ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2015
Mdig, a lung cancer-associated gene, regulates cell cycle progression through p27(KIP1).
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 7 citations in OpenAlex.
- Possibility of inducing tumor cell senescence during therapy.Oncology letters · 2021Review
- MDIG promotes cisplatin resistance of lung adenocarcinoma by regulating ABC transporter expression via activation of the WNT/β-catenin signaling pathway.Oncology letters · 2019Article
- From biological mechanisms to clinical implications: the role of mineral dust-induced gene in lung cancers.Journal of thoracic disease · 2017Article
- Functional characterization of AMP-activated protein kinase signaling in tumorigenesis.Biochimica et biophysica acta · 2016Review
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4 authors at 1 institution in 1 country.
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Abstract
Mineral dust-induced gene (mdig) can accelerate cell proliferation. The aim of this study is to investigate the mechanism by which mdig regulates cell proliferation. A549 cells were transfected with siRNA specifically targeting mdig. Cell proliferation and cell cycle progression were measured using MTT assay and cell cycle analysis, respectively. Furthermore, real-time reverse transcription quantitative-polymerase chain reaction (RT-qPCR) was performed in A549 cells transfected with mdig siRNA to examine the expression levels of the cell cycle related genes such as p18(INK4c), p19(INK4d), p21(WAF/CIP1), p27(KIP1), p57(KIP2), cyclin D1, and cyclin E. To further explore the effect of mdig on p27(KIP1), the expression levels of total p27(KIP1) and its subtypes pT187-p27(KIP1) and pS10-p27(KIP1) were assessed by Western blotting. In vivo, Western blotting was performed to check the expression levels of mdig and p27(KIP1) in human lung cancer tissues, para-cancerous normal lung tissues, and para-bronchial stumps. Knockdown of mdig induced increases in p27(KIP1), both on mRNA and protein levels. Furthermore, the phosphorylation of p27(KIP1) at its Thr187 site was also inhibited. Importantly, in lung cancer tissues, upregulation of mdig expression accompanies with the downregulation of p27(KIP1) expression and in bronchial stump, vice versa. The data suggest that mdig-mediated inhibition of p27(KIP1) is important for cell proliferation and tumor formation and reveal therapeutic potential of p27(KIP1) for lung cancer.
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