Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Oncogenic Functions of the Transcription Factor LSF

ABSTRACT: Overexpression of LSF in less aggressive hepatocellular carcinoma (HCC) cells resulted in highly aggressive, angiogenic and multi-organ metastatic tumors while inhibition of LSF significantly abrogated growth and metastasis of highly aggressive HCC cells in nude mice. We used microarrays to identify the downstream genes mediating the effects of LSF in HCC cells. Gene expression profiles were compared between Control-8 and LSF-17 clones of HepG3 cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Devanand Sarkar

PROVIDER: E-GEOD-19815 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Transcription factor Late SV40 Factor (LSF) functions as an oncogene in hepatocellular carcinoma.

Yoo Byoung Kwon BK Emdad Luni L Gredler Rachel R Fuller Christine C Dumur Catherine I CI Jones Kimberly H KH Jackson-Cook Colleen C Su Zao-Zhong ZZ Chen Dong D Saxena Utsav H UH Hansen Ulla U Fisher Paul B PB Sarkar Devanand D

Proceedings of the National Academy of Sciences of the United States of America 20100419 18

Hepatocellular carcinoma (HCC) is a highly aggressive cancer with no currently available effective treatment. Understanding of the molecular mechanism of HCC development and progression is imperative for developing novel, effective, and targeted therapies for this lethal disease. In this article, we document that the cellular transcription factor Late SV40 Factor (LSF) plays an important role in HCC pathogenesis. LSF protein was significantly overexpressed in human HCC cells compared to normal h ...[more]

PMID: 20404171

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Project description:Background & Aims: Extracellular vesicles (EVs) play a pivotal role in connecting tumor cells and their local and distant microenvironment. Here, we aimed to understand the role and molecular basis of patient-derived EVs in modulating cancer stemness and tumorigenesis in the context of hepatocellular carcinoma (HCC). Methods: EVs were isolated, quantified and characterized from patients’ sera. EVs were tested vigorously, both in vitro and in vivo, by various functional assays. Proteomic analysis was performed to identify the functional components of EVs. The expression level of polymeric immunoglobulin receptor (pIgR) in circulating EVs, tumor and non-tumorous tissues of HCC patients was determined by ELISA, immunoblotting, immunohistochemistry and quantitative PCR. The functional role and underlying mechanism of EVs with an enhanced pIgR expression was elucidated. Blockage of EV-pIgR with neutralizing antibody was performed in nude mice implanted with patient-derived tumor xenograft (PDTX). Results: Circulating EVs of late-stage HCC (L-HCC) patient had significantly elevated pIgR expression when compared to the EVs released by control individuals. The augmenting effect of L-HCC patient in cancer stemness and tumorigenesis was hindered by anti-pIgR antibody. EVs enriched with pIgR consistently promoted cancer stemness and cancerous phenotypes in the recipient cells. Mechanistically, EV-pIgR-induced cancer aggressiveness was abrogated by Akt and β-catenin inhibitors, ascertaining the role of EV-pIgR through the activation of PDK1/Akt/GSK3β/β-catenin signaling axis. Furthermore, anti-pIgR neutralizing antibody attenuated the tumor growth in mice implanted with PDTX. Conclusion: The study illustrates an unrevealed role of EV-pIgR in regulating cancer stemness and aggressiveness, in which EV-pIgR activates PDK1/Akt/GSK3β/β-catenin signaling cascades. The blockage of intercellular communications mediated by EV-pIgR in the tumor microenvironment may provide a new therapeutic strategy for cancer patients.

Dataset Information

Oncogenic Functions of the Transcription Factor LSF

Publications

Transcription factor Late SV40 Factor (LSF) functions as an oncogene in hepatocellular carcinoma.

Similar Datasets

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