Malignant T-cell-amplified sequence 1

Definition:

Anti-oncogene that plays a role in cell cycle regulation; decreases cell doubling time and anchorage-dependent growth; shortens the duration of G1 transit time and G1/S transition. When constitutively expressed, increases CDK4 and CDK6 kinases activity and CCND1/cyclin D1 protein level, as well as G1 cyclin/CDK complex formation. Involved in translation initiation; promotes recruitment of aminoacetyled initiator tRNA to P site of 40S ribosomes. Can promote release of deacylated tRNA and mRNA from recycled 40S subunits following ABCE1-mediated dissociation of post-termination ribosomal complexes into subunits. Plays a role as translation enhancer; recruits the density-regulated protein/DENR and binds to the cap complex of the 5'-terminus of mRNAs, subsequently altering the mRNA translation profile; up-regulates protein levels of BCL2L2, TFDP1, MRE11, CCND1 and E2F1, while mRNA levels remains constant. Hyperactivates DNA damage signaling pathway; increased gamma-irradiation-induced phosphorylation of histone H2AX, and induces damage foci formation. Increases the overall number of chromosomal abnormalities such as larger chromosomes formation and multiple chromosomal fusions when overexpressed in gamma-irradiated cells. May play a role in promoting lymphoid tumor development: lymphoid cell lines overexpressing MCTS1 exhibit increased growth rates and display increased protection against apoptosis. May contribute to the pathogenesis and progression of breast cancer via promotion of angiogenesis through the decline of inhibitory THBS1/thrombospondin-1, and inhibition of apoptosis. Involved in the process of proteasome degradation to down-regulate Tumor suppressor p53/TP53 in breast cancer cell; Positively regulates phosphorylation of MAPK1 and MAPK3. Involved in translation initiation; promotes aminoacetyled initiator tRNA to P site of 40S ribosomes. Can promote release of deacylated tRNA and mRNA from recycled 40S subunits following ABCE1-mediated dissociation of post-termination ribosomal complexes into subunits.

References:

[1]. M Prosniak, et al. A novel candidate oncogene, MCT-1, is involved in cell cycle progression. Cancer Res. 1998 Oct 1;58(19):4233-7. [Content Brief]

[2]. Bo Shi, et al. Expression of the candidate MCT-1 oncogene in B- and T-cell lymphoid malignancies. Blood. 2003 Jul 1;102(1):297-302. [Content Brief]

[3]. G B Herbert, et al. Expression and stabilization of the MCT-1 protein by DNA damaging agents. Oncogene. 2001 Oct 11;20(46):6777-83. [Content Brief]

[4]. J Dierov, et al. Increased G1 cyclin/cdk activity in cells overexpressing the candidate oncogene, MCT-1. J Cell Biochem. 1999 Sep 15;74(4):544-50. [Content Brief]

[5]. S Nandi, et al. Phosphorylation of MCT-1 by p44/42 MAPK is required for its stabilization in response to DNA damage. Oncogene. 2007 Apr 5;26(16):2283-9. [Content Brief]

[6]. Line S Reinert, et al. MCT-1 protein interacts with the cap complex and modulates messenger RNA translational profiles. Cancer Res. 2006 Sep 15;66(18):8994-9001. [Content Brief]

[7]. Maxim A Skabkin, et al. Activities of Ligatin and MCT-1/DENR in eukaryotic translation initiation and ribosomal recycling. Genes Dev. 2010 Aug 15;24(16):1787-801. [Content Brief]

[8]. Hsin-Ling Hsu, et al. The MCT-1 oncogene product impairs cell cycle checkpoint control and transforms human mammary epithelial cells. Oncogene. 2005 Jul 21;24(31):4956-64. [Content Brief]

[9]. Hsin-Ling Hsu, et al. MCT-1 oncogene downregulates p53 and destabilizes genome structure in the response to DNA double-strand damage. DNA Repair (Amst). 2007 Sep 1;6(9):1319-32. [Content Brief]

[10]. Anait S Levenson, et al. MCT-1 oncogene contributes to increased in vivo tumorigenicity of MCF7 cells by promotion of angiogenesis and inhibition of apoptosis. Cancer Res. 2005 Dec 1;65(23):10651-6. [Content Brief]

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