Identification of a hTid‐1 mutation which sensitizes gliomas to apoptosis

Trentin, Grace A.; He, Yonghong; Wu, D.; Tang, Damu; Rozakis-Adcock, Maria

doi:10.1016/j.febslet.2004.11.034

Cited by 26 publications

(26 citation statements)

References 41 publications

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“…Recently, Canamasas et al showed that loss of Tid1 expression was associated with human basal cell carcinoma but not with normal keratinocytes (4). Similarly, Trentin et al also reported a Tid1 mutation in human glioma cells and introduction of wild-type Tid1 into these cancer cells induced their apoptosis (5). These observations suggest that Tid1 plays a role in human carcinogenesis.…”

Section: Introductionmentioning

confidence: 74%

Tid1 Negatively Regulates the Migratory Potential of Cancer Cells by Inhibiting the Production of Interleukin-8

Kim

Hayashi

et al. 2005

Cancer Research

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Tid1 is the human homologue of the Drosophila tumor suppressor, Tid56. Reducing the expression of Tid1 in MDA-MB231 breast cancer cells enhanced their migration without affecting their survival or growth rate. From microarray screening, we discovered that after Tid1 depletion, the mRNA level of interleukin-8 (IL-8) was significantly increased in these cancer cells, which consequently increased secretion of IL-8 protein by 3.5-fold. The enhanced migration of these Tid1-knockdown cells was blocked by reducing the IL-8 expression or by adding an IL-8 neutralizing antibody to the culture medium, suggesting that enhancement of cell motility in these Tid1-deficient cells is dependent on the de novo synthesis of IL-8. Subsequently, we found that abrogating the nuclear factor KB binding site in the IL-8 promoter completely blocked the Tid1 depletion-induced IL-8 expression in the breast cancer cells. As increased IL-8 levels are known to promote tumor metastasis, we tested the effect of Tid1 knockdown on tumor metastasis and found that Tid1 depletion enhanced the metastasis of breast cancer cells in animals. Together, these results indicate that Tid1 negatively regulates the motility and metastasis of breast cancer cells, most likely through attenuation of nuclear factor KB activity on the promoter of the IL8 gene. (Cancer Res 2005; 65(19): 8784-91)

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Section: Introductionmentioning

confidence: 74%

Tid1 Negatively Regulates the Migratory Potential of Cancer Cells by Inhibiting the Production of Interleukin-8

Kim

Hayashi

et al. 2005

Cancer Research

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“…There is a body of evidence indicating that hTid1 plays an important role in apoptosis and/or cell proliferation in various cell types (38,40). In addition, it was shown that hTid regulates apoptosis of glioma cells and suppresses growth of head and neck cancer cells both in vitro and in vivo (61,62). The mechanisms involved in hTid1-mediated growth suppression remain elusive because hTid1 modulates the activity of many proteins involved in signal transduction and hence in the survival/apoptosis and/or cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

The Tumor Suppressor hTid1 Inhibits STAT5b Activity via Functional Interaction

Dhennin‐Duthille¹,

Nyga²,

Yahiaoui³

et al. 2011

Journal of Biological Chemistry

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STAT5a and -5b (signal transducers and activators of transcription 5a and 5b) proteins play an essential role in hematopoietic cell proliferation and survival and are frequently constitutively active in hematologic neoplasms and solid tumors. Because STAT5a and STAT5b differ mainly in the carboxylterminal transactivation domain, we sought to identify new proteins that bind specifically to this domain by using a bacterial two-hybrid screening. We isolated hTid1, a human DnaJ protein that acts as a tumor suppressor in various solid tumors. hTid1 interacts specifically with STAT5b but not with STAT5a in hematopoietic cell lines. This interaction involves the cysteine-rich region of the hTid1 DnaJ domain. We also demonstrated that hTid1 negatively regulates the expression and transcriptional activity of STAT5b and suppresses the growth of hematopoietic cells transformed by an oncogenic form of STAT5b. Our findings define hTid1 as a novel partner and negative regulator of STAT5b.STAT transcription factors play a central role in cytokinedependent survival, proliferation, and differentiation of a large spectrum of cells. Following cytokine addition, STAT proteins become tyrosine-phosphorylated and subsequently dimerize, forming homo-or heterodimers, and translocate into the nucleus, where they bind to specific elements in the promoter of target genes and activate transcription (1). The STAT protein family comprises seven members, including the two closely related STAT5a and STAT5b molecules (2, 3). Mice in which stat5a and stat5b genes were deleted revealed redundant and specific functions of both proteins. stat5a

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“…In MCJ, the J domain is located at the C-terminal unlike other DNAJ proteins where the J domain is at the N-terminal. In ovarian carcinoma, the expression of MCJ has been associated with enhanced sensitivity to paclitaxel, topotecan, and cisplatin [47]. Epigenetic inactivation of MCJ is reported in malignant pediatric brain tumors [69].…”

Section: Abstract Hsp40 á Dnaj á Cancermentioning

confidence: 99%

“…However, the recent flurry of activity in this emerging field is certainly noticeable. Reports describing the involvement of some HSP40 family members of distinct classes such as hTid I (class DNAJA3), HLJ1 (class DNAJB4) in modulation of tumor growth are opening new frontiers for studies on this family [45][46][47][48][49][50][51]. In the next few paragraphs, we will review the published research articles describing members of human HSP40 in cancer.…”

Section: Abstract Hsp40 á Dnaj á Cancermentioning

confidence: 99%

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Multi-faceted role of HSP40 in cancer

Mitra

Shevde

Samant

2009

Clin Exp Metastasis

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HSP40 (DNAJ) is an understudied family of co-chaperones. The human genome codes for over 41 members of HSP40 family that reside at distinct intracellular locations. Despite their large numbers, little is known about their physiologic roles. Recent research has revealed involvement of some of the DNAJ family members in various types of cancers. In this article we summarize the information about the involvement of human DNAJ family members in various aspects of cancer biology. Furthermore we discuss the potential role of the J domain of DNAJ proteins in cancer biology.

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Identification of a hTid‐1 mutation which sensitizes gliomas to apoptosis

Cited by 26 publications

References 41 publications

Tid1 Negatively Regulates the Migratory Potential of Cancer Cells by Inhibiting the Production of Interleukin-8

Tid1 Negatively Regulates the Migratory Potential of Cancer Cells by Inhibiting the Production of Interleukin-8

The Tumor Suppressor hTid1 Inhibits STAT5b Activity via Functional Interaction

Multi-faceted role of HSP40 in cancer

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