Isolation of a new member of DnaJ-like heat shock protein 40 (Hsp40) from human liver

Hoe, Kwang Lae; Won, Mi Sun; Chung, Kwansoo; Jang, Young Joo; Lee, Sang Bong; Kim, Dong Uk; Lee, Ji Won; Yun, Jean Ho; Yoo, Hyang Sook

doi:10.1016/s0167-4838(97)00207-0

Cited by 25 publications

(19 citation statements)

References 29 publications

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“…Specific primers were designed from the 5 0 -end of the known HLJ1 cDNA sequence (Hoe et al, 1998) and from the bioinformatic search in GenBank. CL1-0 cell genomic DNA was isolated by a QIAamp DNA blood mini kit (Qiagen) and served as a PCR template.…”

Section: Microarray Analysismentioning

confidence: 99%

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The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion

et al. 2005

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By using microarray and an invasion/metastasis lung cell line model, we identified the DnaJ-like heat shock protein 40, HLJ1, and found that the expression of HLJ1 correlates negatively with cancer cell invasion ability. Overexpression of HLJ1 can suppress cancer cell invasion in vitro. We further characterize the putative promoter region and investigate the transcriptional regulations of human HLJ1. A serial deletion of the 1.2 kb at the 5 0 -flanking region of the human HLJ1 gene was subcloned into a vector containing reporter gene and transfected into human lung adenocarcinoma cell line CL1-0, followed by luciferase activity assay. The results indicated that the region from -232 to þ 176 could drive the basal transcriptional activity of the HLJ1 gene. Sequence analysis of the HLJ1 gene promoter region showed absence of a TATA box, but identified an inverted CCAAT box and four YY1 transcriptional factor-binding sites, which may be important in the regulation of HLJ1 expression. Co-transfection of the YY1 and HLJ1 basal promoter regions, site-directed mutagenesis, and electrophoretic mobility shift assay confirmed that YY1 could upregulate HLJ1 basal promoter activity. Furthermore, we also demonstrated that overexpression of YY1 in CL1-0 cells can increase HLJ1 expression and reduce cell invasive capability. The reduction of cancer cell invasive ability is, at least in part, through upregulation of Ecadherin expression. The increase in HLJ1 and Ecadherin expression, as well as the suppression of invasion ability, can be reversed specifically by HLJ1 siRNA.

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Section: Microarray Analysismentioning

confidence: 99%

“…The DNA sequence analysis showed that it contained the J and G/F domain sequence of the Hsp40 family members (Hoe et al, 1998;Ohtsuka and Hata, 2000). The amino-acid sequencing revealed that human Hsp40 is a mammalian homologue of the bacterial DnaJ HSP (Hattori et al, 1992;Ohtsuka, 1993).…”

Section: Introductionmentioning

confidence: 99%

The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion

et al. 2005

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“…9). HSP40 proteins occur ubiquitously in cells and display significant diversity in eukaryotic genomes (10,11), with at least 44 genes in the human genome (12).…”

Section: Introductionmentioning

confidence: 99%

Synergistic Activation of the Tumor Suppressor, HLJ1, by the Transcription Factors YY1 and Activator Protein 1

et al. 2007

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HLJ1 is a novel tumor and invasion suppressor that inhibits tumorigenesis and cancer metastasis. However, the mechanism of HLJ1 activation is currently unclear. Here, we identify an enhancer segment in the HLJ1 gene at À2,125 to À1,039 bp upstream of the transcription start site. A 50-bp element between À1,492 and À1,443 bp is the minimal enhancer segment, which includes the activator protein 1 (AP-1) site (À1,457 to À1,451 bp), an essential regulatory domain that binds the transcriptional factors FosB, JunB, and JunD. Chromatin immunoprecipitation assays confirm that these AP-1 family members bind to a specific site in the HLJ1 enhancer segment in vivo. Overexpression of either YY1 at promoter or AP-1 at enhancer results in a 3-fold increase in the transcriptional activity of HLJ1. We propose a novel mechanism whereby expression of the tumor suppressor, HLJ1, is upregulated via enhancer AP-1 binding to promoter YY1 and the coactivator, p300, through DNA bending and multiprotein complex formation. The combined expression of AP-1 and YY1 enhances HLJ1 expression by more than five times and inhibits in vitro cancer cell invasion. Elucidation of the regulatory mechanism of HLJ1 expression may facilitate the development of personalized therapy by inhibiting cancer cell proliferation, angiogenesis, and metastasis. [Cancer Res 2007;67(10):4816-26]

