Transgelin Silencing Induces Different Processes in Different Breast Cancer Cell Lines

Dvořáková, Monika; Lapčík, Petr; Bouchalová, Pavla; Bouchal, Pavel

doi:10.1002/pmic.201900383

Cited by 5 publications

(7 citation statements)

References 44 publications

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“…22 Growth factor-stimulated proliferation of human umbilical vein and aortic endothelial cells was found to be highly dependent on IQGAP1. 23 The non-detection of TAGLN we observed (Figure 1(f)) from the MCF-7 cells coincides with the findings of Dvorakova et al 24 Prior studies stated that PIP2 and IQGAP1 are both expressed in MCF-7 cells. 25,26 However, the non-existence of variances observed with PIP2 and IQGAP1 levels between TAGLN knockdown and control cells (Figure 1(f)) means that no coactions among TAGLN, PIP2, and IQGAP1 have transpired.…”

Section: Resultssupporting

confidence: 90%

“…Growth factor‐stimulated proliferation of human umbilical vein and aortic endothelial cells was found to be highly dependent on IQGAP1 23 . The non‐detection of TAGLN we observed (Figure 1(f)) from the MCF‐7 cells coincides with the findings of Dvorakova et al 24 . Prior studies stated that PIP2 and IQGAP1 are both expressed in MCF‐7 cells 25,26 .…”

Section: Resultssupporting

confidence: 88%

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Transgelin (TAGLN) Regulates IQGAP1 and Alters the Functions of Breast Cancer Cells

Raymundo

Xiu

et al. 2020

Bulletin Korean Chem Soc

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Several studies have been conducted on the transgelin (TAGLN) protein and its critical role in cancer biology. However, the regulation of this protein and the way in which this regulation is correlated with the functions of IQ motif-containing GTPase-activating protein 1 (IQGAP1) in MDA-MB231 cells, remain unclear. We generated stable TAGLN-knockdown and TAGLN-overexpressing cells. These cells, along with their control counterparts, were cultured in the presence or absence of 17-AAG. The different cell groups were then subjected to functional assays to assess proliferation, chemotaxis, and invasion. TAGLN regulation was found to affect the efficacy of 17-AAG. The ability of TAGLN to influence the levels of IQGAP1 and its binding partners altered the critical functions of breast cancer cells. Therefore, the altered functionality of MDA-MB-231 cells, as a consequence of TAGLN regulation, is correlated with IQGAP1 signaling.

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Section: Resultssupporting

confidence: 90%

Section: Resultssupporting

confidence: 88%

Transgelin (TAGLN) Regulates IQGAP1 and Alters the Functions of Breast Cancer Cells

Raymundo

Xiu

et al. 2020

Bulletin Korean Chem Soc

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“…These results are consistent with our data in vitro, which showed that TAGLN expression is higher in TNBC cells than in mammary duct cells; these ndings suggest that TAGLN is expressed differently in different types of BC, which may be related to its speci c context [31]. TAGLN expression in TNBC cells is also different, which may be related to its DNA methylation [32]. The growth curve data we generated indicate that compared to the control conditions, TAGLN overexpression promoted MDA-MB-468 cell growth, and TAGLN knockdown attenuated SUM159 and Hs578T cell growth.…”

Section: Discussionsupporting

confidence: 92%

TAGLN promotes triple-negative breast cancer growth by regulating the AKT/CDK2 pathway

Yang

Tang

et al. 2023

Preprint

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On a global scale, breast cancer (BC) is the most prevalent malignancy among women. Triple-negative breast cancer (TNBC) is a subtype with a poor prognosis and high recurrence, metastasis, and mortality rates. Numerous studies have shown that the TAGLN gene participates in tumorigenesis and tumor invasion. However, TAGLN function in TNBC remains unknown. In this study, we screened 201 TNBC differential genes, including 133 up-regulated and 68 down-regulated genes. Gene Set Enrichment Analysis (GSEA) results showed that these differential genes were mainly enriched in DNA metabolic, nucleic acid binding biological process and gene expression, Rho GTPase, RHOBTB3, and cell cycle signaling pathways. Western blot indicated that TAGLN expression is lower in breast tissue than in normal tissue. However, the GSE38959 database showed that TAGLN is highly expressed in TNBC cells compared with mammary duct cells, and the CancerSEA database indicated that TAGLN is positively correlated with EMT, invasion, angiogenesis, differentiation, apoptosis, metastasis, proliferation, and stemness. Functionally, TAGLN promoted TNBC cell proliferation, migration, invasion, and cell cycle progression in vitro and tumor cell growth in vivo. Further mechanistic studies demonstrated that TAGLN promoted TNBC cell growth by regulating the AKT/CDK2 pathway. In sum, TAGLN is highly expressed in TNBC and promotes cell proliferation, migration, and invasion in vitro and tumor cell growth in vivo.

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“…Recent studies revealed that TAGLN expression increases after UV irradiation [ 12 ]. TAGLN is an actin-binding protein that affects the dynamics of the actin cytoskeleton, regulating cell migration and movement [ 13 , 14 ]. However, few studies have investigated whether TAGLN can regulate UV-induced skin aging and whether a relationship exists between TAGLN and ZEB1.…”

Section: Introductionmentioning

confidence: 99%

Interaction of TAGLN and USP1 promotes ZEB1 ubiquitination degradation in UV-induced skin photoaging

Huang

Jin³

et al. 2023

Cell Biosci

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Background Ultraviolet A (UVA) irradiation can lead to skin damage and premature skin aging known as photoaging. This work found that UVA irradiation caused an imbalance between dermal matrix synthesis and degradation through the aberrant upregulation of transgelin (TAGLN) and studied the underlying molecular mechanism. Results Co-immunoprecipitation and proximal ligation assay results showed that TAGLN can interact with USP1. USP1 can be retained in the cytoplasm by TAGLN in UVA-induced cells, which inhibits the interaction between USP1/zinc finger E-box binding homeobox 1 (ZEB1), promote the ubiquitination degradation of ZEB1, and lead to photoaging. TAGLN knockdown can release USP1 retention and help human skin fibroblasts (HSFs) resist UVA-induced damage. The interactive interface inhibitors of TAGLN/USP1 were screened via virtual docking to search for small molecules that inhibit photoaging. Zerumbone (Zer), a natural product isolated from Zingiber zerumbet (L.) Smith, was screened out. Zer can competitively bind TAGLN to reduce the retention of USP1 in the cytoplasm and the degradation of ZEB1 ubiquitination in UV-induced HSFs. The poor solubility and permeability of Zer can be improved by preparing it as a nanoemulsion, which can effectively prevent skin photoaging caused by UVA in wild-type (WT) mice. Zer cannot effectively resist the photoaging caused by UVA in Tagln−/− mice because of target loss. Conclusions The present results showed that the interaction of TAGLN and USP1 can promote ZEB1 ubiquitination degradation in UV-induced skin photoaging, and Zer can be used as an interactive interface inhibitor of TAGLN/USP1 to prevent photoaging.

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Transgelin Silencing Induces Different Processes in Different Breast Cancer Cell Lines

Cited by 5 publications

References 44 publications

Transgelin (TAGLN) Regulates IQGAP1 and Alters the Functions of Breast Cancer Cells

Transgelin (TAGLN) Regulates IQGAP1 and Alters the Functions of Breast Cancer Cells

TAGLN promotes triple-negative breast cancer growth by regulating the AKT/CDK2 pathway

Interaction of TAGLN and USP1 promotes ZEB1 ubiquitination degradation in UV-induced skin photoaging

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