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Báo cáo hóa học: Inhibiting adenoid cystic carcinoma cells growth and metastasis by blocking the expression of ADAM 10 using RNA interference
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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Inhibiting adenoid cystic carcinoma cells growth and metastasis by blocking the expression of ADAM 10 using RNA interference
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Báo cáo hóa học: "Inhibiting adenoid cystic carcinoma cells growth and metastasis by blocking the expression of ADAM 10 using RNA interference"Xu et al. Journal of Translational Medicine 2010, 8:136http://www.translational-medicine.com/content/8/1/136 RESEARCH Open AccessInhibiting adenoid cystic carcinoma cells growthand metastasis by blocking the expression ofADAM 10 using RNA interferenceQin Xu, Xiuming Liu, Wantao Chen, Zhiyuan Zhang* Abstract Background: Adenoid cystic carcinoma is one of the most common types of salivary gland cancers. The poor long-term prognosis for patients with adenoid cystic carcinoma is mainly due to local recurrence and distant metastasis. Disintegrin and metalloprotease 10 (ADAM 10) is a transmembrane protein associated with metastasis in a number of diverse of cancers. The aim of this study was to analyze the relationship between ADAM 10 and the invasive and metastatic potentials as well as the proliferation capability of adenoid cystic carcinoma cells in vitro and in vivo. Methods: Immunohistochemistry and Western blot analysis were applied to detect ADAM 10 expression levels in metastatic cancer tissues, corresponding primary adenoid cystic carcinoma tissues, adenoid cystic carcinoma cell lines with high metastatic potential, and adenoid cystic carcinoma cell lines with low metastatic potential. RNA interference was used to knockdown ADAM 10 expression in adenoid cystic carcinoma cell lines with high metastatic potential. Furthermore, the invasive and metastatic potentials as well as the proliferation capability of the treated cells were observed in vitro and in vivo. Results: It was observed that ADAM 10 was expressed at a significantly higher level in metastatic cancer tissues and in adenoid cystic carcinoma cell lines with high metastatic potential than in corresponding primary adenoid cystic carcinomas and adenoid cystic carcinoma cell lines with low metastatic potential. Additionally, silencing of ADAM 10 resulted in inhibition of cell growth and invasion in vitro as well as inhibition of cancer metastasis in an experimental murine model of lung metastases in vivo. Conclusions: These studies suggested that ADAM 10 plays an important role in regulating proliferation and metastasis of adenoid cystic carcinoma cells. ADAM 10 is potentially an important therapeutic target for the prevention of tumor metastases in adenoid cystic carcinoma.Background metastasis mechanisms are of great significance for theAdenoid cystic carcinoma is one of the most common prognosis, evaluation, and selection of treatmenttypes of salivary gland cancers, characterized by hetero- protocols.geneous phenotypic features and persistently progressive The ADAM (A disintegrin and metalloprotease) familybiological behavior. The poor long-term prognosis for is a class of type I transmembrane proteins that partici-patients with adenoid cystic carcinoma is mainly due to pate in a wide range of physiological functions. Thislocal recurrence related to perineural invasion and family of proteins is named because they have two maindelayed onset of distant metastasis, particularly to the structural domains, the disintegrin domain and thelungs [1,2]. In-depth studies on its invasion and matrix metalloproteinase domain. They can degrade the extracellular matrix (ECM) and control cell adhesion and movement through regulation of intercellular adhe- sion, protease activity and cell activities that are closely* Correspondence: zhang.zhiyuan2010@hotmail.comDepartment of Oral and Maxillofacial Surgery, Ninth People’s Hospital, related to the metastasis of human tumors [3,4]. AmongShanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory the members of the ADAM family, some ADAMs, suchof Stomatology, Shanghai 200011, China © 2010 Xu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http: ...
Nội dung trích xuất từ tài liệu:
Báo cáo hóa học: "Inhibiting adenoid cystic carcinoma cells growth and metastasis by blocking the expression of ADAM 10 using RNA interference"Xu et al. Journal of Translational Medicine 2010, 8:136http://www.translational-medicine.com/content/8/1/136 RESEARCH Open AccessInhibiting adenoid cystic carcinoma cells growthand metastasis by blocking the expression ofADAM 10 using RNA interferenceQin Xu, Xiuming Liu, Wantao Chen, Zhiyuan Zhang* Abstract Background: Adenoid cystic carcinoma is one of the most common types of salivary gland cancers. The poor long-term prognosis for patients with adenoid cystic carcinoma is mainly due to local recurrence and distant metastasis. Disintegrin and metalloprotease 10 (ADAM 10) is a transmembrane protein associated with metastasis in a number of diverse of cancers. The aim of this study was to analyze the relationship between ADAM 10 and the invasive and metastatic potentials as well as the proliferation capability of adenoid cystic carcinoma cells in vitro and in vivo. Methods: Immunohistochemistry and Western blot analysis were applied to detect ADAM 10 expression levels in metastatic cancer tissues, corresponding primary adenoid cystic carcinoma tissues, adenoid cystic carcinoma cell lines with high metastatic potential, and adenoid cystic carcinoma cell lines with low metastatic potential. RNA interference was used to knockdown ADAM 10 expression in adenoid cystic carcinoma cell lines with high metastatic potential. Furthermore, the invasive and metastatic potentials as well as the proliferation capability of the treated cells were observed in vitro and in vivo. Results: It was observed that ADAM 10 was expressed at a significantly higher level in metastatic cancer tissues and in adenoid cystic carcinoma cell lines with high metastatic potential than in corresponding primary adenoid cystic carcinomas and adenoid cystic carcinoma cell lines with low metastatic potential. Additionally, silencing of ADAM 10 resulted in inhibition of cell growth and invasion in vitro as well as inhibition of cancer metastasis in an experimental murine model of lung metastases in vivo. Conclusions: These studies suggested that ADAM 10 plays an important role in regulating proliferation and metastasis of adenoid cystic carcinoma cells. ADAM 10 is potentially an important therapeutic target for the prevention of tumor metastases in adenoid cystic carcinoma.Background metastasis mechanisms are of great significance for theAdenoid cystic carcinoma is one of the most common prognosis, evaluation, and selection of treatmenttypes of salivary gland cancers, characterized by hetero- protocols.geneous phenotypic features and persistently progressive The ADAM (A disintegrin and metalloprotease) familybiological behavior. The poor long-term prognosis for is a class of type I transmembrane proteins that partici-patients with adenoid cystic carcinoma is mainly due to pate in a wide range of physiological functions. Thislocal recurrence related to perineural invasion and family of proteins is named because they have two maindelayed onset of distant metastasis, particularly to the structural domains, the disintegrin domain and thelungs [1,2]. In-depth studies on its invasion and matrix metalloproteinase domain. They can degrade the extracellular matrix (ECM) and control cell adhesion and movement through regulation of intercellular adhe- sion, protease activity and cell activities that are closely* Correspondence: zhang.zhiyuan2010@hotmail.comDepartment of Oral and Maxillofacial Surgery, Ninth People’s Hospital, related to the metastasis of human tumors [3,4]. AmongShanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory the members of the ADAM family, some ADAMs, suchof Stomatology, Shanghai 200011, China © 2010 Xu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http: ...
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