TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells

Kim, Patrick Y.; Rahmanto, Aldwin Suryo; Tan, Owen; Norris, Murray D.; Haber, Michelle; Marshall, Glenn M.; Cheung, Belamy B.

doi:10.1007/s10495-013-0813-y

Cited by 25 publications

(23 citation statements)

References 36 publications

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“…Another estrogen-responsive protein, TRIM16, which inhibits hepatocellular carcinoma cell migration and invasion by suppression of ZEB2 expression as well as suppresses cancer cell viability by involving interaction and stabilization of TDP43 with consequent eff ects on E2F1 and pRb proteins (Kim et al 2016), is also up-regulated in glioma cells without IRE1 signaling enzyme function. Moreover, TRIM16 inhibits neuroblastoma cells proliferation through cell cycle regulation and induces apoptosis via activation of caspase-2 (Bell et al 2013;Kim et al 2013). Th erefore, our results conform to data that FAM162A, PGRMC2, TRIM16, and SLC39A6 have mainly anti-proliferative functions through interaction with diff erent transcription coregulators and signaling pathways of ER stress in cell specifi c manner.…”

Section: Discussionsupporting

confidence: 88%

“…Moreover, recently was shown that TRIM16 inhibits cancer cell viability by a novel mechanism involving interaction and stabilization of TDP43 with consequent eff ects on E2F1 and pRb proteins (Kim et al 2016). Th ere is also data that TRIM16 inhibits neuroblastoma cells proliferation through cell cycle regulation and melanoma cells proliferation and migration through regulation of interferon beta 1 as well as induces apoptosis through activation of caspase-2 in cancer cells (Bell et al 2013;Kim et al 2013;Sutton et al 2014).…”

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confidence: 99%

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Hypoxic regulation of the expression of genes encoded estrogen related proteins in U87 glioma cells: eff ect of IRE1 inhibition

et al. 2017

Endocrine Regulations

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Objective. Th e aim of the present study was to examine the eff ect of inhibition of endoplasmic reticulum stress signaling, mediated by IRE1 (inositol requiring enzyme 1), which is a central mediator of the unfolded protein response on the expression of genes encoded estrogen related proteins (NRIP1/RIP140, TRIM16/EBBP, ESRRA/NR3B1, FAM162A/E2IG5, PGRMC2/PMBP, and SLC39A6/LIV-1) and their hypoxic regulation in U87 glioma cells for evaluation of their possible signifi cance in the control of glioma cells proliferation.Methods. Th e expression of NRIP1, EBBP, ESRRA, E2IG5, PGRMC2, and SLC39A6 genes in U87 glioma cells, transfected by empty vector pcDNA3.1 (control) and cells without IRE1 signaling enzyme function (transfected by dnIRE1) upon hypoxia, was studied by a quantitative polymerase chain reaction.Results. Inhibition of both enzymatic activities (kinase and endoribonuclease) of IRE1 signaling enzyme function up-regulates the expression of EBBP, E2IG5, PGRMC2, and SLC39A6 genes is in U87 glioma cells in comparison with the control glioma cells, with more signifi cant changes for E2IG5 and PGRMC2 genes. At the same time, the expression of NRIP1 and ESRRA genes is strongly down-regulated in glioma cells upon inhibition of IRE1. We also showed that hypoxia increases the expression of E2IG5, PGRMC2, and EBBP genes and decreases NRIP1 and ESRRA genes expression in control glioma cells. Furthermore, the inhibition of IRE1 in U87 glioma cells decreases the eff ect of hypoxia on the expression of E2IG5 and PGRMC2 genes, eliminates hypoxic regulation of NRIP1 gene, and enhances the sensitivity of ESRRA gene to hypoxic condition. Furthermore, the expression of SLC39A6 gene is resistant to hypoxia in both the glioma cells with and without IRE1 signaling enzyme function. Conclusions.Results of this investigation demonstrate that inhibition of IRE1 signaling enzyme function aff ects the expression of NRIP1, EBBP, ESRRA, E2IG5, PGRMC2, and SLC39A6 genes in U87 glioma cells in gene specifi c manner and these changes possibly contribute to the suppression of the cell proliferation. Most of these genes are regulated by hypoxia and preferentially through IRE1 signaling pathway of endoplasmic reticulum stress.

