ArticleJournal of cancer research and clinical oncology2010
Mina53, a novel c-Myc target gene, is frequently expressed in lung cancers and exerts oncogenic property in NIH/3T3 cells.
Article in Journal of cancer research and clinical oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Predicting role of Myc-induced nuclear antigen 53 in determining the development and severity of systemic lupus erythematosus.Frontiers in immunology · 2024Article
- MYC-targeted genes predict distant recurrence in patients with ocular adnexal extranodal marginal zone lymphoma.Annals of hematology · 2023Article
- Substrate selectivity and inhibition of histidine JmjC hydroxylases MINA53 and NO66.RSC chemical biology · 2023Article
- MDIG, a 2‑oxoglutarate‑dependent oxygenase, acts as an oncogene and predicts the prognosis of multiple types of cancer.International journal of oncology · 2022Article
- The bioinformatics analysis of RIOX2 gene in lung adenocarcinoma and squamous cell carcinoma.PloS one · 2021Article
- Molecular Signatures ofCancers · 2020Article
- [Significance of expression of Myc-induced nuclear antigen 53 in hepatocellular carcinoma and its relationship with patient prognosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020Article
- The small members of the JMJD protein family: Enzymatic jewels or jinxes?Biochimica et biophysica acta. Reviews on cancer · 2019Review
- Effects of mdig on proliferation and apoptosis of lung cancer cells.Oncology letters · 2018Article
- The emerging roles of ribosomal histidyl hydroxylases in cell biology, physiology and disease.Cellular and molecular life sciences : CMLS · 2018Review
- MINA53 deficiency leads to glioblastoma cell apoptosis via inducing DNA replication stress and diminishing DNA damage response.Cell death & disease · 2018Article
- Dysfunction of IKZF1/MYC/MDIG axis contributes to liver cancer progression through regulating H3K9me3/p21 activity.Cell death & disease · 2017Article
- From biological mechanisms to clinical implications: the role of mineral dust-induced gene in lung cancers.Journal of thoracic disease · 2017Article
- MINA controls proliferation and tumorigenesis of glioblastoma by epigenetically regulating cyclins and CDKs via H3K9me3 demethylation.Oncogene · 2017Article
- SETDB2 and RIOX2 are differentially expressed among renal cell tumor subtypes, associating with prognosis and metastization.Epigenetics · 2017Article
- Mdig, a lung cancer-associated gene, regulates cell cycle progression through p27(KIP1).Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Current understanding of mdig/MINA in human cancers.Genes & cancer · 2015Review
- Gene signatures of drug resistance predict patient survival in colorectal cancer.The pharmacogenomics journal · 2015Article
- Potential effects of Mina53 on tumor growth in human pancreatic cancer.Cell biochemistry and biophysics · 2014Article
- Carcinogenic metalloid arsenic induces expression of mdig oncogene through JNK and STAT3 activation.Cancer letters · 2014Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMina53, whose expression is directly induced by c-Myc, is overexpressed in various cancers and plays an important role in cell growth. To clarify the involvement of Mina53 in lung cancers, we investigated its expression in human lung cancer tissues as well as in various lung cancer cell lines.
methodsMina53 expression was determined by real-time RT-PCR, western blotting, and immunohistochemistry using lung cancer cell lines, normal human bronchial epithelial cells, and lung cancer tissues. Biological effects of Mina53 were evaluated by soft agar colony formation assay and tumorigenicity in nude mice using Mina53-transfected NIH/3T3 cells. cDNA microarray analysis was performed to determine the gene alteration by Mina53 and confirmation was made using real-time RT-PCR with mina53 expression plasmid or mina53 shRNA-transfected NIH/3T3 cells.
resultsWe observed that 62% of patients evidenced overexpression of Mina53 from the early clinical stages of lung cancer. Differences according to gender, smoking status, or histologic type were not statistically significant. Forced expression of Mina53 in NIH/3T3 cells induced cell transformation, and mina53-transfected NIH/3T3 clones produced tumors in nude mice, demonstrating that Mina53 has oncogenic potential. cDNA microarray revealed that 254 genes had altered expression in a mina53-transfected NIH/3T3 clone. Mina53 regulates several genes related to cell adhesion and metabolism, which have also been reported to be regulated by c-Myc. Genes regulated by Mina53, but not by c-Myc included cytokine/growth factor related genes such as EGFR, IL-6, and HGF.
conclusionOur results suggest that Mina53 plays an important role in carcinogenesis and may be a target for cancer prevention.
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