This SuperSeries is composed of the SubSeries listed below.
Cytidine Deaminase Axis Modulated by miR-484 Differentially Regulates Cell Proliferation and Chemoresistance in Breast Cancer.
Disease, Cell line
View SamplesGemcitabine was approved to be sufficient effects on most solid tumors, including breast cancer and others. There has been little study of how the evolution of chemoresistance in cancer affects other aspects of disease pathogenesis.
Cytidine Deaminase Axis Modulated by miR-484 Differentially Regulates Cell Proliferation and Chemoresistance in Breast Cancer.
Disease, Cell line
View SamplesTo develop and validate novel multigene signatures to facilitate individualized treatment of TNBC patients By integrating expression profiles of messenger RNAs (mRNAs) and long non-coding RNAs (lncRNAs).
Comprehensive Transcriptome Profiling Reveals Multigene Signatures in Triple-Negative Breast Cancer.
Sex, Specimen part, Disease stage
View SamplesMicroarray analyses for the identification of differences in gene expression patterns have increased our understanding of the molecular genetic events in colorectal cancer.
A molecular signature for the prediction of recurrence in colorectal cancer.
Sex
View SamplesWith stringent filtering criteria (fold change>2, p<0.001 and False Discovery Rate (FDR) <0.01), we identified 133 lncRNAs and 370 mRNAs that were the most highly differentially expressed. Of all the lncRNAs, 61 were upregulated, and 72 were downregulated.
No associated publication
Sex, Specimen part, Disease, Disease stage
View SamplesAlthough many protein-coding genes have been identified to be aberrantly expressed in gallbladder cancer, the mechanism that account for the development and progression of gallbladder cancer remains unclear. In recent years, long noncoding RNAs have been shown to play vital roles in mammalian cell biology. In this study, we found that a small number of lncRNAs that are aberrantly expressed.
Long Noncoding RNA GCASPC, a Target of miR-17-3p, Negatively Regulates Pyruvate Carboxylase-Dependent Cell Proliferation in Gallbladder Cancer.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MicroRNA-181c negatively regulates the inflammatory response in oxygen-glucose-deprived microglia by targeting Toll-like receptor 4.
Specimen part
View SamplesMigroglia cells were exposed to oxygen-glucose deprivation (OGD) for 3 h. The mRNA was isolated and the expression profiles of OGD-activated cells were compared with the profiles of resting cells.
MicroRNA-181c negatively regulates the inflammatory response in oxygen-glucose-deprived microglia by targeting Toll-like receptor 4.
Specimen part
View SamplesBackground: Estrogen receptor-positive (ER+) breast cancers represent approximately two-thirds of all breast cancers and have a sustained risk of late disease recurrence. Cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors have shown significant efficacy in ER+ breast cancer. However, their effects are still limited by drug resistance. In this study, we aim to explore the role of long noncoding RNA TROJAN in ER+ breast cancer. Methods: The expression level of TROJAN in breast cancer tissue and cell lines was determined by quantitative real-time PCR. In vitro and in vivo assays as well as patient derived organoids were preformed to explore the phenotype of TROJAN in ER+ breast cancer. The TROJAN-NKRF-CDK2 axis were screened and validated by RNA pull-down, mass spectrometry, RNA immunoprecipitation, microarray, dual-luciferase reporter and chromatin immunoprecipitation assays. Results: Herein, we showed that TROJAN was highly expressed in ER+ breast cancer. TROJAN promoted cell proliferation and resistance to a CDK4/6 inhibitor and was associated with poor survival in ER+ breast cancer. TROJAN can bind to NKRF and inhibit its interaction with RELA, upregulating the expression of CDK2. The inhibition of TROJAN abolished the activity of CDK2, reversing the resistance to CDK4/6 inhibitor. A TROJAN antisense oligonucleotide sensitized breast cancer cells and organoids to the CDK4/6 inhibitor palbociclib both in vitro and in vivo. Conclusions: TROJAN promotes ER+ breast cancer proliferation and is a potential target for reversing CDK4/6 inhibitor resistance.
LncRNA TROJAN promotes proliferation and resistance to CDK4/6 inhibitor via CDK2 transcriptional activation in ER+ breast cancer.
Cell line
View SamplesIdentify the PDX model of DLBCL subtypes by the microarray expression profiling
No associated publication
Specimen part, Subject
View Samples