Opposite regulation of MDM2 and MDMX expression in acquisition of mesenchymal phenotype in benign and cancer cells

Slabáková, Eva; Kharaishvili, Gvantsa; Smějová, Monika; Pernicová, Zuzana; Suchánková, Tereza; Remšík, Ján; Lerch, Stanislav; Straková, Nicol; Bouchal, Jan; Král, Milan; Čulig, Zoran; Kozubı́k, Alois; Souček, Karel

doi:10.18632/oncotarget.5392

Cited by 20 publications

(25 citation statements)

References 52 publications

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“…Strikingly, although each of those commonly used cell lines is of epithelial origin, they displayed variable surface expression of the tested epitopes ( Fig. 3A and 3B; pairs: MCF 10A LXSN vs. MCF 10A LXSN V12, BPH-1 vs. CAFTD03, and HMLE vs. HMLE-EMT; the EMT phenotypes of the pairs were described previously (13,27,28)]. S3A-C).…”

Section: Surface Fibroblast Markers Are Also Expressed By Breast and mentioning

confidence: 78%

“…BPH-1 cells (10) and the BPH-1-derived tumorigenic clone CAFTD03 (11) were obtained from Dr. S. W. Hayward, Vanderbilt University, TN, USA; MCF 10A cells (CRL-10317 TM ) were obtained from ATCC; MCF 10A LXSN and LXSN V12 cells (12) were obtained from Prof. B. H. Park, The Johns Hopkins University, MD, USA; cultivation of these cells was described previously (13). The HPrF (#4430) cell line was obtained from ScienCell and cultivated in Fibroblast Medium (FM, #2301, ScienCell, Carlsbad, CA).…”

Section: Cell Lines Cultivationmentioning

confidence: 99%

“…S3A-C). We used a model of EMT induction by TGF-b1 treatment in cell lines that were previously established and are regularly used in our laboratory (13,27,29). 3A and 3B; pairs: MCF 10A LXSN vs. MCF 10A LXSN V12, BPH-1 vs. CAFTD03, and HMLE vs. HMLE-EMT; the EMT phenotypes of the pairs were described previously (13,27,28)].…”

Section: Surface Fibroblast Markers Are Also Expressed By Breast and mentioning

confidence: 99%

“…The HPrF (#4430) cell line was obtained from ScienCell and cultivated in Fibroblast Medium (FM, #2301, ScienCell, Carlsbad, CA). BPH-1 cells (10) and the BPH-1-derived tumorigenic clone CAFTD03 (11) were obtained from Dr. S. W. Hayward, Vanderbilt University, TN, USA; MCF 10A cells (CRL-10317 TM ) were obtained from ATCC; MCF 10A LXSN and LXSN V12 cells (12) were obtained from Prof. B. H. Park, The Johns Hopkins University, MD, USA; cultivation of these cells was described previously (13). PC-3 (CRL-1435 TM ) and DU 145 cells (HTB-81 TM ) were obtained from ATCC and cultivated as described previously (14).…”

Section: Cell Lines Cultivationmentioning

confidence: 99%

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The fibroblast surface markers FAP, anti‐fibroblast, and FSP are expressed by cells of epithelial origin and may be altered during epithelial‐to‐mesenchymal transition

et al. 2017

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The identification of fibroblasts and cancer-associated fibroblasts from human cancer tissue using surface markers is difficult, especially because the markers used currently are usually not expressed solely by fibroblasts, and the identification of fibroblast-specific surface molecules is still under investigation. It was aimed to compare three commercially available antibodies in the detection of different surface epitopes of fibroblasts (anti-fibroblast, fibroblast activation protein α, and fibroblast surface protein). The specificity of their expression, employing fibroblast cell lines and tumor-derived fibroblasts from breast and prostate tissues was investigated. Both the established fibroblast cell line HFF-1 and ex vivo primary fibroblasts isolated from breast and prostate cancer tissues expressed the tested surface markers to different degrees. Surprisingly, those markers were expressed also by permanent cell lines of epithelial origin, both benign and cancer-derived (breast-cell lines MCF 10A, HMLE and prostate-cell lines BPH-1, DU 145, and PC-3). The expression of fibroblast activation protein α increased on the surface of previously described models of epithelial cells undergoing epithelial-to-mesenchymal transition in response to treatment with TGF-β1. To prove the co-expression of the fibroblast markers on cells of epithelial origin, we used freshly dissociated human prostate and breast cancer tissues. The results confirmed the co-expression of anti-fibroblast and fibroblast surface protein on CD31/CD45-negative/EpCAM-positive epithelial cells. In summary, our data support the findings that the tested fibroblast markers are not fibroblast specific and may be expressed also by cells of epithelial origin (e.g., cells undergoing EMT). Therefore, the expression of these markers should be interpreted with caution, and the combination of several epitopes for both positive (anti-fibroblast or fibroblast activation protein α) and negative (EpCAM) identification of fibroblasts from breast and prostate tumor tissues is advised. © 2017 International Society for Advancement of Cytometry.

