Identification of a Novel Role of ZMIZ2 Protein in Regulating the Activity of the Wnt/β-Catenin Signaling Pathway

Lee, Suk Hyung; Zhu, Chunfang; Peng, Yue; Johnson, Daniel T.; Lehmann, Lynn; Sun, Zijie

doi:10.1074/jbc.m113.529727

Cited by 21 publications

(21 citation statements)

References 61 publications

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“…It is reported that ECT2 depletion impairs tumorigenic growth of NSCLC cell 20 . ZMIZ2 plays a role in regulating the activity of the Wnt/β-catenin signaling pathway 21 . FMNL3 is involved in regulation of cell morphology and cytoskeletal organization 22 .…”

Section: Resultsmentioning

confidence: 99%

Modulation of alternative splicing induced by paclitaxel in human lung cancer

et al. 2018

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Paclitaxel is utilized as the first-line chemotherapeutic regimen for the majority of advanced non-small-cell lung carcinoma. However, whether paclitaxel could suppress cancer progression through modulating RNA alternative splicing remains largely unknown. Here, we demonstrated the effects of paclitaxel on cell proliferation inhibition, cell cycle arrest, and apoptosis. Mechanistically, paclitaxel leads to transcriptional alteration of networks involved in DNA replication and repair, chromosome segregation, chromatin silencing at rDNA, and mitosis at the transcriptional level. Moreover, paclitaxel regulates a number of cancer-associated RNA alternative splicing events, including genes involved in cellular response to DNA damage stimulus, preassembly of GPI anchor in ER membrane, transcription, and DNA repair. In particular, paclitaxel modulates the splicing of ECT2, a key factor involved in the regulation of cytokinesis. Briefly, paclitaxel favors the production of ECT2-S, the short splicing isoforms of ECT2, thereby inhibiting cancer cell proliferation. Our study provides mechanistic insights of paclitaxel on RNA alternative splicing regulation, thus to offer a potential novel route for paclitaxel to inhibit cancer progression.

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Section: Resultsmentioning

confidence: 99%

Modulation of alternative splicing induced by paclitaxel in human lung cancer

et al. 2018

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“…Recently, it has been shown that Zimp7 has a role in regulating the activity of the Wnt/β-Catenin signaling pathway in mammalian cells. Zimp7 is shown to physically interact with β-Catenin and enhance Wnt/ β-Catenin-mediated transcription (Lee et al, 2013). Moreover, in this report Zmiz2 null mice exhibit down-regulation of Axin2, a downstream target gene of β-Catenin.…”

Section: Introductionmentioning

confidence: 83%

PIAS-like protein Zimp7 is required for the restriction of the zebrafish organizer and mesoderm development

Moreno-Ayala

Schnabel

Salas‐Vidal

et al. 2015

Developmental Biology

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The Zmiz2 (Zimp7) protein and its homolog Zmiz1 (Zimp10) were initially identified in humans as androgen receptor co-activators. Sequence analysis revealed the presence of an SP-RING/Miz domain, which is highly conserved in members of the PIAS family and confers SUMO-conjugating activity. Zimp7 has been shown to interact with components of the Wnt/β-Catenin signaling pathway and with Brg1 and BAF57, components of the ATP-dependent mammalian SWI/SNF-like BAF chromatin-remodeling complexes. In this work, we analyze the role of zygotic Zimp7 in zebrafish development. We describe evidence indicating that Zimp7 is required for mesoderm development and dorsoventral patterning. Morpholino-mediated reduction of zygotic Zimp7 produced axial mesodermal defects that were preceded by up-regulation of organizer genes such as bozozok, goosecoid and floating head at the onset of gastrulation and by down-regulation of the ventral markers vox, vent and eve1 indicating loss of the ventrolateral mesoderm. Consistently, embryos overexpressing zimp7 RNA exhibited midline defects such as loss of forebrain and cyclopia accompanied by transcriptional changes directly opposite of those found in the morphants. In addition, the patterning of ventralized embryos produced by the overexpression of vox and vent was restored by a reduction of Zimp7 activity. Altogether, our findings indicate that Zimp7 is involved in transcriptional regulation of factors that are essential for patterning in the dorsoventral axis.

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“…The viral supernatant was centrifuged briefly to remove cellular debris and stored at -80°C. Lentivirus infection was carried out in the presence of 6 mg/ml Polybrene [54,55].…”

Section: Methodsmentioning

confidence: 99%

The comprehensive role of E-cadherin in maintaining prostatic epithelial integrity during oncogenic transformation and tumor progression

Olson

Aldahl

et al. 2019

PLoS Genet

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E-cadherin complexes with the actin cytoskeleton via cytoplasmic catenins and maintains the functional characteristics and integrity of the epithelia in normal epithelial tissues. Lost expression of E-cadherin disrupts this complex resulting in loss of cell polarity, epithelial denudation and increased epithelial permeability in a variety of tissues. Decreased expression of E-cadherin has also been observed in invasive and metastatic human tumors. In this study, we investigated the effect of E-cadherin loss in prostatic epithelium using newly developed genetically engineered mouse models. Deletion of E-cadherin in prostatic luminal epithelial cells with modified probasin promoter driven Cre (PB-Cre4) induced the development of mouse prostatic intraepithelial neoplasia (PIN). An increase in levels of cytoplasmic and nuclear β-catenin appeared in E-cadherin deleted atypical cells within PIN lesions. Using various experimental approaches, we further demonstrated that the knockdown of E-cadherin expression elevated free cytoplasmic and nuclear β-catenin and enhanced androgen-induced transcription and cell growth. Intriguingly, pathological changes representing prostatic epithelial cell denudation and increased apoptosis accompanied the above PIN lesions. The essential role of E-cadherin in maintaining prostatic epithelial integrity and organization was further demonstrated using organoid culture approaches. To directly assess the role of loss of E-cadherin in prostate tumor progression, we generated a new mouse model with bigenic Cdh1 and Pten deletion in prostate epithelium. Early onset, aggressive tumor phenotypes presented in the compound mice. Strikingly, goblet cell metaplasia was observed, intermixed within prostatic tumor lesions of the compound mice. This study provides multiple lines of novel evidence demonstrating a comprehensive role of E-cadherin in maintaining epithelial integrity during the course of prostate oncogenic transformation, tumor initiation and progression.

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Identification of a Novel Role of ZMIZ2 Protein in Regulating the Activity of the Wnt/β-Catenin Signaling Pathway

Cited by 21 publications

References 61 publications

Modulation of alternative splicing induced by paclitaxel in human lung cancer

Modulation of alternative splicing induced by paclitaxel in human lung cancer

PIAS-like protein Zimp7 is required for the restriction of the zebrafish organizer and mesoderm development

The comprehensive role of E-cadherin in maintaining prostatic epithelial integrity during oncogenic transformation and tumor progression

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