Differential expression of cell adhesion molecules in an ionizing radiation-induced breast cancer model system

Calaf, Gloria M.; Roy, Debasish; Narayan, Gopeshwar; Balajee, Adayabalam S.

doi:10.3892/or.2013.2448

Cited by 9 publications

(13 citation statements)

References 26 publications

(62 reference statements)

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“…[39,40]. In this context, we hypothesized that radiation modulates SP-B expression and that this change is involved in tumor progression in response to radiation.…”

Section: Radiation Exposure Decreases Sp-b Mrna and Protein Levelsmentioning

confidence: 99%

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

Lee

Kim

Kang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Radiotherapy is applied to patients with inoperable cancer types including advanced stage non-small cell lung cancer (NSCLC) and radioresistance functions as a critical obstacle in radiotherapy. This study was aimed to investigate the mechanism of radioresistance regulated by surfactant protein B (SP-B). Methods: To investigate the role of SP-B in radioresistance, ΔSFTPB A549 cell line was established and SP-B expression was analyzed. In response to ionizing radiation (IR), the change of SP-B expression was analyzed in A549 and NCI-H441 cell lines. Conditioned media (CM) from NSCLC cells were utilized to evaluate the downstream signaling pathway. The in vivo effects of SP-B were assessed through mouse xenograft model with intratumoral injection of CM. Results: In response to IR, NSCLC cell lines showed decreased SP-B regulated by the TGF-β signaling and decreased SP-B stimulated cell survival and epithelial-mesenchymal transition. Treatment with CM from irradiated cells activated sPLA 2 , enhanced protein kinase Cδ-MAPKs signaling pathway, and increased arachidonic acid production. We confirmed the in vivo roles of SP-B through mouse xenograft model. Conclusion: Our results revealed that down-regulation of SP-B was involved in the radiation-induced metastatic conversion of NSCLC and provided evidence that SP-B acted as a suppressor of NSCLC progression.S. Lee and D. Kim contributed equally to this work.

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“…[39,40]. In this context, we hypothesized that radiation modulates SP-B expression and that this change is involved in tumor progression in response to radiation.…”

Section: Radiation Exposure Decreases Sp-b Mrna and Protein Levelsmentioning

confidence: 99%

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

Lee

Kim

Kang

et al. 2017

Cell Physiol Biochem

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“…E-cadherin, as a marker of epithelial cells, can mediate the adhesion between cells. A decline in E-cadherin expression would cause cells to lose its polarity, decrease cell junction stability, and contribute to the invasion and metastasis of tumor cells[36,37]. Previous studies have confirmed that E-cadherin is a cancer metastasis inhibitory molecule, and that decreased expression of E-cadherin may be used as a molecular marker to evaluate the malignant degree of gastric cancer[8,36].…”

Section: Discussionmentioning

confidence: 99%

Clinical significance of expression of proliferating cell nuclear antigen and E-cadherin in gastric carcinoma

et al. 2017

WJG

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AIMto investigate the expression of proliferating cell nuclear antigen (PCNA) and E-cadherin in gastric carcinoma and to analyze their clinical significance.METHODSA total of 146 patients were selected for this study, including 38 patients with intestinal metaplasia, 42 with dysplasia, and 66 with primary gastric cancer. In addition, 40 patients with normal gastric tissues were selected as controls. The expression of PCNA and E-cadherin was detected by immunohistochemistry. Differences in PCNA and the E-cadherin labeling indexes among normal gastric mucosa, intestinal metaplasia, dysplasia, and gastric carcinoma were compared. Subjects with normal gastric tissues were assigned to a normal group, while gastric cancer patients were assigned to a gastric cancer group. The difference in PCNA and E-cadherin expression between these two groups was compared. The relationship between expression of PCNA and E-cadherin and clinicopathological features was also explored in gastric cancer patients. Furthermore, prognosis-related factors, as well as the expression of PCNA and E-cadherin, were analyzed in patients with gastric cancer to determine the 3-year survival of these patients.RESULTSThe difference in PCNA and the E-cadherin labeling indexes among normal gastric mucosa, intestinal metaplasia, dysplasia, and gastric carcinoma was statistically significant (P < 0.05). During the transition of normal gastric mucosa to gastric cancer, the PCNA labeling index gradually increased, while the E-cadherin labeling index gradually decreased (P < 0.05). The PCNA labeling index was significantly higher and the E-cadherin labeling index was significantly lower in gastric cancer than in dysplasia (P < 0.05). The expression of PCNA was significantly higher in the gastric cancer group than in the normal group, but E-cadherin was weaker (P < 0.05). There was a negative correlation between the expression of PCNA and E-cadherin in gastric carcinoma (r = -0.741, P = 0.000). PCNA expression differed significantly between gastric cancer patients with and without lymph node metastasis and between patients at different T stages. E-cadherin expression also differed significantly between gastric cancer patients with and without lymph node metastasis (P < 0.05). High T stage and positive PCNA expression were risk factors for the prognosis of patients with gastric cancer (RR > 1), while the positive expression of E-cadherin was a protective factor (RR < 1). The sensitivity, specificity, and accuracy of PCNA positivity in predicting the 3-year survival of patients with gastric cancer were 93.33%, 38.89%, and 0.64, respectively; while these values for E-cadherin negativity were 80.0%, 41.67%, and 0.59, respectively. When PCNA positivity and E-cadherin negativity were combined, the sensitivity, specificity, and accuracy were 66.67%, 66.67%, and 0.67, respectively.CONCLUSIONCombined detection of PCNA and E-cadherin can improve the accuracy of assessing the prognosis of patients with gastric cancer.

