BACKGROUNDHematopoietic pre-B-cell leukemia transcription factor-interacting protein (HPIP) is a corepressor of pre-B-cell leukemia homeobox (PBX) 1 and is known to play a role in hematopoiesis. Recently, HPIP was demonstrated to promote breast cancer cell proliferation and hepatocellular carcinoma growth. Moreover, it has been revealed that homeobox and PBX proteins, the expression of which is regulated by HPIP, play key roles in cancer of various organs, including oral squamous cell carcinoma (OSCC). Nevertheless, there has not been any study regarding the role of HPIP in OSCC. This study investigated the expression of HPIP in normal oral mucosa, epithelial precursor lesion (OEPL), and OSCC, and the functional roles of HPIP in OSCC cells and normal keratinocytes.MATERIALS AND METHODSImmunohistochemical analysis of HPIP, Ki-67, and involucrin was performed in OSCC specimens, and the change in involucrin expression following RNA interference treatment against HPIP was examined by quantitative RT-PCR and Western blot analysis in SCC9 and NHEK cells undergoing extracellular calcium-induced differentiation. Matrigel transwell and cell proliferation assays for both cell lines transfected with HPIP siRNA were also conducted.RESULTSHPIP expression increased in OEPL and OSCC specimens. In vitro analysis revealed that HPIP suppressed differentiation and proliferation of SCC9 cells and transwell migration of NHEK cells, while HPIP promoted invasion of SCC9 and proliferation of NHEK cells. However, HPIP has no significant effect on NHEK cell differentiation.CONCLUSIONHPIP may play a critical role in oral carcinogenesis and is thus a potential target for anticancer therapy, with particular emphasis on its involvement in differentiation and migration/metastasis.
Lymph node metastasis is a major factor for poor prognosis in oral squamous cell carcinoma (OSCC). However, the molecular mechanisms of lymph node metastasis are unclear. We determined that angiopoietin-like protein 4 (ANGPTL4) mRNA and protein expression were increased in OSCC cells established from the primary site in metastatic cases. In addition, ANGPTL4 expression in biopsy specimens was correlated with the presence of lymph node metastasis. Therefore, our initial findings suggest that OSCC cells expressing ANGPTL4 may possess metastatic ability. Furthermore, cell culture supernatants from OSCC cells that metastasized to the lymph node contain ANGPTL4 and promote invasive ability. These findings suggest that secreted ANGPTL4 may affect the invasive ability of OSCC. Moreover, the rates of positive ANGPTL4 expression at the primary site were significantly higher in the lymph node metastasis group. These results demonstrate that ANGPTL4 contributes to OSCC metastasis by stimulating cell invasion. Therefore, ANGPTL4 is a potential therapeutic target for preventing cancer metastasis.
Pathology InternationalVolume 62, Issue 1 p. 75-76 Sclerosing odontogenic carcinoma Tarou Irié, Tarou Irié Department of Oral Pathology, Showa University School of Dentistry, Tokyo, Department of Pathology, Asahi General Hospital, Chiba, JapanSearch for more papers by this authorIkuko Ogawa, Ikuko Ogawa Center of Oral Clinical Examination, Hiroshima University Hospital, HiroshimaSearch for more papers by this authorTakashi Takata, Takashi Takata Department of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical Sciences, Hiroshima University, HiroshimaSearch for more papers by this authorSatoru Toyosawa, Satoru Toyosawa Department of Oral Pathology, Osaka University Graduate School of Dentistry, OsakaSearch for more papers by this authorTomohide Isobe, Tomohide Isobe Department of Oral Pathology, Showa University School of Dentistry, Tokyo,Search for more papers by this authorChie Hokazono, Chie Hokazono Department of Oral Pathology, Showa University School of Dentistry, Tokyo,Search for more papers by this authorTetsuhiko Tachikawa, Tetsuhiko Tachikawa Department of Oral Pathology, Showa University School of Dentistry, Tokyo,Search for more papers by this authorYoshio Suzuki, Yoshio Suzuki Department of Pathology, Asahi General Hospital, Chiba, JapanSearch for more papers by this author Tarou Irié, Tarou Irié Department of Oral Pathology, Showa University School of Dentistry, Tokyo, Department of Pathology, Asahi General Hospital, Chiba, JapanSearch for more papers by this authorIkuko Ogawa, Ikuko Ogawa Center of Oral Clinical Examination, Hiroshima University Hospital, HiroshimaSearch for more papers by this authorTakashi Takata, Takashi Takata Department of Oral and Maxillofacial Pathobiology, Graduate School of Biomedical Sciences, Hiroshima University, HiroshimaSearch for more papers by this authorSatoru Toyosawa, Satoru Toyosawa Department of Oral Pathology, Osaka University Graduate School of Dentistry, OsakaSearch for more papers by this authorTomohide Isobe, Tomohide Isobe Department of Oral Pathology, Showa University School of Dentistry, Tokyo,Search for more papers by this authorChie Hokazono, Chie Hokazono Department of Oral Pathology, Showa University School of Dentistry, Tokyo,Search for more papers by this authorTetsuhiko Tachikawa, Tetsuhiko Tachikawa Department of Oral Pathology, Showa University School of Dentistry, Tokyo,Search for more papers by this authorYoshio Suzuki, Yoshio Suzuki Department of Pathology, Asahi General Hospital, Chiba, JapanSearch for more papers by this author First published: 22 December 2011 https://doi.org/10.1111/j.1440-1827.2011.02749.xCitations: 4Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume62, Issue1January 2012Pages 75-76 RelatedInformation
