Browsing by Subject "Lung carcinoma"

Now showing 1 - 5 of 5
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    Comparison of the dysadherin and E-cadherin expression in primary lung cancer and metastatic sites
    (Murcia : F. Hernández, 2010) Mitselou, Antigony; Batistatou, Anna; Nakanishi, Yukihiro; Hirohashi, Setsuo; Vougiouklakis, Theodoros; Charalabopoulos, Konstantinos
    Dysadherin, a cancer associated cell membrane glycoprotein, has been reported to downregulate E-cadherin. Aberrant expression of Ecadherin has been associated with the development of metastases in patients with cancer. Even though the expression of dysadherin and E-cadherin has been studied in primary non-small cell lung carcinoma, little is known about its expression at the distant metastases sites. We investigate by immunohistochemistry the relationship between E-cadherin and dysadherin in 111 cases of primary lung carcinomas (53 squamous cell carcinomas, 21 adenocarcinomas, 13 large cell carcinomas, and 24 small cell carcinomas), and their distant metastases. The intensity, the expression pattern and the percentage of neoplastic cell staining were recorded and the results were correlated with clinicopathological findings of the subjects. Dysadherin immunostain was expressed in 61 (54.95%) of the cases, and increased dysadherin expression was significantly correlated with tumour size (p=0.003), distant metastases (p=0.0034), and metastasis size (p=0.0008). Reduced Ecadherin expression was noted in 46 (41.45%) of the cases, and was correlated with high-grade tumour (p=0.02), infiltrative growth pattern (p=0.042), and advanced stage (p=0.032). Although the correlation between the expression of dysadherin and E-cadherin was not significant, a group of patients showed reduced E-cadherin expression with dysadherin overexpression. In lung carcinomas dysadherin expression seems to reflect tumour aggressiveness and may be considered a positive marker of poor prognosis when considered alone or/and in combination with down-regulation of Ecadherin.
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    Glucose transporter expression in developing fetal lungs and lung neoplasms
    (Murcia : F. Hernández, 1999) Ito, T.; Noguchi, Y.; Udaka, N.; Kitamura, H.; Satoh, S.
    Glucose uptake and metabolism are essential for proliferation and survival of cells, and are supposed to be enhanced in actively proliferating cell systems such as embryonic and cancer tissues. Glucose uptake is usually carried out through glucose transporters. In the developing fetal lung, metabolism of glucose is thought to be an important process in cell proliferation, differentiation and maturation. Active glucose uptake could result in accumulation of glycogen in epithelial cells, and utilization of glycogen could be a critical phenomenon for lung epithelia1 development. In hamsters, although facilitative glucose transporter isoform 1 (GLUTl) and isoform 4 (GLUT4) are not detected in adult lungs, expression of them is detected with immunohistochemical and Western blot analyses in the developing fetal lungs. In human lung carcinomas, GLUTl expression is seen in most cases of lung carcinoma, and is seen especially frequently in squamous cell carcinoma. GLUTl expression in adenocarcinoma of the lung is correlated with reduced cell differentiation, larger tumor size and positive lymph node metastasis. A few cases of lung carcinoma show positive staining for GLUT3 and GLUT4. Thus, expression of some facilitative glucose transporter isoforms is detected in developing fetal epithelium and in lung carcinomas. Overexpression of them could enhance uptake of glucose into these cells, and the increased influx of glucose could be involved in active cell proliferation, which is a common character of the developing lung epithelium and carcinoma.
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    Lidocaine represses the malignant behavior of lung carcinoma cells via the circ_PDZD8/miR-516b-5p/GOLT1A axis
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Zi, Huafen; Chen, Li; Ruan, Qian
    Lung carcinoma is the most prevalent malignancy in adults. Lidocaine (Lido) has been confirmed to exert an anti-tumor role in many human cancers. However, the role and underlying mechanism of Lido in lung carcinoma remain poorly understood. Cell proliferation ability, migration, invasion, and apoptosis were measured by Colony formation, 5-ethynyl-2'- deoxyuridine (EdU), Cell Counting Kit-8 (CCK-8), transwell, and flow cytometry assays. Circ_PDZD8, microRNA-516b-5p (miR-516b-5p), and Golgi transport 1A (GOLT1A) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Protein levels of proliferating cell nuclear antigen (PCNA) and GOLT1A were examined by western blot assay. The binding relationship between miR-516b-5p and circ_PDZD8 or GOLT1A was predicted by circular RNA Interactome or Starbase 3.0 and then verified by a dual-luciferase reporter assay. The biological roles of circ_PDZD8 and Lido on lung carcinoma cell growth were examined by the xenograft tumor model in vivo. Lido suppressed proliferation, migration, invasion, and induced apoptosis in lung carcinoma cells. Circ_PDZD8 and GOLT1A were increased, miR-516b-5p was decreased in lung carcinoma tissues and cell lines. Their expression presented the opposite trend in Lido-triggered lung carcinoma cells. Circ_PDZD8 might overturn the repression of Lido on cell growth ability and metastasis in this tumor. Mechanically, circ_PDZD8 might regulate GOLT1A expression by sponging miR-516b-5p. Circ_PDZD8 weakened the anti-lung carcinoma effect of Lido in vivo. Circ_PDZD8 might mitigate the inhibitory effect of Lido on tumor cell malignancy by modulating the miR-516b-5p/GOLT1A axis, providing a novel insight for lung carcinoma treatment.
