What we know about ST13, a co-factor of heat shock protein, or a tumor suppressor?

Shi, Zheng Zheng; Zhang, Jia Wei; Zheng, Shu

doi:10.1631/jzus.2007.b0170

Cited by 36 publications

(28 citation statements)

References 48 publications

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“…This region harbours several genes, for instance, ST13 (suppression of tumourigenicity 13), which encodes a cofactor of the heat shock protein 70. ST13 has been found to be down-regulated in gastric and colorectal cancers (Shi et al 2007), and a potent antitumour effect of ST13 has recently been reported in vitro and in an animal model of colorectal carcinoma (Yang et al 2008). A second MOR of deletion at 22q13.2-22q13.31 involved 50% of the tumour samples.…”

Section: Discussionmentioning

confidence: 99%

Recurrent genomic alterations in benign and malignant pheochromocytomas and paragangliomas revealed by whole-genome array comparative genomic hybridization analysis

Sandgren

Ståhl²,

Andersson³

et al. 2010

Endocrine-Related Cancer

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Pheochromocytomas and abdominal paragangliomas are adrenal and extra-adrenal catecholamine-producing tumours. They arise due to heritable cancer syndromes, or more frequently occur sporadically due to an unknown genetic cause. The majority of cases are benign, but malignant tumours are observed. Previous comparative genomic hybridization (CGH) and loss of heterozygosity studies have shown frequent deletions of chromosome arms 1p, 3q and 22q in pheochromocytomas. We applied high-resolution whole-genome array CGH on 53 benign and malignant pheochromocytomas and paragangliomas to narrow down candidate regions as well as to identify chromosomal alterations more specific to malignant tumours. Minimal overlapping regions (MORs) were identified on 16 chromosomes, with the most frequent MORs of deletion (R32%) occurring on chromosome arms 1p, 3q, 11p/q, 17p and 22q, while the chromosome arms 1q, 7p, 12q and 19p harboured the most common MORs of gain (R14%). The most frequent MORs (61-75%) in the pheochromocytomas were identified at 1p, and the four regions of common losses encompassed 1p36, 1p32-31, 1p22-21 and 1p13. Tumours that did not show 1p loss generally demonstrated aberrations on chromosome 11. Gain of chromosomal material was significantly more frequent among the malignant cases. Moreover, gain at 19q, trisomy 12 and loss at 11q were positively associated with malignant pheochromocytomas, while 1q gain was commonly observed in the malignant paragangliomas. Our study revealed novel and narrow recurrent chromosomal regions of loss and gain at several autosomes, a prerequisite for identifying candidate tumour suppressor genes and oncogenes involved in the development of adrenal and extra-adrenal catecholamine-producing tumours.

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Section: Discussionmentioning

confidence: 99%

Recurrent genomic alterations in benign and malignant pheochromocytomas and paragangliomas revealed by whole-genome array comparative genomic hybridization analysis

Sandgren

Ståhl²,

Andersson³

et al. 2010

Endocrine-Related Cancer

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“…(19)(20)(21) By collaborating with other positive cofactors such as Hsp40 and the Hsp70-Hsp90 organizing protein, or competing with negative cofactors such as Bcl2-associated athanogen 1, Hsp70-interacting protein may facilitate the chaperone function of Hsc70 and Hsp70 in protein folding and repair, and in controlling the activity of regulatory proteins such as steroid receptors and regulators of proliferation or apoptosis. (21)(22)(23) Our recent findings suggest that overexpression of ST13 can inhibit the growth of wild-type and mutant p53 colorectal cancer cells by inducing mitochondrial apoptotic cell death.(24) This evidence clearly proves that ST13 is a colorectal cancer-specific suppressor gene.To create an oncolytic adenovirus with stronger antitumor targeting efficacy and reduced side effects on normal cells, the novel adenovirus variant SG500 was constructed, in which the tumor-selective expression of both the E1A and E1B genes was replaced with the hTERT promoter and HRE promoter, respectively.(12) The ST13 expression cassette controlled by the cytomegalovirus promoter was inserted into SG500 to form SG500-ST13 constructs, allowing for increased cancer cell targeting specificity and decreased adverse side effects. Its antitumor efficacy was explored both in vitro and in vivo.…”

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confidence: 99%

Potent antitumor activity of double‐regulated oncolytic adenovirus‐mediated ST13 for colorectal cancer