Cytokeratin is commonly used diagnostic markers of oral squamous cell carcinoma (OSCC). Especially, Keratin17 (K17) is reported to be up-regulated in OSCC. Recently, identification and quantification of proteins from tissue section become possible by using laser microdissection and LC/MS/MS method. In this study, we performed nano-flow liquid chromatography, mass spectrometry and protein identification by tandem mass spectrometry (LC/MS/MS) analysis on pooled protein extracts from OSCC tissue section and compared the results with those from normal epithelium. As a result, Keratin 6hf is considered as a candidate marker of OSCC. From more validation, the expression of K6hf may be associated with malignancy of oral epithelial lesion. In previous study, K6hf is known to be specifically expressed in a hair follicle and specifically cross a partner with K17. But, there are no report about correlation between K6hf and carcinoma. In conclusion, K6hf expression may play an important role in the carcinogenesis progression of OSCC. However, further studies on the molecular function of K6hf are encouraged to clear the precise mechanism of K6hf in OSCC.
Abstract When we perform profiling analysis using tissue of Homo sapiens, individual difference becomes one of large problems. We use a laser microdissection as one of the solutions for this problem and try profiling analysis from tissue section. This technique can collect the part where morphologic evidence varies from the same tissue section, and comparison in an equivalence case besides in same lesion become possible. In addition, a laser microdissection method is effective in hyperplasia, papilloma, border domain, complicated differentiation form, such as lesion difficult to obtain a cultured cell. In this study, we collected area of normal epithelium, epithelial dysplasia and squamous cell carcinoma from tissue section by using laser microdissection. Collected tissue was dissolved in lysis buffer and digested by trypsin to make samples. Each sample was analyzed and quantified by LC/MS/MS, then, obtained data was referred to the protein database (SWISS PROT). From this procedure, we found over 100 different types of protein in every area. In comparison with each protein profiling list, many already known marker of oral squamous cell carcinoma, such as keratin 17, keratin 13, lumican and CD98, was detected. Two new candidate markers of oral squamous cell carcinoma are discovered at present: one is keratin superfamily, and another is tumor related protein. About extracted new candidate markers, we perform real time PCR, immunohistochemistry and Western blot from tissue section for validation. In conclusion, Laser microdissection and LC/MS/MS were useful method to search for markers of oral squamous cell carcinoma, and detected candidate marker was thought to be effective for diagnosis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2004.
A case of sclerosing odontogenic carcinoma (SOC) admixed with a benign fibro-osseous lesion (BFOL) is reported herein. A 67-year-old male had paresthesia in the mental region. Computed tomography detected an intragnathic mass that was focally expansile with disappearance of cortical bone, and contained admixed radiolucency and radio-opacity. Under the pathological diagnosis as benign fibro-osseous lesion, it was surgically removed by curettage. Microscopic analysis showed that a few parts of the resected materials contained dispersed thin cords and small nests of epithelial cells accompanied by fibrous stroma. Cellular atypia and mitotic figures were not evident. The diagnosis of BFOL with hyperplastic and metaplastic odontogenic epithelia was ultimately made. Eight months after the operation, the lesion recurred and segmental mandibulectomy was carried out. Histologically, the lesion was predominantly occupied by the fibro-osseous component with irregular-shaped foci of epithelial component. The epithelial component exhibited mostly thin cord or small nest patterns and showed definite perineural infiltration. Immunohistochemically, the epithelial cells were positive for p63, cytokeratin (CK) 6 and CK19, and focally positive for CK7 but negative for vimentin. MIB-1 positive nuclei were inconspicuous. To the best of our knowledge, this report is the first case of SOC with BFOL.