To explore the biological changes of keratinocytes in condyloma acuminata (CA) warts, we performed mRNA and lncRNA expression profiling of keratinocytes from normal skins and warts of condyloma acuminata patients to compare the gene expression.
Enhanced Glycogen Metabolism Supports the Survival and Proliferation of HPV-Infected Keratinocytes in Condylomata Acuminata.
Specimen part
View SamplesReprogramming metabolism plays an important role in tumor cells for maintaining their abnormal biologic behaviors. Therefore, special factors could regulate metabolic processes and influence the overall status of tumor cells. This phenomenon was obviously found in melanoma. Fumarylacetoacetate hydrolase (fumarylacetoacetase, FAH) is an enzyme encoded by the FAH gene located on the chromosome 15q25.1 region and contains 14 exons. FAH enzyme catalyzes the hydrolysis of 4- fumarylacetoacetase into fumarate and acetoacetate. It is the last enzyme in the subpathway from L-phenylalanine and tyrosine degradation. Mutations in the FAH gene cause type I tyrosinemia, which is a hereditary error of metabolism that is characterized by increased tyrosine levels in the blood and urine of patients. In the present study, we will explore whether FAH is an essential enzyme to promote multiple metabolic processes and elucidate the functions of FAH in melanoma. Gene microarrays and bioinformatics analysis of the differentially expressed genes (DEGs) were performed using A375 cells, and we concentrated on the biologic functions of FAH. In general, our work revealed several functional mechanisms of FAH in melanoma, which indicated FAH might be a potentially therapeutic target and an independent prognostic indicator for this disease.
CDC5L drives FAH expression to promote metabolic reprogramming in melanoma.
Cell line
View SamplesThe role of lymphangiogenesis in tumor metastasis remains unclear. This study addressed this issue in lymphatic endothelial cells (LECs) derived from primary invasive breast cancer specimens.
Tumor-associated Lymphatic Endothelial Cells Promote Lymphatic Metastasis By Highly Expressing and Secreting SEMA4C.
Specimen part, Disease
View SamplesL-DOPA-induced dyskinesia (LID) represents one of the major problems of the long-term therapy of patients with Parkinson's disease (PD). Although the pathophysiologic mechanisms underlying LID are not completely understood, activation of the extracellular signal regulated kinase (ERK) is recognized to play a key role. ERK is phosphorylated by mitogen-activated protein kinase kinase (MEK), and thus MEK inhibitor can prevent ERK activation. Here the effect of the MEK inhibitor PD98059 on LID and the associated molecular changes were examined. Rats with unilateral 6-OHDA lesions of the nigrostriatal pathway received daily L-DOPA treatment for three weeks, and abnormal involuntary movements (AIMs) were assessed every other day. PD98059 was injected in the lateral ventricle daily for 12 days starting from day 10 of L-DOPA treatment. Striatal molecular markers of LID were analyzed together with gene regulation using microarray. The administration of PD98059 significantly reduced AIMs. In addition, ERK activation and other associated molecular changes including FosB were reversed in rats treated with the MEK inhibitor. PD98059 induced significant up-regulation of 418 transcripts and down-regulation of 378 transcripts in the striatum. Tyrosine hydroxylase (Th) and aryl hydrocarbon receptor nuclear translocator (Arnt) genes were down-regulated in lesioned animals and up-regulated in L-DOPA-treated animals. Analysis of protein levels showed that PD98059 reduced the striatal TH. These results support the association of p-ERK1/2, FosB, p-H3 to the regulation of TH and ARNT in the mechanisms of LID, and pinpoint other gene regulatory changes, thus providing clues for identifying new targets for LID therapy.
No associated publication
Sex, Specimen part, Disease, Disease stage
View SamplesLittle is known about the roles of methyl-CpG-binding domain protein 2 (MBD2), a reader of DNA methylation, in T-cell acute lymphoblastic leukemia (T-ALL). Here, we investigated the role of MBD2 in T-ALL by using an Mbd2 knockout mouse model. We found that MBD2 ablation impeded the progression and maintenance of Notch1-driven T-ALL.Our data reveals essential roles for MBD2 in lymphopoiesis and T-ALL and support an intriguing potential of MBD2 as a therapeutic target for T-ALL.
MBD2 Ablation Impairs Lymphopoiesis and Impedes Progression and Maintenance of T-ALL.
Specimen part
View SamplesOur previous study screened a novel cancer progression suppressor gene, FAM210B, which encodes an outer mitochondrial membrane protein, by the suppression of mortality by antisense rescue technique (SMART). We demonstrated that FAM210B loss was significantly associated with cancer metastasis and decreased survival in a clinical setting.
No associated publication
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Specimen part, Cell line
View SamplesTo explore the potential targets of Bmi1 in the liver development of hepatic carcinogenesis, we assayed the gene expression level in the liver of Bmi1 knockout mice. We isolated the liver tissue of Bmi1 WT and KO mice around 6-8 weeks. Then we extracted total RNA and run the microarray detection. Gene expression in Bmi1 KO mouse livers was compared with that in Bmi1 WT mouse livers to screen potential targets of Bmi1.
No associated publication
Specimen part
View SamplesBmi1 plays a pivotal role in hepatic carcinoma (HCC), but its targets in HCC is unknown. To screen the potential targets, we transfected HCC cell line Huh7 and Hep3B with Bmi1 shRNA lenti-virus. After confirming the Bmi1 was knocked down using western blotting, we extracted total RNA and then run the microarray detection. Gene expression profiles in Bmi1 KO cells were compared with those in Bmi1 WT cells to screen potential targets of Bmi1.
No associated publication
Cell line
View SamplesTranscriptional profiling of an Fd-GOGAT1/GLU1 mutant in Arabidopsis thaliana reveals a multiple stress response and extensive reprogramming of the transcriptome
Transcriptional profiling of an Fd-GOGAT1/GLU1 mutant in Arabidopsis thaliana reveals a multiple stress response and extensive reprogramming of the transcriptome.
Specimen part
View Samples