Zhong

Yang

et al. 2009

Cancer Science

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Following targeted gene virotherapy, the suppression of tumorigenicity 13 (ST13) gene was inserted into the doubleregulated oncolytic adenovirus SG500 to ensure more safety and potent antitumor activity against colorectal cancer in vitro and in vivo. We generated the ST13-expressing oncolytic adenovirus SG500-ST13, with which colorectal carcinoma cell lines SW620 and HCT116, and the lung fibroblast cell line WI38, were infected. Crystal violet staining was carried out to detect the cytopathic effect in cells, and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method was used to assay cell viability. The effect of apoptosis induced by SG500-ST13 was confirmed by Hoechst staining and the TdT-mediated dUTP-biotin nick-end labeling method. To further identify the antitumor effects of SG500-ST13 on HCT116 xenografts in Balb/c nude mice, the induction of cell death was assessed by hematoxylin-eosin staining. Immunohistochemical study was also carried out. (Cancer Sci 2009; 100: 678-683) C olorectal cancer ranks second in both morbidity and mortality in developed countries. Nearly 945 000 new colorectal cancer cases are diagnosed worldwide each year and its mortality rate is approximately 492 000.(1) Despite advanced progress in technologies for diagnosis and therapy, around 50% of newly diagnosed colorectal cancer patients will die of this disease due to metastases.(2) Surgical resection or surgery coupled with systemic chemotherapy of liver metastasis is the treatment currently available for these patients.(3) These findings underscore the need for improved therapeutic approaches to more efficaciously control this aggressive type of cancer and reduce its metastatic spread.Conditional replicative adenoviruses appear to be attractive anticancer agents that are currently being evaluated in clinical trials.(4,5) CRAd exerts intrinsic anticancer activity through its selective replication in and lysis of cancer cells. In addition, release of CRAd progeny by infected tumor cells provides a potential to amplify the oncolytic effect and its lateral spread through solid tumors.One strategy to ensure tumor targeting is to place the virual essential genes under the control of tumor-specific promoters. Because the hTERT promoter is expected to be active in the majority (~90%) of human cancer cells with upregulated telomerase expression, (6) the hTERT promoter is used to control the essential gene E1A for adenovirus replication in a series of CRAd.(7-9) Hypoxia occurs in virtually all solid tumors as they outgrow their blood supply. Hypoxia augments cellular levels of HIF, a transcription factor that regulates target genes through the binding of HRE. Activation of the HIF pathway enables cancer cells to survive and proliferate in a hypoxic environment and contributes to a more aggressive phenotype.(10,11) Therefore, the HIF-HRE system of gene regulation under hypoxia, or as a result of genetic alterations during cell transformation, is particularly attractive to specifically target solid tumors. Therefore, HRE ha...

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“…ST13 is the gene encoding the HSP70 interacting protein (HIP), a co-chaperone of the 70-kDa HSPs (HSC/HSP70) (Höhfeld et al, 1995;Shi et al, 2007). We originally identified the ST13 gene by subtraction hybridization with normal mucosal tissue and colorectal cancers (Zheng et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

“…ST13 protein (HIP) is composed of an N-terminal region, a central tetratricopeptide repeat (TPR) domain followed by a highly charged region, and a C-terminal region containing glycine-glycine-methionine-proline (GGMP) repeats and a Sti1 motif (Prapapanich et al, 1996a;1998;Irmer and Höhfeld, 1997). HIP may facilitate the chaperone function of HSC/HSP70 in controlling the activities of regulatory proteins such as steroid receptors and regulators of proliferation or apoptosis, and in protein folding and repair (Prapapanich et al, 1996a;1996b;Höhfeld and Jentsch, 1997;Irmer and Höhfeld, 1997;Shi et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

ST13, a proliferation regulator, inhibits growth and migration of colorectal cancer cell lines

Bai

Shi

Zhang

et al. 2012

J. Zhejiang Univ. Sci. B

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Background and objective: ST13, is the gene encoding the HSP70 interacting protein (HIP). Previous research has shown that ST13 mRNA and protein levels are down-regulated in colorectal cancer (CRC) tissues compared with adjacent normal tissues. This study aims at the role of ST13 in the proliferation and migration of CRC cells. Methods: The transcript level of ST13 in different CRC cell lines was evaluated by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). ST13-overexpressed and ST13-knockdown CRC cells were constructed respectively by lentiviral transduction, followed by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, plate colony formation, cell-cycle analysis, and migration assays to evaluate the influence of ST13 on proliferation and migration in vitro. Moreover, a mouse xenograft study was performed to test in vivo tumorigenicity of ST13-knockdown CRC cells. Results: Lentivirus-mediated overexpression of ST13 in CRC cells inhibited cell proliferation, colony formation, and cell migration in vitro. In contrast, down-regulation of ST13 by lentiviralbased short hairpin RNA (shRNA) interference in CRC cells significantly increased cell proliferation and cloning efficiency in vitro. In addition, down-regulation of ST13 expression significantly increased the tumorigenicity of CRC cells in vivo. Conclusions: ST13 gene is a proliferation regulator that inhibits tumor growth in CRC and may affect cell migration.

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What we know about ST13, a co-factor of heat shock protein, or a tumor suppressor?

Cited by 36 publications

References 48 publications

Recurrent genomic alterations in benign and malignant pheochromocytomas and paragangliomas revealed by whole-genome array comparative genomic hybridization analysis

Recurrent genomic alterations in benign and malignant pheochromocytomas and paragangliomas revealed by whole-genome array comparative genomic hybridization analysis

Potent antitumor activity of double‐regulated oncolytic adenovirus‐mediated ST13 for colorectal cancer

ST13, a proliferation regulator, inhibits growth and migration of colorectal cancer cell lines

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