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    Lung carcinoma with rhabdoid component. A series of seven cases associated with uncommon types of non-small cell lung carcinomas and alveolar entrapment
    (Murcia : F. Hernández, 2010) Izquierdo Garcia, Francisco M.; Moreno Mata, Nicolás; Herranz Aladro, María Luisa; Cañizares, Miguel Ángel; Álvarez-Fernández, Emilio
    Rhabdoid tumor, included in the WHO classification among large cell carcinomas of the lung, is an uncommon type of lung carcinoma with poor prognosis. We report a series of 7 cases of lung carcinomas with rhabdoid component in 10% and 80% of the tumor. The associated tumor was adenocarcinoma in 3 cases - one of them with focal micropapillary pattern - large cell carcinoma in 2 cases, squamous cell carcinoma in 1 case and pleomorphic carcinoma in 1 case. Two adenocarcinomas showed a focal spindle cell component. Micropapillary and pleomorphic types had not been reported before as a component associated with rhabdoid carcinomas. All cases were positive for vimentin, and AE1/AE3 cytokeratin and 5 cases for cytokeratin 7. All cases were negative for muscle and endothelial markers and for chromogranin A. Synaptophysin was focally positive only in one case. Alveolar trapping inside the tumor was present in 3 cases - a phenomenon not well studied in lung carcinomas and also not reported in tumors with rhabdoid component. Five patients died because of the tumor within 2 to 31 months after diagnosis, one of myocardial infarction and only one is alive and disease free 123 months after the diagnosis. In summary, we describe 7 new cases of this uncommon lung tumor with aggressive clinical course, associated with infrequent histological types in nonrhabdoid component and with alveolar trapping, a nondescribed finding.
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    Parafibromin expression in lung normal tissue and carcinoma: its comparison with clinicopathological parameters of carcinoma
    (Murcia: F. Hernández y Juan F. Madrid, Universidad de Murcia, Departamento de Biología Celular e Histología, 2011) Xia, Pu; Wang, Wei; Xu, Xiao-yan; Wang, Jian-ping; Takano, Yasuo; Zheng, Hua-Chuan
    Parafibromin is a protein encoded by the hyperparathyroidism 2 oncosuppressor gene and its down-regulated expression is involved in the pathogenesis of parathyroid, gastric and colorectal carcinomas. To clarify the roles of parafibromin expression in lung carcinomas, it was examined by immunohistochemistry and in situ hybridization on tissue microarray containing lung carcinomas (n=144) and normal lung tissue (n=20), with a comparison to clinicopathological parameters of carcinomas. Lung carcinoma cell lines and tissues were studied for parafibromin expression by Western blot and RT-PCR. Down-regulated expression of parafibromin mRNA was found in lung carcinoma in comparison with matched normal tissue (p<0.05). Parafibromin protein was found in the cilia and nuclei of pseudo-stratified columnar epithelium, and the nuclei of lung carcinoma. According to immunostaining and in situ hybridization, there was no difference in parafibromin expression between histological subtypes of lung carcinoma (p>0.05). The Kaplan-Meier method indicated that nuclear parafibromin expression was positively correlated with adenocarcinoma patients (p<0.05). Down-regulated parafibromin mRNA expression might play an important role in lung carcinogenesis, but not in its histogenesis. Strong parafibromin expression in cilia of the pseudostratified columnar epithelium indicated its possible involvement in cell mobility. Parafibromin expression could be employed to indicate the favorable prognosis of patients with adenocarcinoma.