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Section: Surface Fibroblast Markers Are Also Expressed By Breast and mentioning

confidence: 78%

Section: Cell Lines Cultivationmentioning

confidence: 99%

Section: Surface Fibroblast Markers Are Also Expressed By Breast and mentioning

confidence: 99%

Section: Cell Lines Cultivationmentioning

confidence: 99%

See 2 more Smart Citations

The fibroblast surface markers FAP, anti‐fibroblast, and FSP are expressed by cells of epithelial origin and may be altered during epithelial‐to‐mesenchymal transition

et al. 2017

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“…The staining of patients' samples was performed on a Discovery-XT staining device (Ventana, Tucson, AZ, USA). The histoscore (H-score) was used to semiquantitatively assess the staining considering percentage of positive cells (0-100%) multiplied by staining intensity (0-3), which results in a final H-score between 0 and 300 (Slabáková et al 2015). The nuclear NCOA1 and the cytoplasmic PRKD1 staining in luminal cells were considered for analysis.…”

Section: Immunohistochemistrymentioning

confidence: 99%

The AR/NCOA1 axis regulates prostate cancer migration by involvement of PRKD1

Luef

Handle

Kharaishvili

et al. 2016

Endocrine-Related Cancer

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Due to the urgent need for new prostate cancer (PCa) therapies, the role of androgen receptor (AR)-interacting proteins should be investigated. In this study we aimed to address whether the AR coactivator nuclear receptor coactivator 1 (NCOA1) is involved in PCa progression. Therefore, we tested the effect of long-term NCOA1 knockdown on processes relevant to metastasis formation. [ 3 H]-thymidine incorporation assays revealed a reduced proliferation rate in AR-positive MDA PCa 2b and LNCaP cells upon knockdown of NCOA1, whereas AR-negative PC3 cells were not affected. Furthermore, Boyden chamber assays showed a strong decrease in migration and invasion upon NCOA1 knockdown, independently of the cell line's AR status. In order to understand the mechanistic reasons for these changes, transcriptome analysis using cDNA microarrays was performed. Protein kinase D1 (PRKD1) was found to be prominently up-regulated by NCOA1 knockdown in MDA PCa 2b, but not in PC3 cells. Inhibition of PRKD1 reverted the reduced migratory potential caused by NCOA1 knockdown. Furthermore, PRKD1 was negatively regulated by AR. Immunohistochemical staining of PCa patient samples revealed a strong increase in NCOA1 expression in primary tumors compared with normal prostate tissue, while no final conclusion could be drawn for PRKD1 expression in tumor specimens. Thus, our findings directly associate the AR/NCOA1 complex with PRKD1 regulation and cellular migration and support the concept of therapeutic inhibition of NCOA1 in PCa.

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Extracellular vesicles as drivers of epithelial‐mesenchymal transition and carcinogenic characteristics in normal prostate cells

Souza

Silva

Campos-Fernández

et al. 2018

Molecular Carcinogenesis

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There is increasing evidence that cancer dissemination and metastasis establishment may not only be due to the movement of tumor cells. Content of extracellular vesicles (EVs) secreted by tumor cells may also reflect the origin of these cells. Some molecules that constitute these EVs have already been used as targets for detection of specific tumors. However, to the best of our knowledge, EVs from biopsies and plasma have not yet been compared nor thoroughly investigated as triggers of malignant transformation and metastatic niche formation. To evaluate the role of EVs in the cellular microenvironment, we have treated the normal epithelial prostate cell lines, RWPE-1 and PNT-2, with a pool of EVs from biopsies of prostate primary tumors (bEVs), biopsies of benign prostate hyperplasia (hEVs), plasma of prostate cancer (PCa) patients (pEVs) or plasma of healthy individuals (pnEVs). Each of the four pools consisted of isolated EVs from several subjects, of which PCa patients were in different stages of cancer. Migration and proliferation profiles, cytokine release, and a panel of PCa-associated genes' expression of epithelial-mesenchymal transition in the cell lines were evaluated after 24 h incubation with EVs. When compared to the control groups, cells treated with the pool of EVs isolated from tumor biopsies and plasma of PCa patients showed greater migration and proliferation, significant alterations in gene expression, and high levels of IL-8, factors that are associated with cancer development. Specifically, isolated bEVs and pEVs may induce malignant features in non-tumor cells by activating several cellular events associated with cancer progression, suggesting that future PCa therapy may target multiple elements found in tumor-derived EVs.

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Opposite regulation of MDM2 and MDMX expression in acquisition of mesenchymal phenotype in benign and cancer cells

Cited by 20 publications

References 52 publications

The fibroblast surface markers FAP, anti‐fibroblast, and FSP are expressed by cells of epithelial origin and may be altered during epithelial‐to‐mesenchymal transition

The fibroblast surface markers FAP, anti‐fibroblast, and FSP are expressed by cells of epithelial origin and may be altered during epithelial‐to‐mesenchymal transition

The AR/NCOA1 axis regulates prostate cancer migration by involvement of PRKD1

Extracellular vesicles as drivers of epithelial‐mesenchymal transition and carcinogenic characteristics in normal prostate cells

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