Altered gene expression profiles of NIH3T3 cells regulated by human lung cancer associated gene CT120

He, Xiang; Li, Jinjun; Xie, Yihu; Tang, Yingjie; Yao, Gen Fu; Qin, Wen; Wan, Da Fang; Gu, Jiafeng

doi:10.1038/sj.cr.7290252

Cited by 14 publications

(17 citation statements)

References 19 publications

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“…It has been reported that cathepsin B is required for reovirusmediated oncolysis, and transformed NIH3T3 cells are susceptible to the reovirus-mediated oncolysis, but normal NIH3T3 cells are not (Alain et al, 2007). Cathepsin B expression is significantly (more than 50 times) elevated by transformation of NIH3T3 cells (Chambers et al, 1992;He et al, 2004). These results suggest that cathepsin B activity in normal NIH3T3 cells is negative or much lower than that in transformed NIH3T3 cells, consistent with our result.…”

Section: Discussionsupporting

confidence: 91%

Cathepsin L is required for ecotropic murine leukemia virus infection in NIH3T3 cells

et al. 2009

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Recently it has been reported that a cathepsin B inhibitor, CA-074Me, attenuates ecotropic murine leukemia virus (Eco-MLV) infection in NIH3T3 cells, suggesting that cathepsin B is required for the Eco-MLV infection. However, cathepsin B activity was negative or extremely low in NIH3T3 cells. How did CA-074Me attenuate the Eco-MLV infection? The CA-074Me treatment of NIH3T3 cells inhibited cathepsin L activity, and a cathepsin L specific inhibitor, CLIK148, attenuated the Eco-MLV vector infection. These results indicate that the suppression of cathepsin L activity by CA-074Me induces the inhibition of Eco-MLV infection, suggesting that cathepsin L is required for the Eco-MLV infection in NIH3T3 cells. The CA-074Me treatment inhibited the Eco-MLV infection in human cells expressing the exogenous mouse ecotropic receptor and endogenous cathepsins B and L, but the CLIK148 treatment did not, showing that only the cathepsin L suppression by CLIK148 is not enough to prevent the Eco-MLV infection in cells expressing both of cathepsins B and L, and CA-074Me inhibits the Eco-MLV infection by suppressing both of cathepsins B and L. These results suggest that either cathepsin B or L is sufficient for the Eco-MLV infection.

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Section: Discussionsupporting

confidence: 91%

Cathepsin L is required for ecotropic murine leukemia virus infection in NIH3T3 cells

et al. 2009

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“…Fam57A (CT120), a membrane-associated gene important for amino acid transport (35), was found to be 2.6- and 2.5-fold downregulated in DDLS8817 and LPS141, respectively. CT120 has been implicated in lung carcinogenesis and its ectopic expression in NIH3T3 cells has been associated with Raf/MEK/Erk and PI3K/Akt signaling pathways driving cell proliferation, cell survival, and anti-apoptotic pathways (36). EIF3M, eukaryotic initiation factor 3 subunit M, is an essential gene for global cellular protein synthesis and polysome formation and appears to be associated with the bulk of cellular mRNAs (37).…”

Section: Discussionmentioning

confidence: 99%

ZIC1 Overexpression Is Oncogenic in Liposarcoma

et al. 2010

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Liposarcomas are aggressive mesenchymal cancers with poor outcomes that exhibit remarkable histologic diversity, with five recognized subtypes. Currently, the mainstay of therapy for liposarcoma is surgical excision since liposarcomas are often resistant to traditional chemotherapy. In light of the high mortality associated with liposarcoma and the lack of effective systemic therapy, we sought novel genomic alterations driving liposarcomagenesis that might serve as therapeutic targets. ZIC1, a critical transcription factor for neuronal development, is overexpressed in all five subtypes of liposarcoma compared with normal fat and in liposarcoma cell lines compared with adipose-derived stem cells (ASC). Here we show that ZIC1 contributes to the pathogenesis of liposarcoma. ZIC1 knockdown inhibits proliferation, reduces invasion, and induces apoptosis in dedifferentiated and myxoid/round cell liposarcoma cell lines, but not in either ASC or a lung cancer cell line with low ZIC1 expression. ZIC1 knockdown is associated with increased nuclear expression of p27 protein, and the down-regulation of pro-survival target genes: BCL2L13, JunD, Fam57A, and EIF3M. Our results demonstrate that ZIC1 expression is essential for liposarcomagenesis and that targeting ZIC1 or its downstream targets may lead to novel therapy for liposarcoma.

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“…It has also been shown that knocking down CT120 in SPC-A-1 cells results in reduced in vitro cell growth rate and in a decrease of tumorigenicity in nude mice 7 , 14 . In addition to these findings the study revealed that proliferation of the NIH3T3 and A549 cells is promoted by CT120 expression 7 , 12 .…”

Section: Discussionmentioning

confidence: 57%

“…On the other hand, it has also been shown that CT120A is expressed in various tumor cell lines and its expression is significantly higher in lung cancer than in control tissue or in normal lung tissue 7 . He et al 12 also reported that ectopic CT120 gene expression in the NIH3T3 cells activates two major signaling pathways which are involved in cell proliferation, survival and apoptosis. Silencing of CT120A results in reduced cell growth rates and tumorigenicity in nude mice and in tumor cell lines 13 , 14 .…”

Section: Introductionmentioning

confidence: 99%

CT120A Acts as an Oncogene in Head and Neck Squamous Cell Carcinoma

Baltaci¹,

Ekizoglu²,

Sarı³

et al. 2015

J. Cancer

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Squamous cell carcinoma of the head and neck (HNSCC) is among the most frequent cancers worldwide. The etiology and pathogenesis of HNSCC are influenced by multiple genetic factors in addition to environmental and lifestyle-related factors. However, the mechanism underlying the HNSCC is still far from clear.The membrane associated gene CT120 was previously identified from chromosome 17p13.3 as a lung cancer-associated gene. Its function as an activator of the Erk and Akt signaling pathways in human lung cancer cell lines suggested that CT120 has an oncogenic function. However, there is no data in the literature on the role of CT120 in any other cancer type. Therefore, the aim of this study was to determine the expression rate and probable function of CT120 in HNSCC.Tumor tissues from 50 patients were analyzed by real-time quantitative RT-PCR to investigate the expression rate and by direct sequencing to differentiate the CT120A and CT120B variants. CT120 overexpression was observed in 58% of tumors compared to non-cancerous tissue samples and this up-regulation was directly associated with the upregulation of the CT120A variant and with the stage of the disease (p=0.001).Our results indicate that the CT120 gene may function in the development of HNSCC.

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Altered gene expression profiles of NIH3T3 cells regulated by human lung cancer associated gene CT120

Cited by 14 publications

References 19 publications

Cathepsin L is required for ecotropic murine leukemia virus infection in NIH3T3 cells

Cathepsin L is required for ecotropic murine leukemia virus infection in NIH3T3 cells

ZIC1 Overexpression Is Oncogenic in Liposarcoma

CT120A Acts as an Oncogene in Head and Neck Squamous Cell Carcinoma

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