Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Differential gene expression profiling of MIHA cells transfected with C-terminal truncated HBx mutants

ABSTRACT: To compare the differentially expressed transcriptomes between MIHA cells transfected with empty vector control or different C-terminal truncated HBx mutants (14 or 35 amino acid carboxyl-terminal truncation - i.e. d14 and d35) mRNA profiles of MIHA cells stably overexpressing empty vector control or different C-terminal truncated HBx mutants (delta 14 and delta 35) were generated by PolyA mRNA sequencing using Illumina HiSeq 1500 platform

ORGANISM(S): Homo sapiens

SUBMITTER: Chi Ho Lin

PROVIDER: E-GEOD-71993 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties.

Ng Kai-Yu KY Chai Stella S Tong Man M Guan Xin-Yuan XY Lin Chi-Ho CH Ching Yick-Pang YP Xie Dan D Cheng Alfred Sze-Lok AS Ma Stephanie S

Oncotarget 20160401 17

Tumor relapse after chemotherapy typifies hepatocellular carcinoma (HCC) and is believed to be attributable to residual cancer stem cells (CSCs) that survive initial treatment. Chronic infection with hepatitis B virus (HBV) has long been linked to the development of HCC. Upon infection, random HBV genome integration can lead to truncation of hepatitis B virus X (HBx) protein at the C-terminus. The resulting C-terminal-truncated HBx (HBx-ΔC) was previously shown to confer enhanced invasiveness an ...[more]

PMID: 27006468

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Project description:Reactivation of androgen receptor (AR) may drive recurrent prostate cancer in castrate patients. Ack1 tyrosine kinase is overexpressed in prostate cancer and promotes castrate resistant xenograft tumor growth and enhances androgen target gene expression and AR recruitment to enhancers. Ack1 phosphorylates AR at Tyr-267 in the N-terminal transactivation domain. In this study, the role of this phosphorylation site was investigated by characterizing the phosphorylation site mutant in the context of full length and truncated AR lacking the ligand-binding domain. The Y267F mutant showed decreased transactivation of reporters. Expression of wild type full length and truncated AR in LNCaP cells increased cell proliferation in androgen-depleted conditions and increased colony formation. However, the Y267F mutant of full length and truncated AR was defective in stimulating cell proliferation. The full length AR Y267F mutant was defective in nuclear translocation induced by androgen or Ack1 kinase. The truncated AR was constitutively localized to the nucleus. Chromatin immunoprecipitation analysis showed that it was recruited to the target enhancers without androgen. The truncated Y267F AR mutant did not exhibit constitutive nuclear localization and androgen enhancer binding activity. Expression of AR responsive genes in cells expressing truncated AR wt and AR-Y267F mutant under androgen deprived conditions was assessed by microarray gene expression analysis. The AR pathway score was increased in cells expressing truncated AR wt and decreased in cells expressing truncated AR-Y267F. These results support the concept that phosphorylation of Tyr-267 is required for AR nuclear translocation and recruitment and DNA binding and transcription of AR responsive genes. Gene expression profiling was performed using RNA samples from LNCaP cells expressing truncated AR-wt and truncated AR-Y267F growing in androgen deprived conditions. The RNA sample from vector control cells were used as reference sample. Two biological replicates were used per each cell line.

Dataset Information

Differential gene expression profiling of MIHA cells transfected with C-terminal truncated HBx mutants

Publications

C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties.

Similar Datasets

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