Overexpression of c-myc induces epithelial mesenchymal transition in mammary epithelial cells

Cho, Kyoung Bin; Cho, Min Kyong; Lee, Won Young; Kang, Keon Wook

doi:10.1016/j.canlet.2010.01.013

Cited by 112 publications

(87 citation statements)

References 38 publications

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“…NF-κB was reported to be involved in Snail generegulated EMT (19,20). Additionally, our lab previously demonstrated that the p65 subunit of NF-κB plays a role in MTDH-induced EMT (21).…”

Section: Low-dose Radiation-induced Emt Is Related To the Nf-κbmentioning

confidence: 87%

Low-dose radiation-induced epithelial-mesenchymal transition through NF-κB in cervical cancer cells

Shi

Wang

Yang

et al. 2013

International Journal of Oncology

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Abstract. Cervical cancer is the leading cause of death from cancer among women. Radiotherapy for cervical cancer is an effective treatment method; however, the response to radiotherapy varies among patients. Epithelial-mesenchymal transition (EMT) is a morphogenesis process involved in embryonic and organismal development. During tumour progression, EMT may enhance cancer cell invasion, promoting tumour metastasis. We hypothesised that EMT was involved in the enhanced invasiveness of cervical cancer cells after low-dose radiation and aimed to elucidate the underlying mechanism of this process in low-dose radiation of cervical cancer. The irradiated cells (FIR cells) were derived from the parental cells (N cells) with a cumulative dose of 75 Gy. After resting and reorganisation, the effect of low-dose radiation on the FIR cells was analysed. The expression of E-cadherin, N-cadherin and p65 was detected by real-time qPCR and western blotting in parental cancer cells and irradiated cancer cells. Motility was detected using the migration/invasion assay. After silencing of NF-κB p65 expression using siRNA against p65, the expression of E-cadherin and N-cadherin was examined by real-time qPCR and western blotting. We found that low-dose radiation induced morphological changes of cells. The expression of epithelial markers was downregulated and mesenchymal markers were induced in irradiated cells, both of which are characteristics of EMT. Additionally, in irradiated cells, migration and invasion were enhanced and the expression of p65 was increased. To investigate whether p65 was involved in EMT, we silenced the expression of p65 in irradiated cells using siRNA and found that the features of EMT were suppressed. In summary, p65-regulated EMT induced by low-dose irradiation of cervical cancer cell lines promoted the invasiveness and metastasis of cervical cancer cells. The reversal of EMT may be a new therapeutic target for improving the effectiveness of radiotherapy for cervical cancer.

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“…NF-κB was reported to be involved in Snail generegulated EMT (19,20). Additionally, our lab previously demonstrated that the p65 subunit of NF-κB plays a role in MTDH-induced EMT (21).…”

Section: Low-dose Radiation-induced Emt Is Related To the Nf-κbmentioning

confidence: 87%

Low-dose radiation-induced epithelial-mesenchymal transition through NF-κB in cervical cancer cells

Shi

Wang

Yang

et al. 2013

International Journal of Oncology

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“…This process could also be facilitated by the ability of MYC to promote cell "stemness" [28,232,233], which in turn leaves migrated cells in a better state to thrive in distal, foreign, tissues. Directly, MYC stimulates the expression of factors that enhance tumor invasion [234] and reduce cell adhesion [235], and regulates key micro-RNAs to promote the epithelial mesenchymal transition [236][237][238]. As the switch of polarized epithelial cells to the motile mesenchymal phenotype is recognized as a major contributor to tumor invasion and metastasis [239], the ability of MYC to tap into this process arguably contributes to the all-toofrequent poor prognoses of cancer patients with frank MYC overexpression [132].…”

Section: Influencing the Tumor Environmentmentioning

confidence: 99%

Mammalian MYC Proteins and Cancer

Tansey

2014

New Journal of Science

135

160

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The MYC family of proteins is a group of basic-helix-loop-helix-leucine zipper transcription factors that feature prominently in cancer. Overexpression of MYC is observed in the vast majority of human malignancies and promotes an extraordinary set of changes that impact cell proliferation, growth, metabolism, DNA replication, cell cycle progression, cell adhesion, differentiation, and metastasis. The purpose of this review is to introduce the reader to the mammalian family of MYC proteins, highlight important functional properties that endow them with their potent oncogenic potential, describe their mechanisms of action and of deregulation in cancer cells, and discuss efforts to target the unique properties of MYC, and of MYC-driven tumors, to treat cancer.

