Similar Datasets
Project description:B-cell acute lymphoid leukemias (B-ALL) are the most common neoplastic diseases in children. Survival rates in Hispanics are lower than in non-Hispanic children. It is, therefore, necessary to find predictive and prognostic biomarkers of relapse and death in this population. Our aim was to identify biomarkers of treatment response, which may also predict relapse and death, through identifying differentially expressed and methylated genes between patients who responded or did not respond to induction treatment. DNA and RNA samples were extracted from 27 bone marrow samples from Hispanic children newly diagnosed with B-ALL. mRNA was sequenced using the NextSeq550 Illumina platform. Bisulfite-treated DNA was annealed to Illumina Infinium EPIC Methylation chips. Gene expression and differential methylation were compared between responders and non-responders at day 15 and at the end of induction chemotherapy. DAPK1, CNKSR3, MIR4435-HG2, CTHRC1, NPDC1, SLC45A3, ITGA6, and ASCL2 were overexpressed and hypomethylated in non-responders. The overexpression of MIR4435-2HG, DAPK1, ASCL2, SCL45A3, CNKSR3, and NPDC1 can predict non-response at day 15 and refractoriness. Additionally, higher expression of MIR4435-2HG increases the probability of non-response, death, and the risk of death. DAPK1, CNKSR3, and MIR4435-2HG are also overexpressed in relapse samples. Finally, MIR4435-2HG overexpression, together with positive minimal residual disease, is associated with poorer survival, and together with high expression of DAPK1 and ASCL2, it could improve the risk classification of patients with normal karyotype. In conclusion, MIR4435-2HG is a potential predictive biomarker in children with B-ALL, and its detection at diagnosis could improve survival rates in our patients.
2024-05-22 | GSE229052 | GEO
Project description:B-cell acute lymphoid leukemias (B-ALL) are the most common neoplastic diseases in children. Survival rates in Hispanics are lower than in non-Hispanic children. It is, therefore, necessary to find predictive and prognostic biomarkers of relapse and death in this population. Our aim was to identify biomarkers of treatment response, which may also predict relapse and death, through identifying differentially expressed and methylated genes between patients who responded or did not respond to induction treatment. DNA and RNA samples were extracted from 28 bone marrow samples from Hispanic children newly diagnosed with B-ALL. mRNA was sequenced using the NextSeq2000 Illumina platform. Bisulfite-treated DNA was annealed to Illumina Infinium EPIC Methylation chips. Gene expression and differential methylation were compared between responders and non-responders at day 15 and at the end of induction chemotherapy. DAPK1, CNKSR3, MIR4435-HG2, CTHRC1, NPDC1, SLC45A3, ITGA6, and ASCL2 were overexpressed and hypomethylated in non-responders. The overexpression of MIR4435-2HG, DAPK1, ASCL2, SCL45A3, CNKSR3, and NPDC1 can predict non-response at day 15 and refractoriness. Additionally, higher expression of MIR4435-2HG increases the probability of non-response, death, and the risk of death. DAPK1, CNKSR3, and MIR4435-2HG are also overexpressed in relapse samples. Finally, MIR4435-2HG overexpression, together with positive minimal residual disease, is associated with poorer survival, and together with high expression of DAPK1 and ASCL2, it could improve the risk classification of patients with normal karyotype. In conclusion, MIR4435-2HG is a potential predictive and prognostic biomarker in children with B-ALL, and its detection at diagnosis could improve survival rates in our patients
2024-05-22 | GSE229046 | GEO
Project description:MIR4435-2HG as a novel predictive biomarker of chemotherapy response and death in pediatric B-cell ALL
| PRJNA952650 | ENA
Project description:MIR4435-2HG as a novel predictive biomarker of chemotherapy response and death in pediatric B-cell ALL [methylation]
| PRJNA952644 | ENA
Project description:MIR4435-2HG as a novel predictive biomarker of chemotherapy response and death in pediatric B-cell ALL [RNA-seq]
| PRJNA952635 | ENA
Project description:The abnormal expression of long non-coding RNAs(lncRNAs) is closely related to the prognosis of patients. This finding may indicate a new target for the treatment of malignant tumors. Non-muscle invasive bladder cancer (NMIBC) is the most common subtype of bladder cancer, and BCG intravesical therapy is the first-line treatment for NMIBC, but about half of NMIBC patients relapse within two years after BCG treatment. Therefore, it is necessary to screen out lncRNAs related to the prognosis and treatment of BGC-resistant patients. Here, we performed differential expression analysis of lncRNAs in the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets, and screened MIR4435-2HG as the only BCG-response-related lncRNA. Then, the prognosis value of MIR4435-2HG was validated in several publicly available cohorts, and confirmed its prognostic value in bladder cancer of different stages. In addition, we also analyzed its genetic alterations, clinical relevance, function enrichment, and association with other biomarkers. Further validation of the expression of MIR4435-2HG might be helpful to instruct NMIBC prognosis and treatment.
