Novobiocin decreases SMYD3 expression and inhibits the migration of MDA‐MB‐231 human breast cancer cells

Luo, Xue‐Gang; Zou, Jianing; Wang, Shuzhen; Zhang, Tongcun; Xi, Tao

doi:10.1002/iub.288

Cited by 37 publications

(26 citation statements)

References 20 publications

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“…1 and Supplementary Table S4), were verteporfin (33), resveratrol (34), and novobiocin (35), all of which have already been shown to inhibit migration and/or the metastatic development of cancer cells (Table 1; refs. [33][34][35]. Upon drug treatment by any of these three drugs (Fig.…”

Section: Prediction Of Novel Drug Compounds For Metastatic Colorectalmentioning

confidence: 99%

Novel Drug Candidates for the Treatment of Metastatic Colorectal Cancer through Global Inverse Gene-Expression Profiling

et al. 2014

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Drug-induced gene-expression profiles that invert disease profiles have recently been illustrated to be a starting point for drug repositioning. In this study, we validate this approach and focus on prediction of novel drugs for colorectal cancer, for which there is a pressing need to find novel antimetastatic compounds. We computationally predicted three novel and still unknown compounds against colorectal cancer: citalopram (an antidepressant), troglitazone (an antidiabetic), and enilconazole (a fungicide). We verified the compounds by in vitro assays of clonogenic survival, proliferation, and migration and in a subcutaneous mouse model. We found evidence that the mode of action of these compounds may be through inhibition of TGFb signaling. Furthermore, one compound, citalopram, reduced tumor size as well as the number of circulating tumor cells and metastases in an orthotopic mouse model of colorectal cancer. This study proposes citalopram as a potential therapeutic option for patients with colorectal cancer, illustrating the potential of systems pharmacology. Cancer Res; 74(20); 5690-9. Ó2014 AACR.

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Section: Prediction Of Novel Drug Compounds For Metastatic Colorectalmentioning

confidence: 99%

Novel Drug Candidates for the Treatment of Metastatic Colorectal Cancer through Global Inverse Gene-Expression Profiling

et al. 2014

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“…The effect on the cell proliferation was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium (MTT; Sigma, St. Louis, MO, USA) assay was performed as described before (20). Absorbance was directly proportional to the number of survival cells.…”

Section: Microrna-135b Promotes Proliferation Invasion and Migrationmentioning

confidence: 99%

MicroRNA-135b promotes proliferation, invasion and migration of osteosarcoma cells by degrading myocardin

Shang

Cong

et al. 2014

International Journal of Oncology

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Abstract. functions as an oncogene in malignant tumors suggesting that it might be a target for malignant tumor therapy, but its role in osteosarcoma has not been investigated to date. In this study, we found that myocardin expression is specifically attenuated in MG63 osteosarcoma cells. Silencing miR-135b restores the expression of myocardin and miR-135b inhibits the expression of myocardin by targeting its 3'UTR in MG63 osteosarcoma cells. In additional experiments, we found that miR-135b was highly expressed in osteosarcoma tissues and it promoted MG63 cell proliferation, migration and invasion. Myocardin had the opposite effects of miR-135b, which suppressed proliferation, migration and invasion in MG63 cells. Thus, it is probably that miR-135b promotes proliferation, invasion and migration of osteosarcoma cells by degrading myocardin.

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“…Reverse-transcription PCR (RT-PCR) analysis was carried out as described previously (16). Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as an internal control to show equal loading of the cDNA samples.…”

Section: Reverse-transcription Polymerase Chain Reaction (Pcr) and Rementioning

confidence: 99%

Cooperation of myocardin and smad2 in inducing differentiation of mesenchymal stem cells into smooth muscle cells

et al. 2012

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SummarySeveral reports demonstrated that mesenchymal stem cells (MSCs) might differentiate into smooth muscle cells (SMCs) in vitro and in vivo. It has been shown that myocardin protein is a strong inducer of smooth muscle genes and MSCs can differentiate into SMCs in response to transforming growth factor-b (TGF-b). However, the relationship or link between myocardin and TGF-b3-induced MSC differentiation has not been fully elucidated. Here, we demonstrated that both myocardin and TGF-b3 were able to induce differentiation of rat bone marrow-derived MSCs toward smooth-muscle-like cell types, as evidenced by increasing expression of SMC-specific genes. Of note, myocardin cooperated with Smad2 to synergistically activate SM22a promoter and significantly enhance the expression of SM22a. Report assays with site-direct mutation analysis of SM22a promoter demonstrated that myocardin and Smad2 coactivated SM22a promoter mainly depending on CArG box and less on smad binding elements (SBE) sites as well. These findings reveal the cooperation of myocardin and Smad2 in process of MSC differentiation into SMCs.2012 IUBMB IUBMB Life, 64(4): [331][332][333][334][335][336][337][338][339] 2012

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Novobiocin decreases SMYD3 expression and inhibits the migration of MDA‐MB‐231 human breast cancer cells

Cited by 37 publications

References 20 publications

Novel Drug Candidates for the Treatment of Metastatic Colorectal Cancer through Global Inverse Gene-Expression Profiling

Novel Drug Candidates for the Treatment of Metastatic Colorectal Cancer through Global Inverse Gene-Expression Profiling

MicroRNA-135b promotes proliferation, invasion and migration of osteosarcoma cells by degrading myocardin

Cooperation of myocardin and smad2 in inducing differentiation of mesenchymal stem cells into smooth muscle cells

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