Expression of Mina53, a novel c-Myc target gene, is a favorable prognostic marker in early stage lung cancer

Komiya, Kazutoshi; Sueoka‐Aragane, Naoko; Sato, Akemi; Hisatomi, Takashi; Sakuragi, Tohru; Mitsuoka, Masahiro; Sato, Tachio; Hayashi, Shinichiro; Izumi, Hiroto; Tsuneoka, Makoto; Sueoka, Eisaburo

doi:10.1016/j.lungcan.2009.10.010

Cited by 31 publications

(20 citation statements)

References 21 publications

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“…The present study also used HUVEC cells to verify the above molecular mechanisms, and the same conclusions were obtained. Collectively, our results elucidated the molecular mechanism underlying the inhibitory effects of mdig on the invasion and metastasis of NSCLC by demonstrating a strong correlation between the expression levels of mdig and the examined proteins in tumor cells and normal cells, as observed previously (6,9), and supported the clinical findings that mdig-positive NSCLC is associated with a better prognosis than the mdig-negative form in patients at the advanced stage because of mdig inhibiting invasion and metastasis of NSCLC (22). The present study focused on the regulation of tumor cell biological behavior by mdig, and advanced our understanding of the underlying regulatory mechanism regarding downstream target genes.…”

Section: Discussionsupporting

confidence: 87%

Mdig suppresses epithelial-mesenchymal transition and inhibits the invasion and metastasis of non-small cell lung cancer via regulating GSK-3β/β-catenin signaling

Geng

Jiang

Song

et al. 2017

International Journal of Oncology

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Mineral dust-induced gene (mdig) can inhibit the invasion and metastasis of A549 cells. The main purpose of this study was to explore the molecular mechanism underlying the inhibitory effect of mdig on cell invasion and metastasis. Mdig-knockdown and mdig-overexpressing A549 cells and an mdig-overexpressing human umbilical vein endothelial cell (HUVEC) line were constructed using lentiviral vectors, and western blot analysis was performed to verify the silencing and overexpression of the mdig protein. A Transwell invasion assay was used to detect the invasive abilities of each experimental group, and Transwell migration and scratch assays were used to detect cell migration ability. Western blotting was subsequently conducted to detect the major biochemical indices of the GSK-3β/β-catenin pathway and the protein expression levels and modifications of epithelial‑mesenchymal transition (EMT) transcription factors, as well as changes in the expression levels of EMT molecular markers and intercellular adhesion proteins. The results indicated that overexpression of mdig in A549 cells inhibited cell invasion and metastasis, while silencing of mdig increased the invasive and metastatic properties of cells. The molecular mechanism underlying the effects of mdig downregulation on A549 cell invasion and metastasis was found to involve the inhibition of GSK-3β phosphorylation, which in turn promoted the phosphorylation and destabilization of β-catenin. This was associated with downregulation of the downstream transcription factors slug, snail and ZEB1, thus leading to increased expression levels of epithelial cell markers and upregulation of the intercellular adhesion molecules E-cadherin, claudin‑1, ZO‑1, integrin β1 and integrin β4, which was accompanied by downregulation of the mesenchymal cell markers vimentin and N-cadherin. The HUVECs were used to validate the aforementioned molecular mechanisms and the same conclusions were obtained. The present results indicate that mdig can inhibit the phosphorylation of GSK-3β and promote the phosphorylation and destabilization of β-catenin, in order to suppress the expression of slug, snail, and ZEB1 and the occurrence of EMT, and thereby inhibit the invasion and metastasis of non-small cell lung cancer (NSCLC).

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Section: Discussionsupporting

confidence: 87%

Mdig suppresses epithelial-mesenchymal transition and inhibits the invasion and metastasis of non-small cell lung cancer via regulating GSK-3β/β-catenin signaling

Geng

Jiang

Song

et al. 2017

International Journal of Oncology

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“…Overexpression of the c-myc gene has been found to be associated to the carcinogenesis, development and bad prognosis in a variety of tumors (He et al, 1995;Komiya et al, 2010;Joensuu et al, 2011). Moreover, previous reports have shown c-myc gene was amplification and overexpression in esophageal cancer cell lines (Jones et al, 1993;Kanda et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Luteolin Induced-growth Inhibition and Apoptosis of Human Esophageal Squamous Carcinoma Cell Line Eca109 Cells in vitro

Wang¹,

Wang²,

Huang³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Luteolin is a plant flavonoid which exhibits anti-oxidative, anti-inflammatory and anti-tumor effects. However, the antiproliferative potential of luteolin is not fully understood. In this study, we investigated the effect of luteolin on cell cycling and apoptosis in human esophageal squamous carcinoma cell line Eca109 cells. MTT assays showed that luteolin had obvious cytotoxicity on Eca109 with an IC 50 of 70.7±1.72μM at 24h. Luteolin arrested cell cycle progression in the G0/G1 phase and prevented entry into S phase in a dose-and time-dependent manner. as assessed by FCM. Luteolin induced apoptosis of Eca109 cells was demonstrated by AO/EB staining assay and annexin V-FITC/PI staining. Moreover, luteolin downregulated the expression of cyclin D1, survivin and c-myc, and it also upregulated the expression of p53, in line with the fact that luteolin was able to inhibit Eca109 cell proliferation.

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“…There are reports that upregulation of MINA in lung cancer cells promoted cell proliferation, 11 and downregulation of MINA in cells of esophageal carcinoma, 14 cervical carcinoma, 5 colon cancer 13 or pancreatic cancer 8 inhibited cell proliferation. However, the molecular mechanisms of how MINA contributed to cell proliferation remain to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

MINA controls proliferation and tumorigenesis of glioblastoma by epigenetically regulating cyclins and CDKs via H3K9me3 demethylation

Huang

Xuan

et al. 2016

Oncogene

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It is generally known that histone demethylases regulate gene transcription by altering the methylate status on histones, but their roles in cancers and the underlying molecular mechanisms still remain unclear. MYC-induced nuclear antigen (MINA) is reported to be a histone demethylase and highly expressed in many cancers. Here, for the first time, we show that MINA is involved in glioblastoma carcinogenesis and reveal the probable mechanisms of it in cell-cycle control. Kaplan-Meier analysis of progression-free survival showed that high MINA expression was strongly correlated with poor outcome and advancing tumor stage. MINA knockdown significantly repressed the cell proliferation and tumorigenesis abilities of glioblastoma cells in vitro and in vivo that were rescued by overexpressing the full-length MINA afterwards. Microarray analysis after knockdown of MINA revealed that MINA probably regulated glioblastoma carcinogenesis through the predominant cell-cycle pathways. Further investigation showed that MINA deficiency led to a cell-cycle arrest in G1 and G2 phases. And among the downstream genes, we found that cyclins and cyclin-dependent kinases were directly activated by MINA via the demethylation of H3K9me3.

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Expression of Mina53, a novel c-Myc target gene, is a favorable prognostic marker in early stage lung cancer

Cited by 31 publications

References 21 publications

Mdig suppresses epithelial-mesenchymal transition and inhibits the invasion and metastasis of non-small cell lung cancer via regulating GSK-3β/β-catenin signaling

Mdig suppresses epithelial-mesenchymal transition and inhibits the invasion and metastasis of non-small cell lung cancer via regulating GSK-3β/β-catenin signaling

Luteolin Induced-growth Inhibition and Apoptosis of Human Esophageal Squamous Carcinoma Cell Line Eca109 Cells in vitro

MINA controls proliferation and tumorigenesis of glioblastoma by epigenetically regulating cyclins and CDKs via H3K9me3 demethylation

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