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“…If this mechanism is stimulated within the adult organism, it promotes pathological conditions or tumour metastasis (40). Members of the Snail family have been shown to induce EMT, and c-myc seems also to be involved in this process (35,41). Moreover, in transformed epithelial cells it has been found that EMT correlates with the presence of ß-catenin in the nucleus (42).…”

Section: Discussionmentioning

confidence: 99%

Apoptosis and cell growth arrest in A375 human melanoma cells by diorganotin(IV) and triorganotin(IV) complexes of [meso-Tetra(4-sulfonatophenyl)porphine] manganese(III)chloride

Costa

Zito

Emma³

et al. 2011

Int J Oncol

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Abstract.In previous studies we have demonstrated that two derivatives of meso-Tetra(4-sulfonatophenyl)porphine (TPPS), (Bu 2 Sn) 2 TPPS and (Bu 3 Sn) 4 TPPS, cause apoptotic death of A375 melanoma cells and, at lower concentrations, arrest of cell proliferation. In the present study, we examined if the manganese metal inside the porphyrin cavity could improve the efficacy of this class of compounds. Thus, [mesoTetra(4-sulfonatophenyl)porphine]Mn(III)Cl (=MnTPPS) derivatives, namely (Me 2 Sn) 2 MnTPPS, (Bu 2 Sn) 2 MnTPPS, (Me 3 Sn) 4 MnTPPS and (Bu 3 Sn) 4 MnTPPS, were tested on the A375 human melanoma cell line. A cytotoxicity assay showed that (Bu 2 Sn) 2 MnTPPS and (Bu 3 Sn) 4 MnTPPS were highly cytotoxic by inducing apoptosis in melanoma cells, as shown by DNA fragmentation analysis and by apoptotic nuclei fluorescence, and when used at lower concentrations, they affected only cellular proliferation. An arrest of cell proliferation was also observed with (Me 3 Sn) 4 MnTPPS, but at the highest concentrations used. Moreover, the lower concentration of (Bu 3 Sn) 4 MnTPPS induced a change in cell morphology, from a polygonal to an elongated and spindleshaped phenotype, likewise to its cognate (Bu 3 Sn) 4 TPPS, previously tested. Western blotting analysis showed indeed that both tributyltin compounds, i.e. (Bu 3 Sn) 4 MnTPPS and (Bu 3 Sn) 4 TPPS, lowered levels of the major proteins involved in tumorigenesis: ß-catenin, c-myc and snail. We also demonstrated that all compounds entered the cells and localized in the nuclei. In conclusion, our results show that, in spite of the Mn(III) metal introduction, the butyl derivatives always have a higher efficacy than methyl derivatives, and the tributyltin compounds in particular have an interesting effect in vitro on A375 cell proliferation.

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Overexpression of c-myc induces epithelial mesenchymal transition in mammary epithelial cells

Cited by 112 publications

References 38 publications

Low-dose radiation-induced epithelial-mesenchymal transition through NF-κB in cervical cancer cells

Low-dose radiation-induced epithelial-mesenchymal transition through NF-κB in cervical cancer cells

Mammalian MYC Proteins and Cancer

Apoptosis and cell growth arrest in A375 human melanoma cells by diorganotin(IV) and triorganotin(IV) complexes of [meso-Tetra(4-sulfonatophenyl)porphine] manganese(III)chloride

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