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Article: Decreased brain-expressed X-linked 4 (BEX4) expression promotes growth of oral squamous cell carcinoma
Title | Decreased brain-expressed X-linked 4 (BEX4) expression promotes growth of oral squamous cell carcinoma |
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Authors | |
Keywords | Squamous cell carcinoma S100A family Oral cancer Brain-expressed X-linked family BEX4 Tumor growth |
Issue Date | 2016 |
Citation | Journal of Experimental and Clinical Cancer Research, 2016, v. 35, n. 1 How to Cite? |
Abstract | © 2016 Gao et al.Background: Brain-expressed X-linked (BEX) 4 is a member of BEX family. The functional role of BEX4 in oral squamous cell carcinoma (OSCC) remains unknown. Methods: Expression level of BEX family members (BEX1-5) in OSCC tissues and the paired normal epithelial were examined. Functions of epigenetic changes (DNA methylation and histone modifications) on BEX4 suppression in OSCC were examined by zebularine and trichostatin A (TSA) treatment on OSCC cell lines. Lentivector containing full-length BEX4 was used to generate OSCC cell lines with stable BEX4 expression. Effects of BEX4 expression on OSCC proliferation were monitored with xCELLigence RTCA real-time cell analyzer. BEX4-overexpressing CAL27 was implanted into nude mice to evaluate the effects on tumor growth in vivo. The signaling pathways regulated by BEX4 in OSCC was explored using human whole-transcript expression microarray. Results: Among the 5 BEX family members, BEX1 and BEX4 showed significant down-regulation in OSCC (P < 0.001). BEX3, in comparison, was overexpressed in the primary tumor. BEX4 expression in OSCC cell lines was re-activated after zebularine and TSA treatment. High BEX4 expression could suppress proliferation of OSCC in vitro. Subcutaneous tumor volume of BEX4-overexpressing CAL27 was remarkably reduced in nude mice. Microarray experiment showed that S100A family members (S100A7, S100A7A, S100A8, S100A9 & S100A12) might be the downstream targets of BEX4 in OSCC. Conclusions: BEX4 functions as tumor suppressor by inhibiting proliferation and growth of oral cancer. Decreased BEX4 contributes to the increased proliferative propensity of OSCC. |
Persistent Identifier | http://hdl.handle.net/10722/235964 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Gao, Wei | - |
dc.contributor.author | Li, John Zeng Hong | - |
dc.contributor.author | Chen, Si Qi | - |
dc.contributor.author | Chu, Chiao Yun | - |
dc.contributor.author | Chan, Jimmy Yu Wai | - |
dc.contributor.author | Wong, Thian Sze | - |
dc.date.accessioned | 2016-11-10T07:11:50Z | - |
dc.date.available | 2016-11-10T07:11:50Z | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | Journal of Experimental and Clinical Cancer Research, 2016, v. 35, n. 1 | - |
dc.identifier.uri | http://hdl.handle.net/10722/235964 | - |
dc.description.abstract | © 2016 Gao et al.Background: Brain-expressed X-linked (BEX) 4 is a member of BEX family. The functional role of BEX4 in oral squamous cell carcinoma (OSCC) remains unknown. Methods: Expression level of BEX family members (BEX1-5) in OSCC tissues and the paired normal epithelial were examined. Functions of epigenetic changes (DNA methylation and histone modifications) on BEX4 suppression in OSCC were examined by zebularine and trichostatin A (TSA) treatment on OSCC cell lines. Lentivector containing full-length BEX4 was used to generate OSCC cell lines with stable BEX4 expression. Effects of BEX4 expression on OSCC proliferation were monitored with xCELLigence RTCA real-time cell analyzer. BEX4-overexpressing CAL27 was implanted into nude mice to evaluate the effects on tumor growth in vivo. The signaling pathways regulated by BEX4 in OSCC was explored using human whole-transcript expression microarray. Results: Among the 5 BEX family members, BEX1 and BEX4 showed significant down-regulation in OSCC (P < 0.001). BEX3, in comparison, was overexpressed in the primary tumor. BEX4 expression in OSCC cell lines was re-activated after zebularine and TSA treatment. High BEX4 expression could suppress proliferation of OSCC in vitro. Subcutaneous tumor volume of BEX4-overexpressing CAL27 was remarkably reduced in nude mice. Microarray experiment showed that S100A family members (S100A7, S100A7A, S100A8, S100A9 & S100A12) might be the downstream targets of BEX4 in OSCC. Conclusions: BEX4 functions as tumor suppressor by inhibiting proliferation and growth of oral cancer. Decreased BEX4 contributes to the increased proliferative propensity of OSCC. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Experimental and Clinical Cancer Research | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | Squamous cell carcinoma | - |
dc.subject | S100A family | - |
dc.subject | Oral cancer | - |
dc.subject | Brain-expressed X-linked family | - |
dc.subject | BEX4 | - |
dc.subject | Tumor growth | - |
dc.title | Decreased brain-expressed X-linked 4 (BEX4) expression promotes growth of oral squamous cell carcinoma | - |
dc.type | Article | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1186/s13046-016-0355-6 | - |
dc.identifier.scopus | eid_2-s2.0-84974588991 | - |
dc.identifier.hkuros | 259253 | - |
dc.identifier.volume | 35 | - |
dc.identifier.issue | 1 | - |
dc.identifier.eissn | 1756-9966 | - |
dc.identifier.isi | WOS:000379551400001 | - |
dc.identifier.issnl | 1756-9966 | - |