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- Publisher Website: 10.1016/j.humpath.2014.05.002
- Scopus: eid_2-s2.0-84908885320
- PMID: 25017435
- WOS: WOS:000341409300007
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Article: The potential contributions of a Y-located protooncogene and its X homologue in sexual dimorphisms in hepatocellular carcinoma
Title | The potential contributions of a Y-located protooncogene and its X homologue in sexual dimorphisms in hepatocellular carcinoma |
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Authors | |
Keywords | Gonadoblastoma gene Hepatocellular carcinoma Sex chromosomes Sexual dimorphism TSPX |
Issue Date | 2014 |
Publisher | WB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath |
Citation | Human Pathology, 2014, v. 45 n. 9, p. 1847-1858 How to Cite? |
Abstract | There is a significant sex disparity favoring males among hepatocellular carcinoma (HCC) patients. Although various risk factors have been identified, the exact etiology of such sexual dimorphism(s) in HCC is uncertain. Previous studies showed that overexpression of the Y-located protooncogene, testis-specific protein Y encoded (TSPY), promotes cell proliferation and oncogenesis whereas its X-located homologue, TSPYhomologue X (TSPX), retards cell cycle and oncogenic progression. Furthermore, TSPX promotes proteasomal degradation of hepatitis B virus-encoded X oncoprotein and hence could serve as a tumor suppressor in virus-associated HCC. Using immunohistochemistry and reverse-transcription polymerase chain reaction analysis, we had examined the expression of TSPY and TSPX with reference to other established biomarkers in HCC and related liver cancers. Our results demonstrated that 55 (19.2%) of 287 male cases were TSPY positive in immunohistochemistry of tissue arrays, and 15 (46.9%) of 32 male cases were TSPY positive in reverse-transcription polymerase chain reaction analysis of clinical samples. TSPY expression was closely associated with the expression of HCC biomarkers, such as glypican 3. In contrast, TSPX expression was down-regulated in 54.5% of total tumor/nontumorous paired samples (18/33) and negatively associated with those of TSPY, glypican 3, and forkhead box M1 (FOXM1) and was positively associated with that of a tumor suppressor, insulin-like growth factor binding protein 3. The present findings support the hypothesis that the oncogenic events leading to an ectopic activation of the Y-located protooncogene TSPY and/or inactivating mutation/epigenetic silencing of the X-located tumor suppressor gene TSPX could collectively contribute to the sexual dimorphism(s) in HCC and related liver cancers in male-biased manners. |
Persistent Identifier | http://hdl.handle.net/10722/219203 |
ISSN | 2022 Impact Factor: 3.3 2020 SCImago Journal Rankings: 1.213 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Kido, T | - |
dc.contributor.author | Lo, CLR | - |
dc.contributor.author | Li, Y | - |
dc.contributor.author | Lee, J | - |
dc.contributor.author | Tabatabai, ZL | - |
dc.contributor.author | Ng, IOL | - |
dc.contributor.author | Lau, YF | - |
dc.date.accessioned | 2015-09-18T07:17:25Z | - |
dc.date.available | 2015-09-18T07:17:25Z | - |
dc.date.issued | 2014 | - |
dc.identifier.citation | Human Pathology, 2014, v. 45 n. 9, p. 1847-1858 | - |
dc.identifier.issn | 0046-8177 | - |
dc.identifier.uri | http://hdl.handle.net/10722/219203 | - |
dc.description.abstract | There is a significant sex disparity favoring males among hepatocellular carcinoma (HCC) patients. Although various risk factors have been identified, the exact etiology of such sexual dimorphism(s) in HCC is uncertain. Previous studies showed that overexpression of the Y-located protooncogene, testis-specific protein Y encoded (TSPY), promotes cell proliferation and oncogenesis whereas its X-located homologue, TSPYhomologue X (TSPX), retards cell cycle and oncogenic progression. Furthermore, TSPX promotes proteasomal degradation of hepatitis B virus-encoded X oncoprotein and hence could serve as a tumor suppressor in virus-associated HCC. Using immunohistochemistry and reverse-transcription polymerase chain reaction analysis, we had examined the expression of TSPY and TSPX with reference to other established biomarkers in HCC and related liver cancers. Our results demonstrated that 55 (19.2%) of 287 male cases were TSPY positive in immunohistochemistry of tissue arrays, and 15 (46.9%) of 32 male cases were TSPY positive in reverse-transcription polymerase chain reaction analysis of clinical samples. TSPY expression was closely associated with the expression of HCC biomarkers, such as glypican 3. In contrast, TSPX expression was down-regulated in 54.5% of total tumor/nontumorous paired samples (18/33) and negatively associated with those of TSPY, glypican 3, and forkhead box M1 (FOXM1) and was positively associated with that of a tumor suppressor, insulin-like growth factor binding protein 3. The present findings support the hypothesis that the oncogenic events leading to an ectopic activation of the Y-located protooncogene TSPY and/or inactivating mutation/epigenetic silencing of the X-located tumor suppressor gene TSPX could collectively contribute to the sexual dimorphism(s) in HCC and related liver cancers in male-biased manners. | - |
dc.language | eng | - |
dc.publisher | WB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath | - |
dc.relation.ispartof | Human Pathology | - |
dc.subject | Gonadoblastoma gene | - |
dc.subject | Hepatocellular carcinoma | - |
dc.subject | Sex chromosomes | - |
dc.subject | Sexual dimorphism | - |
dc.subject | TSPX | - |
dc.title | The potential contributions of a Y-located protooncogene and its X homologue in sexual dimorphisms in hepatocellular carcinoma | - |
dc.type | Article | - |
dc.identifier.email | Lo, CLR: loregina@hku.hk | - |
dc.identifier.email | Ng, IOL: iolng@hku.hk | - |
dc.identifier.authority | Lo, CLR=rp01359 | - |
dc.identifier.authority | Ng, IOL=rp00335 | - |
dc.identifier.doi | 10.1016/j.humpath.2014.05.002 | - |
dc.identifier.pmid | 25017435 | - |
dc.identifier.scopus | eid_2-s2.0-84908885320 | - |
dc.identifier.hkuros | 252156 | - |
dc.identifier.volume | 45 | - |
dc.identifier.issue | 9 | - |
dc.identifier.spage | 1847 | - |
dc.identifier.epage | 1858 | - |
dc.identifier.isi | WOS:000341409300007 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0046-8177 | - |