To investigate the important roles of the cancer-promoting long non-coding RNAs (lncRNAs) in cervical cancer, the up-regulated lncRNAs and prognostic analysis were identified through Lnc2Cancer and Lncar. LncRNA-regulated miRNA and miRNA-target mRNA were analyzed based on starBase v2.0 and miTarbase to predict the lncRNA-miRNA-mRNA ceRNA network. Based on the above findings, the abnormally expressed histocompatibility leukocyte antigen complex P5 (HCP5) was identified in 31 cervical cancer patients through RT-qPCR. The stable cell lines were constructed to explore the effect of HCP5 on the promotion of cervical cancer and the regulatory role on the expression of miR-216a-5p and CDC42. Cell Counting Kit-8 (CCK8) assay, cell clone formation, and transwell assay were used to examine proliferation and migration ability of cervical cancer cells. The results displayed that the overexpression of HCP5 promoted cervical cancer cell proliferation and migration in vitro, and the elevated HCP5 can also promote tumor growth in vivo. Besides, RT-qPCR and western blot assay revealed that elevated HCP5 suppressed miR-216a-5p expression and then up-regulated the expression of CDC42. In contrast, knocking down HCP5 resulted in increased expression of miR-216a-5p and then downregulated the expression of CDC42. Rescue experiments also demonstrated that miR-216a-5p could in part intercept in promotion impact caused by HCP5 on cervical cancer cells. Above all, HCP5, as an oncogene, can promote proliferation and migration ability of cervical cancer via the regulation of the miR-216a-5p/CDC42 axis.
Background: Glioblastoma (GBM) is an intracranial brain tumor characterized by a high final lethality rate and recurrence rate, and limited available therapies. With the development of high-throughput sequencing technology, the genomic and transcriptomic features of GBM have been fully characterized. Therefore, our study aimed to identify its underlying genetic mechanisms, thus facilitating the development of novel therapies for GBM.Methods: Based on the Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases, differential expression of RNAs in GBM and control group was analyzed. After constructing the long noncoding RNA (lncRNA)-miRNA-mRNA regulatory network of GBM, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGGs) were performed to analyze related key nodes and the lncRNAs interacting with them. Further univariate Cox regression was conducted to explore independent factors, and then multivariate Cox regression was performed to construct risk prediction models.Results: We first constructed the lncRNA-miRNA-mRNA regulatory network of GBM and two effective prediction models that included 2 mRNAs [transcription factor 12 (TCF12) and discoidin, CUB and LCCL domain containing 2 (DCBLD2)] and 5 lncRNAs (C10orf25, LINC00343, HOXA transcript antisense RNA, myeloid-specific 1 (HOTAIRM1), FGF12 antisense RNA 2 (FGF12-AS2) and H19). Additionally, we identified several key molecules [TCF12, integrin β3 (ITGB3), high mobility group AT-hook 2 (HMGA2), C10orf25 and LINC00336] closely associated with GBM prognosis. C10orf25/miR-218/DCBLD2 may be an important regulatory pathway in GBM.Conclusions: Key molecules (TCF12, ITGB3, HMGA2, C10orf25, LINC00336 and H19) that are independent prognostic factors may be possible biomarkers to further optimize GBM prognosis. Two effective prognostic risk models that include 2 mRNAs (TCF12 and DCBLD2) and 5 lncRNAs (C10orf25, LINC00343, HOTAIRM1, FGF12-AS2 and H19) were constructed. C10orf25/miR-218/DCBLD2 may be an important regulatory pathway associated with the pathogenesis of GBM. Our findings contribute to further understanding the pathogenesis of GBM and finding possible candidate genes for prognostic and therapeutic usage with GBM.
Objective:To identify aberrant gene expression in primary human T-cell acute lymphoblastic leukemia (T-ALL) and to evaluate the differently expressed level of Lyll and LMO2 genes in human LMO2 positive/TALl negative T-ALL tumors. Methods: Three methods, representational difference analysis (RDA) of cDNA, cDNA microarrays and RT-PCR were used to detect if Lyll and LMO2 genes were differently expressed in human LMO2 positive/tall negative T-ALL tumors. Results: The results of cDNA RDA and cDNA array shown that Lyll and LMO2 genes are differently expressed in human T-cell tumors. The result of RT-PCR also shown Lyll and LMO2 are high expressed in human T-cell tumors and very low level or no expressed in normal group. Conclusion: We have found that cDNA RDA and cDNA microarray can be successfully used to identify aberrant gene expression in T-ALL cells. In the study described in this manuscript we found that Lyll and LMO2 are aberrantly expressed in human T-ALL LMO2 positive/TALl negative T-ALL tumors.Recurrent translocations are commonly found in T-cell acute lymphoblastic leukemia (T-ALL) [13]. Examples of these translocations include t(1; 14), t(10; 14), t(7; 11), t(7; 19) and t(ll; 14). The break points of the translocations have been cloned, and the adjacent genes were identified. The gene at lp32 is TAL-1/scll, at 10q24 is HOXll, at llp15 is rhombotin/Lim motif only-1 (LMO1), at llp13 is rhombotin2/LMO2 and at 19p13 is Lyll t4-81. The oncogenic potential of each of these genes has been demonstrated by the development of leukemia in transgenic mice over-expressing the genes tg' 105. Tall, HOXll and LMO1 and 2 are nuclear proteins
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.