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“…HLJ1, consisting 337 amino acids, was first identified from the human liver cDNA library and was classified as a member of the HSP40 family [46] . HLJ1, also known as DNAJB4, belongs to the type Ⅱ homologues of the Hsp40 family and comprises the following four conserved functional domains: a highly conserved J domain, a glycine/phenylalanine-rich region, a cysteinerich region, and a COOH terminal domain [47] .…”

Section: Hlj1 Expression In Lung Cancermentioning

confidence: 99%

“…HLJ1 mRNA is highly expressed in skeletal muscle and in the heart, pancreas, brain, lung, and other organs but is weakly expressed in the liver and kidney. Although the HLJ1 gene was cloned from the liver cDNA library, the expression of HLJ1 in liver tissue is relatively low [46] . Gene expression profiles have been used to identify possible associations with lung cancer behaviour or clinical outcome to better predict patient prognosis.…”

Section: Hlj1 Expression In Lung Cancermentioning

confidence: 99%

Tumour suppressor HLJ1: A potential diagnostic, preventive and therapeutic target in non-small cell lung cancer

Tsai¹

2014

WJCO

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Lung cancer is the leading cause of cancer-related mortality throughout the world. Non-small cell lung cancer (NSCLC) accounts for 85% of all diagnosed lung cancers. Despite considerable progress in the diagnosis and treatment of the disease, the overall 5-year survival rate of NSCLC patients remains lower than 15%. The most common causes of death in lung cancer patients are treatment failure and metastasis. Therefore, developing novel strategies that target both tumour growth and metastasis is an important and urgent mission for the next generation of anticancer therapy research. Heat shock proteins (HSPs), which are involved in the fundamental defence mechanism for maintaining cellular viability, are markedly activated during environmental or pathogenic stress. HSPs facilitate rapid cell division, metastasis, and the evasion of apoptosis in cancer development. These proteins are essential players in the development of cancer and are prime therapeutic targets. In this review, we focus on the current understanding of the molecular mechanisms responsible for HLJ1's role in lung cancer carcinogenesis and progression. HLJ1, a member of the human HSP 40 family, has been characterised as a tumour suppressor. Research studies have also reported that HLJ1 shows promising dual anticancer effects, inhibiting both tumour growth and metastasis in NSCLC. The accumulated evidence suggests that HLJ1 is a potential biomarker and treatment target for NSCLC.© 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Non-small cell lung cancer; Metastasis; HLJ1; Anticancer; Biomarker Core tip: HLJ1, a member of the human heat shock proteins 40 family, has been characterised as a tumour suppressor. Research studies have reported that HLJ1 shows promising dual anticancer effects, inhibiting both tumour growth and metastasis in non-small cell lung cancer (NSCLC). The accumulated evidence suggests that HLJ1 is a potential biomarker and treatment target for NSCLC. We propose a hypothetical model for the roles of HLJ1 stimulator in suppressing lung cancer tumourigenesis. Investigating the integrated and coordinated molecular mechanisms of HLJ1 may shed new light on the treatment of lung cancer. The development of drug targeting HLJ1 may be an effective approach for lung cancer therapy.Tsai MF, Wang CC, Chen JJW. Tumour suppressor HLJ1: A potential diagnostic, preventive and therapeutic target in nonsmall cell lung cancer.

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Isolation of a new member of DnaJ-like heat shock protein 40 (Hsp40) from human liver

Cited by 25 publications

References 29 publications

The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion

The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion

Synergistic Activation of the Tumor Suppressor, HLJ1, by the Transcription Factors YY1 and Activator Protein 1

Tumour suppressor HLJ1: A potential diagnostic, preventive and therapeutic target in non-small cell lung cancer

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