• Title/Summary/Keyword: TMEM39A

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Recognition of Transmembrane Protein 39A as a Tumor-Specific Marker in Brain Tumor

  • Park, Jisoo;Lee, Hyunji;Tran, Quangdon;Mun, Kisun;Kim, Dohoon;Hong, Youngeun;Kwon, So Hee;Brazil, Derek;Park, Jongsun;Kim, Seon-Hwan
    • Toxicological Research
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    • v.33 no.1
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    • pp.63-69
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    • 2017
  • Transmembrane protein 39A (TMEM39A) belongs to the TMEM39 family. TMEM39A gene is a susceptibility locus for multiple sclerosis. In addition, TMEM39A seems to be implicated in systemic lupus erythematosus. However, any possible involvement of TMEM39A in cancer remains largely unknown. In the present report, we provide evidence that TMEM39A may play a role in brain tumors. Western blotting using an anti-TMEM39A antibody indicated that TMEM39A was overexpressed in glioblastoma cell lines, including U87-MG and U251-MG. Deep-sequencing transcriptomic profiling of U87-MG and U251-MG cells revealed that TMEM39A transcripts were upregulated in such cells compared with those of the cerebral cortex. Confocal microscopic analysis of U251-MG cells stained with anti-TMEM39A antibody showed that TMEM39A was located in dot-like structures lying close to the nucleus. TMEM39A probably located to mitochondria or to endosomes. Immunohistochemical analysis of glioma tissue specimens indicated that TMEM39A was markedly upregulated in such samples. Bioinformatic analysis of the Rembrandt knowledge base also supported upregulation of TMEM39A mRNA levels in glioma patients. Together, the results afford strong evidence that TMEM39A is upregulated in glioma cell lines and glioma tissue specimens. Therefore, TMEM39A may serve as a novel diagnostic marker of, and a therapeutic target for, gliomas and other cancers.

TMEM39A and Human Diseases: A Brief Review

  • Tran, Quangdon;Park, Jisoo;Lee, Hyunji;Hong, Youngeun;Hong, Suntaek;Park, Sungjin;Park, Jongsun;Kim, Seon-Hwan
    • Toxicological Research
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    • v.33 no.3
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    • pp.205-209
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    • 2017
  • Transmembrane Protein 39A (TMEM39A) is a member of TMEM family. The understanding about this protein is still limited. The earlier studies indicated that TMEM39A was a key mediator of autoimmune disease. TMEM39A seems to be involved in systemic lupus erythematosus and multiple sclerosis in numerous of populations. All of these works stop at insufficient information by using gene functioning methods such as: Genome-wide association studies (GWASs) and/or follow-up study. It is the fact that the less understood of TMEM39A actually is the attraction to the scientist in near future. In this review the current knowledge about TMEM39A and its possible roles in cell biology, physiology and pathology will be described.

Tazarotene-Induced Gene 1 Enhanced Cervical Cell Autophagy through Transmembrane Protein 192

  • Shyu, Rong-Yaun;Wang, Chun-Hua;Wu, Chang-Chieh;Chen, Mao-Liang;Lee, Ming-Cheng;Wang, Lu-Kai;Jiang, Shun-Yuan;Tsai, Fu-Ming
    • Molecules and Cells
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    • v.39 no.12
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    • pp.877-887
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    • 2016
  • Tazarotene-induced gene 1 (TIG1) is a retinoic acid-inducible protein that is considered a putative tumor suppressor. The expression of TIG1 is decreased in malignant prostate carcinoma or poorly differentiated colorectal adenocarcinoma, but TIG1 is present in benign or well-differentiated tumors. Ectopic TIG1 expression led to suppression of growth in cancer cells. However, the function of TIG1 in cell differentiation is still unknown. Using a yeast two-hybrid system, we found that transmembrane protein 192 (TMEM192) interacted with TIG1. We also found that both TIG1A and TIG1B isoforms interacted and co-localized with TMEM192 in HtTA cervical cancer cells. The expression of TIG1 induced the expression of autophagy-related proteins, including Beclin-1 and LC-3B. The silencing of TMEM192 reduced the TIG1-mediated upregulation of autophagic activity. Furthermore, silencing of either TIG1 or TMEM192 led to alleviation of the upregulation of autophagy induced by all-trans retinoic acid. Our results demonstrate that the expression of TIG1 leads to cell autophagy through TMEM192. Our study also suggests that TIG1 and TMEM192 play an important role in the all-trans retinoic acid-mediated upregulation of autophagic activity.