| S-EPMC9408477 | biostudies-literature
Project description:BackgroundLncRNA MIR4435-2HG is observed in a variety of cancers, while its role in colorectal cancer is unknown. We aimed to demonstrate the relationship between MIR4435-2HG and colorectal cancer based on The Cancer Genome Atlas (TCGA) database.Materials and methodsPatients with colorectal cancer were collected from TCGA. We compared the expression of MIR4435-2HG in colorectal cancer and normal tissues with Wilcoxon rank sum test, and logistic regression was used to evaluate the relationship between MIR4435-2HG and clinicopathological characters. Moreover, Kaplan-Meier and Cox regression was performed to evaluate the correlation between MIR4435-2HG and survival rate. Gene set enrichment analysis (GSEA) was also conducted to annotate biological function of MIR4435-2HG.ResultsMIR4435-2HG level was elevated in colorectal cancer tissues. Increased level of MIR4435-2HG was significantly correlated with TNM stage (OR = 1.66 for T1/T2 vs. T3/T4; OR = 1.68 for N0 vs. N1/N2), stage (OR = 1.66 for stage 1/2 vs. stage 3/4), and carcinoembryonic antigen level before treatment (OR = 1.70 for <5 vs. ≥5) (all P-value <0.05). High MIR4435-2HG expression had a poorer progression-free survival (p = 0.048), and overall survival (OS) (P = 0.028), which were validated in the GSE92921 and GSE29621 datasets. MIR4435-2HG expression (P = 0.040, HR = 1.955 (95% CI [1.031-3.710])) was independently correlated with OS. GSEA demonstrated that the P38/MAPK pathway, the VEGF pathway, the cell adhesion molecules cams, the NOD-like receptor signaling pathway, the cell surface interactions at the vascular wall, and integrin cell surface interactions were differentially enriched in MIR4435-2HG high expression phenotype.ConclusionsIncreased MIR4435-2HG might be a potential biomarker for the diagnosis and prognosis of colorectal cancer. Moreover, MIR4435-2HG might participate in the development of colorectal cancer via the P38/MAPK and VEGF pathway.
| S-EPMC6450379 | biostudies-literature
Project description:Several studies have indicated that dysregulation of long non‑coding RNAs (lncRNAs) participates in the initiation and progression of cancer. The lncRNA MIR4435‑2HG was previously reported to act as an oncogene in human cancer, including liver cancer. However, its role in the pathogenesis in liver cancer is largely unclear. The present study aimed to reveal the molecular mechanism by which MIR4435‑2HG regulates liver cancer. The expression levels of MIR4435‑2HG in liver cancer and adjacent normal tissues were analyzed using The Cancer Genome Atlas database. MIR4435‑2HG expression was validated by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) in cancer cells in vitro. The target genes of MIR4435‑2HG were predicted using bioinformatics analysis. Interactions between miR‑136‑5p, MIR4435‑2HG and B3GNT5 were detected using luciferase reporter assays, and their effects on cell viability, migration and invasion were assessed using Cell Counting Kit‑8, wound healing and Transwell assays. The effects of miR‑136‑5p and MIR4435‑2HG on B3GNT5 expression were confirmed by western blot analysis. The results revealed that MIR4435‑2HG expression was upregulated in primary liver cancer and liver cancer cell lines, and was positively associated with advanced tumor stage, metastasis and poor prognosis in patients with liver cancer. Knockdown of MIR4435‑2HG significantly inhibited the proliferation, migration and invasion of liver cancer cells. Furthermore, miR‑136‑5p was determined to be a direct target of MIR4435‑2HG and suppressed MIR4435‑2HG expression by binding with the seed region of the 3'‑UTR of MIR4435‑2HG in liver cancer cells. Functional studies showed that the inhibitory effects of MIR4435‑2HG knockdown on cell proliferation, migration and invasion were significantly rescued by inhibiting miR‑136‑5p. Furthermore, the target gene, B3GNT5, of miR‑136‑5p was confirmed by bioinformatics analysis and RT‑qPCR. In addition, B3GNT5 expression was regulated by the MIR4435‑2HG/miR‑136‑5p axis. In conclusion, the present study indicated that MIR4435‑2HG facilitated the progression of liver cancer via the MIR4435‑2HG/miR‑136‑5p/B3GNT5 axis, which demonstrated that MIR4435‑2HG may be a potential biomarker for the prognosis and treatment of liver cancer.
| S-EPMC8669657 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-12-01 | E-GEOD-52847 | biostudies-arrayexpress
Project description:Background:Accumulating studies showed that long noncoding RNAs (lncRNAs) played vital roles in cancer progression. LncRNA MIR4435-2HG was proved to act as an oncogene in various tumors. However, the underlying function of MIR4435-2HG in ovarian cancer (OC) remains unclear. Methods:The expression levels of MIR4435-2HG, miR-128-3p and cyclin-dependent kinase 14 (CDK14) were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and apoptosis in OC cells were detected by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and flow cytometric analysis, respectively. Transwell assay was applied to evaluate cell migration and invasion. Wound healing assay was performed to monitor the migration rate. Western blot assay was performed to detect the protein levels of Bcl-2, Cleaved PARP, E-cadherin, Vimentin and CDK14 in OC cells. The binding sites between miR-128-3p and MIR4435-2HG or CDK14 were predicted by online tool starBase and their relationship was confirmed by dual-luciferase reporter assay, RIP assay and pull-down experiment. Results:MIR4435-2HG and CDK14 were over-expressed in OC tissues and cells. Patients with high MIR4435-2HG expression had poorer overall survival (OS) than patients with low MIR4435-2HG expression. MIR4435-2HG knockdown inhibited proliferation, invasion and migration but induced apoptosis of OC cells via miR-128-3p/CDK14 axis. In conclusion, MIR4435-2HG knockdown suppressed the progression of OC cells through downregulating CDK14 expression by the promotion of miR-128-3p.
| S-EPMC7195767 | biostudies-literature