Evaluation of ST13 gene expression in colorectal cancer patients

Dong, Qi; Zheng, Shu; Hu, Yue; Chen, Gong-xing; Ding, Jun

doi:10.1631/jzus.2005.b1170

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…( 30 ) Many previous studies by us have shown that ST13 gene expression levels are significantly decreased in primary colorectal cancers compared with adjacent mucosal tissues. ( 18,31 ) It raises the question of whether the low expression of ST13 is due to hypoxia in colorectal tumors.…”

Section: Discussionmentioning

confidence: 99%

“…( 15 ) The expression of ST13 was significantly lower in colorectal cancer than in adjacent normal colon mucosa. ( 15–18 ) Later studies proved that it encodes the approximately 41 kDa Hsp70‐interacting protein, a cofactor (cochaperone) of the 70‐kDa Hsc70 and Hsp70. ( 19–21 ) 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.…”

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confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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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“…Using Northern blot analysis and quantitative RT-PCR approaches, a decreased level of ST13 mRNA was observed in multiple colorectal cancer samples relative to that in their adjacent normal mucosa (Mo et al, 1996;1997a;1997b;Li and Zhang, 2000). However, the levels of ST13 mRNA showed no significant correlation with a tumor's differentiation grade, Dukes' stage, invasion depth, lymph node metastasis, or disease-specific survival (Dong et al, 2005). Similarly, recent in situ hybridization found that only 3 of 7 colon cancer tissues analyzed were positive for ST13 mRNA, whereas 7 of 7 normal colon tissues were positive (Wang et al, 2005).…”

Section: Physiological and Pathophysiological Rolementioning

confidence: 90%

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

Shi

Zhang

Zheng

2007

J. Zhejiang Univ. - Sci. B

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This article is to summarize the molecular and functional analysis of the gene "suppression of tumorigenicity 13" (ST13). ST13 is in fact the gene encoding Hsp70 interacting protein (Hip), a co-factor (co-chaperone) of the 70-kDa heat shock proteins (Hsc/Hsp70). By collaborating with other positive co-factors such as Hsp40 and the Hsp70-Hsp90 organizing protein (Hop), or competing with negative co-factors such as Bcl2-associated athanogen 1 (Bag1), Hip facilitates may facilitate the chaperone function of Hsc/Hsp70 in protein folding and repair, and in controlling the activity of regulatory proteins such as steroid receptors and regulators of proliferation or apoptosis. Although the nomenclature of ST13 implies a role in the suppression of tumorigenicity (ST), to date available experimental data are not sufficient to support its role in cancer development, except for the possible down-regulation of ST13 in gastric and colorectal cancers. Further investigation of this gene at the physiological level would benefit our understanding of diseases such as endocrinological disorders, cancer, and neurodegeneration commonly associated with protein misfolding.

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“…In previous studies, we have proved that ST13 mRNA and protein levels were lower in colorectal cancer tissues compared with adjacent normal tissues (Mo et al, 1996;Zheng et al, 1997;Dong et al, 2005;Wang et al, 2005). Moreover, increased ST13 protein expression suppressed proliferation of colorectal cancer cells and induced apoptosis in colorectal cancer cell lines (Yang et al, 2008;Yu et al, 2009).…”

Section: Introductionmentioning

confidence: 89%

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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Evaluation of ST13 gene expression in colorectal cancer patients

Cited by 8 publications

References 22 publications

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

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

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

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

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