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|Entity|| Lung cancer|
|Prognosis|| CT120A protein was a potential molecular target for treatment of lung cancers. CT120A was overexpressed in 15 cases of the 16 primary lung cancer specimens. Knockdown of CT120A by small hairpin RNA in the human lung adenocarcinoma cell line SPC-A-1 cells resulted in a reduced cell growth rate in vitro and decrease of the capacity for anchorage-independent growth and tumorigenicity in nude mice. |
The suppression of CT120A expression also sensitized cells to ultraviolet-induced apoptosis. Atlas cDNA expression array revealed that the expressions of several apoptosis- and growth-associated genes were altered underlying the molecular mechanisms of these cell biological behaviors.
|Oncogenesis|| CT120 ectopic expression could promote cell proliferation activity of NIH3T3 cells, and two major signaling pathways involved in cell proliferation, cell survival and anti-apoptosis were overexpressed and activated in response to CT120: one is the Raf/MEK/Erk signal cascades and the other is the PI3K/Akt signal cascades, suggesting that CT120 might contribute, at least in part, to the constitutively activation of Erk and Akt in human lung cancer cells. |
In addition, some tumor metastasis associated genes cathepsin B, cathepsin D, cathepsin L, MMP-2/TIMP-2 were also upregulated by CT120, upon which CT120 might be involved in tumor invasiveness and metastasis.
In addition, CT120 might play an important role in tumor progression through modulating the expression of some candidate "lung tumor progression" genes including B-Raf, Rab-2, BAX, BAG-1, YB-1 and Cdc42.
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| Molecular cloning and characterization of CT120, a novel membrane-associated gene involved in amino acid transport and glutathione metabolism.|
| He X, Di Y, Li J, Xie Y, Tang Y, Zhang F, Wei L, Zhang Y, Qin W, Huo K, Li Y, Wan D, Gu J.|
| Biochem Biophys Res Commun. 2002 Sep 27;297(3):528-36.|
| Altered gene expression profiles of NIH3T3 cells regulated by human lung cancer associated gene CT120.|
| He XH, Li JJ, Xie YH, Tang YT, Yao GF, Qin WX, Wan DF, Gu JR.|
| Cell Res. 2004 Dec;14(6):487-96.|
| Silencing of CT120 by antisense oligonucleotides could inhibit the lung cancer cells growth.|
| Li Z, Shao S, Xie S, Jiao F, Ma Y, Shi S.|
| Ir J Med Sci. 2010 Jun;179(2):217-23. Epub 2009 Dec 20.|
| Down-regulation of CT120A by RNA interference suppresses lung cancer cells growth and sensitizes to ultraviolet-induced apoptosis.|
| Pan D, Wei L, Yao M, Wan D, Gu J.|
| Cancer Lett. 2006 Apr 8;235(1):26-33. Epub 2005 May 31.|
| Inhibitory effect of CT120B, an alternative splice variant of CT120A, on lung cancer cell growth.|
| Pan DN, Li JJ, Wei L, Yao M, Wan DF, Gu JR.|
| Acta Biochim Biophys Sin (Shanghai). 2005 Sep;37(9):588-92.|