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Article: Characterization of Bridging Integrator 1 (BIN1) as a Potential Tumor Suppressor and Prognostic Marker in Hepatocellular Carcinoma

TitleCharacterization of Bridging Integrator 1 (BIN1) as a Potential Tumor Suppressor and Prognostic Marker in Hepatocellular Carcinoma
Authors
Issue Date2012
PublisherThe Feinstein Institute for Medical Research. The Journal's web site is located at http://www.molmed.org/
Citation
Molecular Medicine, 2012, v. 18 n. 3, p. 507-518 How to Cite?
AbstractIt has been shown that bridging integrator 1 (BIN1) can interact with c-myelocytomatosis (c-Myc) oncoprotein in cancer. However, the role of BIN1 in hepatocellular carcinoma (HCC) is not clear. In the present study, we investigated the expression and prognostic role of BIN1 in primary HCC and evaluated the function of BIN1 in hepatocarcinogenesis. Using real-time polymerase chain reaction and Western blot analysis, we found significantly decreased expression of BIN1 in primary HCC tumor tissues (n = 42) compared with adjacent normal tissues and in HCC cell lines. Immunohistochemistry analysis also found decreased BIN1 expression in HCC tumor tissues (n = 117). In clinicopathological analysis, loss of BIN1 expression correlated significantly (P < 0.05) with differentiation scores and tumor size. Importantly, decreased expression of BIN1 in tumors was found to be closely associated with a poor prognosis, and we conclude that BIN1 was an independent prognostic factor in a multivariate analysis. In mechanistic studies, restoring BIN1 expression in BIN1-null HCC cells significantly inhibited cell proliferation and colony formation and induced apoptosis of HCC cells. Furthermore, we found that BIN1 overexpression could significantly suppress the motility and invasion of HCC cells in vitro. Our results indicate that BIN1 may function as a potential tumor suppressor and serve as a novel prognostic marker in HCC patients. The BIN1 molecule might play an important role in tumor growth, cell motility and invasion. Modulation of BIN1 expression may lead to clinical applications of this critical molecule in the control of hepatocellular carcinoma as well as in early and effective diagnosis of this aggressive tumor.
Persistent Identifierhttp://hdl.handle.net/10722/159676
ISSN
2015 Impact Factor: 3.53
2015 SCImago Journal Rankings: 2.372
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorPan, Ken_US
dc.contributor.authorLiang, XTen_US
dc.contributor.authorZhang, HKen_US
dc.contributor.authorZhao, JJen_US
dc.contributor.authorWang, DDen_US
dc.contributor.authorLi, JJen_US
dc.contributor.authorLian, Qen_US
dc.contributor.authorChang, AEen_US
dc.contributor.authorLi, Qen_US
dc.contributor.authorXia, JCen_US
dc.date.accessioned2012-08-16T05:53:55Z-
dc.date.available2012-08-16T05:53:55Z-
dc.date.issued2012en_US
dc.identifier.citationMolecular Medicine, 2012, v. 18 n. 3, p. 507-518en_US
dc.identifier.issn1076-1551en_US
dc.identifier.urihttp://hdl.handle.net/10722/159676-
dc.description.abstractIt has been shown that bridging integrator 1 (BIN1) can interact with c-myelocytomatosis (c-Myc) oncoprotein in cancer. However, the role of BIN1 in hepatocellular carcinoma (HCC) is not clear. In the present study, we investigated the expression and prognostic role of BIN1 in primary HCC and evaluated the function of BIN1 in hepatocarcinogenesis. Using real-time polymerase chain reaction and Western blot analysis, we found significantly decreased expression of BIN1 in primary HCC tumor tissues (n = 42) compared with adjacent normal tissues and in HCC cell lines. Immunohistochemistry analysis also found decreased BIN1 expression in HCC tumor tissues (n = 117). In clinicopathological analysis, loss of BIN1 expression correlated significantly (P < 0.05) with differentiation scores and tumor size. Importantly, decreased expression of BIN1 in tumors was found to be closely associated with a poor prognosis, and we conclude that BIN1 was an independent prognostic factor in a multivariate analysis. In mechanistic studies, restoring BIN1 expression in BIN1-null HCC cells significantly inhibited cell proliferation and colony formation and induced apoptosis of HCC cells. Furthermore, we found that BIN1 overexpression could significantly suppress the motility and invasion of HCC cells in vitro. Our results indicate that BIN1 may function as a potential tumor suppressor and serve as a novel prognostic marker in HCC patients. The BIN1 molecule might play an important role in tumor growth, cell motility and invasion. Modulation of BIN1 expression may lead to clinical applications of this critical molecule in the control of hepatocellular carcinoma as well as in early and effective diagnosis of this aggressive tumor.-
dc.languageengen_US
dc.publisherThe Feinstein Institute for Medical Research. The Journal's web site is located at http://www.molmed.org/-
dc.relation.ispartofMolecular Medicineen_US
dc.subject.meshAdaptor Proteins, Signal Transducing - genetics - metabolism-
dc.subject.meshCarcinoma, Hepatocellular - metabolism-
dc.subject.meshLiver Neoplasms - metabolism-
dc.subject.meshNuclear Proteins - genetics - metabolism-
dc.subject.meshTumor Markers, Biological - metabolism-
dc.titleCharacterization of Bridging Integrator 1 (BIN1) as a Potential Tumor Suppressor and Prognostic Marker in Hepatocellular Carcinomaen_US
dc.typeArticleen_US
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1076-1551&volume=18&issue=3&spage=507&epage=518&date=2012&atitle=Characterization+of+Bridging+Integrator+1+(BIN1)+as+a+Potential+Tumor+Suppressor+and+Prognostic+Marker+in+Hepatocellular+Carcinomaen_US
dc.identifier.emailLian, Q: qzlian@hkucc.hku.hken_US
dc.identifier.authorityLian, Q=rp00267en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.2119/molmed.2011.00319-
dc.identifier.pmid22281836-
dc.identifier.pmcidPMC3356425-
dc.identifier.scopuseid_2-s2.0-84865625703-
dc.identifier.hkuros204430en_US
dc.identifier.hkuros206957-
dc.identifier.volume18en_US
dc.identifier.issue3en_US
dc.identifier.spage507en_US
dc.identifier.epage518en_US
dc.identifier.isiWOS:000304516200018-
dc.publisher.placeUnited States-
dc.customcontrol.immutablejt 130514-

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