Proteomic analysis of a neoplastic mouse lung epithelial cell line whose tumorigenicity has been abrogated by transfection with the gap junction structural gene for connexin 43, Gja1

Peebles, Katherine A.

doi:10.1093/carcin/bgg008

Cited by 34 publications

(26 citation statements)

References 43 publications

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“…An increase in TPI expression was observed in a spontaneous transformant of an immortalized but non-tumorigenic cell line derived from alveolar type II pneumocytes as well as in lung tumor tissues versus normal lung tissues from a chemical carcinogenesis mouse model (Peebles et al, 2003;Kassie et al, 2008). TPI was identified by comparative proteomic analysis as being significantly overexpressed in lung cancer tissues compared with adjacent normal lung tissues (Chen et al, 2002;Kuramitsu and Nakamura, 2006).…”

Section: Discussionmentioning

confidence: 99%

Identification of potential lung cancer biomarkers using an in vitro carcinogenesis model

et al. 2008

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Lung cancer is one of the deadliest and commonly diagnosed neoplasms. Early diagnosis of this disease is critical for improving clinical outcome and prognosis. Because the early stages of lung cancer often produce no symptoms, it is necessary to identify biomarkers for early detection, prognostic evaluation, and recurrence monitoring of the cancer. To identify potential lung cancer biomarkers, we analyzed the differential protein secretion from transformed bronchial epithelial cells (1198 and 1170-I) as compared to immortalized normal bronchial epithelial cells (BEAS-2B) and non-transformed cells (1799) all of which are derived from BEAS-2B and represent multistage bronchial epithelial carcinogenesis. The proteins recovered from the conditioned media of the cells were separated on two-dimensional gels. There was little difference between the secretome of the BEAS-2B and 1799 cells, whereas the patterns between the transformed 1198 and 1170-I cells and non-transformed 1799 cells were significantly different. Using mass spectrometry and database search, we identified 20 proteins including protein gene product 9.5 (PGP9.5), translationally controlled tumor protein (TCTP), tissue inhibitors of metalloproteinases-2 (TIMP-2), and triosephosphate isomerase (TPI), that were either increased or decreased simultaneously in conditioned media of both 1198 and 1170-I cells. Furthermore, levels of PGP9.5, TCTP, TIMP-2, and TPI were significantly increased not only in the conditioned media of both transformed cell lines when compared to those of BEAS-2B and 1799 cells, but also in plasmas and tissues from lung cancer patients when compared to those in normal controls. We suggest the PGP9.5, TCTP, TIMP-2, and TPI as promising candidates for lung cancer serum biomarkers.

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Section: Discussionmentioning

confidence: 99%

Identification of potential lung cancer biomarkers using an in vitro carcinogenesis model

et al. 2008

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“…Previously, several lines of evidence suggested that ENO1 may contribute to tumor malignancy (180). Upregulation of the ENO1 gene has been observed in several highly tumorigenic or metastatic cell lines (181,182) and its enzymatic activity in breast cancer suggests a role of ENO1 in tumor progression. Increased expression of enolase α in human breast cancer confers tamoxifen resistance in humans.…”

Section: +mentioning

confidence: 99%

Mechanisms associated with resistance to tamoxifen in estrogen receptor-positive breast cancer (Review)

et al. 2014

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Abstract. Anti-estrogens such as tamoxifen are widely used in the clinic to treat estrogen receptor-positive breast tumors. Patients with estrogen receptor-positive breast cancer initially respond to treatment with anti-hormonal agents such as tamoxifen, but remissions are often followed by the acquisition of resistance and, ultimately, disease relapse. The development of a rationale for the effective treatment of tamoxifen-resistant breast cancer requires an understanding of the complex signal transduction mechanisms. In the present study, we explored some mechanisms associated with resistance to tamoxifen, such as pharmacologic mechanisms, loss or modification in estrogen receptor expression, alterations in co-regulatory proteins and the regulation of the different signaling pathways that participate in different cellular processes such as survival, proliferation, stress, cell cycle, inhibition of apoptosis regulated by the Bcl-2 family, autophagy, altered expression of microRNA, and signaling pathways that regulate the epithelial-mesenchymal transition in the tumor microenvironment. Delineation of the molecular mechanisms underlying the development of resistance may aid in the development of treatment strategies to enhance response and compromise resistance.

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“…Up-regulation of ENO1 has been reported in several highly tumorigenic or metastatic cell lines derived from either alveolar type II pneumocytes (16), small cell lung cancer (SCLC; ref. 17), or head and neck cancer (18).…”

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confidence: 99%

Identification of α-Enolase as an Autoantigen in Lung Cancer: Its Overexpression Is Associated with Clinical Outcomes

Chang

Liu

Hsieh

et al. 2006

Clinical Cancer Research

142

143

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Purpose: Although existence of humoral immunity has been previously shown in malignant pleural effusions, only a limited number of immunogenic tumor-associated antigens (TAA) have been identified and associated with lung cancer. In this study, we intended to identify moreTAAs in pleural effusion^derived tumor cells. Experimental Design: Using morphologically normal lung tissues as a control lysate inWestern blotting analyses, 54 tumor samples were screened with autologous effusion antibodies. Biochemical purification and mass spectrometric identification of TAAs were done using established effusion tumor cell lines as antigen sources. We identified a p48 antigen as a-enolase (ENO1). Semiquantitative immunohistochemistry was used to evaluate expression status of ENO1 in the tissue samples of 80 patients with non^small cell lung cancer (NSCLC) and then correlated with clinical variables. Results: Using ENO1-specifc antiserum, up-regulation of ENO1expression in effusion tumor cells from 11of 17 patients was clearly observed compared with human normal lung primary epithelial and non-cancer-associated effusion cells. Immunohistochemical studies consistently showed high level of ENO1 expression in all the tumors we have examined thus far. Log-rank and Cox's analyses of ENO1 expression status revealed that its expression level in primary tumors was a key factor contributing to overall-and progression-free survivals of patients (P < 0.05). The same result was also obtained in the early stage of NSCLC patients, showing that tumors expressing relatively higher ENO1level were tightly correlated with poorer survival outcomes. Conclusions: Our data strongly support a prognostic role of ENO1in determining tumor malignancy of patients with NSCLC.

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Proteomic analysis of a neoplastic mouse lung epithelial cell line whose tumorigenicity has been abrogated by transfection with the gap junction structural gene for connexin 43, Gja1

Cited by 34 publications

References 43 publications

Identification of potential lung cancer biomarkers using an in vitro carcinogenesis model

Identification of potential lung cancer biomarkers using an in vitro carcinogenesis model

Mechanisms associated with resistance to tamoxifen in estrogen receptor-positive breast cancer (Review)

Identification of α-Enolase as an Autoantigen in Lung Cancer: Its Overexpression Is Associated with Clinical Outcomes

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