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“… Heatmap of Affymetrix array (U133A) data that allows to compare the following cell lines: MCF-10F (C) /Estrogen (E); C/Alpha3 (A3); E/Alpha5 (A5); A3/Alpha5; A5/Tumor2 (T2) and A3/T2 [ 153 ]. The red color indicates a higher expression in the first cell line, blue a lower expression, and yellow equal expression in both cell lines ( A ).…”

Section: Figurementioning

confidence: 99%

Gene Signatures Induced by Ionizing Radiation as Prognostic Tools in an In Vitro Experimental Breast Cancer Model

Calaf

Crispin

Roy

et al. 2021

Cancers

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This study aimed to analyze the expression of genes involved in radiation, using an Affymetrix system with an in vitro experimental breast cancer model developed by the combined treatment of low doses of high linear energy transfer (LET) radiation α particle radiation and estrogen yielding different stages in a malignantly transformed breast cancer cell model called Alpha model. Altered expression of different molecules was detected in the non-tumorigenic Alpha3, a malignant cell line transformed only by radiation and originally derived from the parental MCF-10F human cell line; that was compared with the Alpha 5 cell line, another cell line exposed to radiation and subsequently grown in the presence 17β-estradiol. This Alpha5, a tumorigenic cell line, originated the Tumor2 cell line. It can be summarized that the Alpha 3 cell line was characterized by greater gene expression of ATM and IL7R than control, Alpha5, and Tumor2 cell lines, it presented higher selenoprotein gene expression than control and Tumor2; epsin 3 gene expression was higher than control; stefin A gene expression was higher than Alpha5; and metallothionein was higher than control and Tumor2 cell line. Therefore, radiation, independently of estrogen, induced increased ATM, IL7R, selenoprotein, GABA receptor, epsin, stefin, and metallothioneins gene expression in comparison with the control. Results showed important findings of genes involved in cancers of the breast, lung, nervous system, and others. Most genes analyzed in these studies can be used for new prognostic tools and future therapies since they affect cancer progression and metastasis. Most of all, it was revealed that in the Alpha model, a breast cancer model developed by the authors, the cell line transformed only by radiation, independently of estrogen, was characterized by greater gene expression than other cell lines. Understanding the effect of radiotherapy in different cells will help us improve the clinical outcome of radiotherapies. Thus, gene signature has been demonstrated to be specific to tumor types, hence cell-dependency must be considered in future treatment planning. Molecular and clinical features affect the results of radiotherapy. Thus, using gene technology and molecular information is possible to improve therapies and reduction of side effects while providing new insights into breast cancer-related fields.

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Differential expression of cell adhesion molecules in an ionizing radiation-induced breast cancer model system

Cited by 9 publications

References 26 publications

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

Clinical significance of expression of proliferating cell nuclear antigen and E-cadherin in gastric carcinoma

Gene Signatures Induced by Ionizing Radiation as Prognostic Tools in an In Vitro Experimental Breast Cancer Model

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