogenous competing RNA of miR-145-5p to up-regulate the expression of YES1,which was proved to be the target gene of miR-145-5p. By promoting YES1-dependent YAP1 nuclear translocation, linc01133 up-regulated the expression of the key cell cycle regulators CDK4, CDK6 and cyclin D1 to promote G1-S phase transition. Thus, our study unveiled the function and mechanism of linc01133 regulating cell cycle progression in gastric cancer.
Project description:Long non-coding RNAs (lncRNAs) may contribute to tumorigenesis and cancer progression by regulating the gene in various cancers, including advanced gastric cancer (AGC). To investigate differentially expressed lncRNAs in AGC, we use whole transcriptome sequencing in 3 pairs of human gastric adenocarcinoma and the corresponding normal tissues.
Project description:Although many protein-coding genes have been identified to be aberrantly expressed in cervical cancer, the mechanisms of development and progression of cervical cancer remain unclear. In recent years, non-coding RNAs, especially including microRNAs and long non-coding RNAs, have been shown to play important regulatory roles in mammalian cell biology. In our study, we investigated the whole genome gene expression level changes by human transcriptome array in tumor tissues and paired adjacent non-tumor tissue of patients with cervical cancer. The functions of different expression microRNAs, long non-coding RNAs and mRNAs were further analyzed in vitro and in vivo using loss-of-function and gain-of-function approaches. A ten chip study using total RNA recovered from five separate cervical cancer tissues and five paired adjacent non-tumor samples.
Project description:Gastric cancer (GC) remains one of the most prevalent tumor worldwide, and ranks third in cancer-related deaths globally. Long non-coding RNAs (lncRNAs) have been reported to play significant role in the progression and metastasis in gastric cancer (GC), however, the molecular mechanism are largely elusive. We aim to identify up-regulated lncRNA in GC and study their function in promoting tumor progression and metastasis.
Project description:Although many protein-coding genes have been identified to be aberrantly expressed in cervical cancer, the mechanisms of development and progression of cervical cancer remain unclear. In recent years, non-coding RNAs, especially including microRNAs and long non-coding RNAs, have been shown to play important regulatory roles in mammalian cell biology. In our study, we investigated the whole genome gene expression level changes by human transcriptome array in tumor tissues and paired adjacent non-tumor tissue of patients with cervical cancer. The functions of different expression microRNAs, long non-coding RNAs and mRNAs were further analyzed in vitro and in vivo using loss-of-function and gain-of-function approaches.
Project description:H. pylori infection induces upregulation of the long non-coding RNA LUCAT1 in gastric cancer cells, which facilitates the exosomal transfer of MIF (macrophage migration inhibitory factor) to the tumor microenvironment. This process shifts macrophages from the M0 to M2 phenotype, contributing to an aggressive gastric cancer progression by enhancing cell proliferation, migration, and invasion. The research suggests potential preventive and therapeutic strategies for gastric cancer by targeting LUCAT1 and MIF, highlighting the critical role of lncRNA-mediated mechanisms in H. pylori driven-cancer development.
Project description:Purpose: To investigate the role and mechanism of mRNAs, long chain non-coding RNAs and circular RNAs in gastric cancer. Methods: RNA-seq of ribosomal RNA-depleted total RNA were performed to screen differential expressed mRNAs, long chain non-coding RNAs between paired gastric cancer tissues and adjacent normal tissues.For the linear RNA was digested with 3 U of RNase R per µg of RNA. Results: A total of 83672 mRNAs, 105998 long chain non-coding RNAs, 25441 distinct circRNAs were identified in these samples, and 13929 of these circRNAs were identified as novel circRNAs.
Project description:Recent research highlights the significant impact of methionine metabolism on glioma progression. An increasing amount of compelling evidence bridges long non-coding RNAs to abnormal metabolism in gliomas. However, the specific role of long non-coding RNAs in methionine metabolism regulating glioma progression remains unclear. This study reveals that methionine deprivation inhibits the proliferation, migration, and invasion capabilities of gliomas. Interestingly, the expression of TP53TG1, a long non-coding RNA, is also suppressed. TP53TG1 is highly expressed in gliomas and associated with poor patient outcomes. Subsequently, our data proves that inhibition of TP53TG1 suppresses glioma cell proliferation and the epithelial-mesenchymal transition process both in vitro and in vivo. Ultimately, we found that the underlying mechanism involves a competing endogenous RNA regulating network, in which TP53TG1 modulates the target protein STK17B by competitively binding to miR-96-5p, thus regulating glioma progression. These findings suggest that targeting methionine deprivation could be a promising approach for the clinical treatment of glioma.
Project description:Long non-coding RNAs (lncRNAs) play important roles in cancer development and progression; however, their contributions to gastric cancer metastasis remain largely unknown. By lncRNA microarray screening, our study showed that 10 lncRNAs are dysregulated in gastric cancer tissues with or without lymph node metastasis, of which lnc-LEMGC ranks as one of the most significantly downregulated lncRNAs. Lnc-LEMGC inhibited cell migration and invasion both in vitro and in vivo, by combining with protein DNA-PKcs. Importantly, nucleotides 1,300–1,800 of lnc-LEMGC prevented DNA-PKcs phosphorylation of serine 2056 and partially abrogated the effects of downstream effectors, transforming growth factor alpha, EGFR, Src kinase, paxillin, and focal adhesion kinase, in the epidermal growth factor receptor (EGFR) pathway. The results of this study extend our knowledge of lncRNA’s molecular mechanisms, in which lnc-LEMGC functions by directly suppressing the phosphorylation of its combined protein DNA-PKcs and inactivating the DNA-PKcs downstream EGFR signaling.