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Section: Discussionsupporting

confidence: 88%

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confidence: 99%

Hypoxic regulation of the expression of genes encoded estrogen related proteins in U87 glioma cells: eff ect of IRE1 inhibition

et al. 2017

Endocrine Regulations

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“…TRIM16, also known as estrogen-responsive B-box protein (EBBP), is a member of the TRIM family and the functions are not yet fully elucidated (12). TRIM16 is a positive transcriptional regulator of the retinoic acid receptor β2 (13).…”

Section: Introductionmentioning

confidence: 99%

“…TRIM16 is a positive transcriptional regulator of the retinoic acid receptor β2 (13). It plays an important role in many different types of cancers, including neuroblastoma, non-small cell lung cancer (NSCLC) and melanoma (12). Overexpression of TRIM16 reduced neuroblastoma cell growth, enhanced retinoid-induced differentiation and decreased tumorigenicity in vivo (14,15).…”

Section: Introductionmentioning

confidence: 99%

TRIM16 suppresses the progression of prostate tumors by inhibiting the Snail signaling pathway

Lü

Sun

et al. 2016

International Journal of Molecular Medicine

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Prostate carcinoma is a devastating disease which is characterized by insidious early symptoms, rapid progression and a poor prognosis. Tripartite motif-containing protein 16 (TRIM16) was identified as an estrogen- and antiestrogen-regulated gene in epithelial cells stably expressing estrogen receptors. The protein encoded by this gene contains two B-box domains and a coiled-coiled region that are characteristic of the B-box zinc finger protein family. Proteins belonging to this family have been reported to be involved in a variety of biological processes including cell growth, differentiation and pathogenesis. TRIM16 expression has been detected in most tissues. However, the funtions of this gene remain to be elucidated. In the present study, immunohistochemical staining revealed that the expression of TRIM16 was decreased in prostate adenocarcinoma compared with that in normal prostate tissues. The patients with high TRIM16-expressing tumors had a significantly greater survival than those with low TRIM16-expressing tumors. Western blot analysis showed that TRIM16 was downregulated in distant metastatic cancer tissues compared with that in non-distant metastatic cancer tissues. The overexpression of TRIM16 inhibited the migration and invasion of prostate cancer cells as well as inhibiting the epithelial-to-mesenchymal transition process, whereas TRIM16 depletion enhanced these processes. Moreover, TRIM16 inhibited the Snail signaling pathway. The silencing of Snail by small interfering RNA was performed in order to determine the role of Snail in the TRIM16-mediated tumor phenotype. Taken together, these findings suggest that TRIM16 may be an important molecular target which may aid in the design of novel therapeutic agents for prostate cancer.

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“…Given the connections to autophagic machinery via TRIM16, the role of Galectin-3 in control of bacteria or pathology associated with mycobacterial infection can now be mechanistically linked to the TRIM-driven process of precision autophagy (Kimura et al, 2016), which differs from bulk autophagy. TRIM16 is also known as estrogen-responsive B box protein, and its role in cancer (a general property of TRIMs (Hatakeyama, 2011)) has been linked to specific effects on immune signaling (Sutton et al, 2014), cell survival (Kim et al, 2013), cell migration and metastasis (Marshall et al, 2010; Sutton et al, 2014) through various mechanisms, including measures of membrane repair (Cheung et al, 2012; Marshall et al, 2010), with the latter potentially overlapping with the processes described in this work.…”

Section: Discussionmentioning

confidence: 86%

TRIMs and Galectins Globally Cooperate and TRIM16 and Galectin-3 Co-direct Autophagy in Endomembrane Damage Homeostasis

et al. 2016

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SUMMARY Selective autophagy performs an array of tasks to maintain intracellular homeostasis, sterility, and organellar and cellular functionality. The fidelity of these processes depends on precise target recognition and limited activation of the autophagy apparatus in a localized fashion. Here we describe cooperation in such processes between the TRIM family and Galectin family of proteins. TRIMs, which are E3 ubiquitin ligases, displayed propensity to associate with Galectins. One specific TRIM, TRIM16, interacted with Galectin-3 in an ULK1-dependent manner. TRIM16, through integration of Galectin- and ubiquitin-based processes, coordinated recognition of membrane damage with mobilization of the core autophagy regulators ATG16L1, ULK1, and Beclin 1 in response to damaged endomembranes. TRIM16 affected mTOR, interacted with TFEB and influenced TFEB’s nuclear translocation. The cooperation between TRIM16 and Galectin-3 in targeting and activation of selective autophagy protects cells from lysosomal damage and Mycobacterium tuberculosis invasion.

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TRIM16 overexpression induces apoptosis through activation of caspase-2 in cancer cells

Cited by 25 publications

References 36 publications

Hypoxic regulation of the expression of genes encoded estrogen related proteins in U87 glioma cells: eff ect of IRE1 inhibition

Hypoxic regulation of the expression of genes encoded estrogen related proteins in U87 glioma cells: eff ect of IRE1 inhibition

TRIM16 suppresses the progression of prostate tumors by inhibiting the Snail signaling pathway

TRIMs and Galectins Globally Cooperate and TRIM16 and Galectin-3 Co-direct Autophagy in Endomembrane Damage Homeostasis

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