title: Decreased expression of profilin 2 in oral squamous cell carcinoma and its clinicopathological implications.
abstract: Profilins are small proteins essential for many normal cellular dynamics and constitute one of the crucial components of actin-based cellular motility. Several recent studies have implicated a role for the profilin (PFN) family in cancer pathogenesis and progression. However, their expression and promising functions are largely unknown in oral squamous cell carcinoma (OSCC). In this study, we analyzed the correlation between PFN1 and PFN2 expression in vitro and in vivo. The protein expression levels were roughly compared between cell lines (HIOEC, HB96) with the employment of mass spectrometry. PFN2 was singled out as one of the significantly down-regulated genes in the cancerous HB96 cells. The expression levels of PFN1 and PFN2 in vitro were validated by RT-PCR, real-time PCR and Western blotting. Laser scanning confocal microscopy was used for the first time to assess the localization of PFN2 expression. In subsequent experiments, we observed the relationship between PFN2 expression levels and the proliferation of transfected HB96 cancer cells. VASP, N-WASP and P27 expression was also examined in the PFN2-transfected or non-transfected HB96 cells. In vivo, antigen expression was determined by immunohistochemical analyses in 88 paired tissue specimens. Decreased protein expression was confirmed in cancerous tissues from 88 OSCC patients compared with paracancerous normal mucous epithelia. Tumors with weak PFN2 expression were associated with a significantly worse prognosis than strongly expressed tumours (P<0.001). Other statistical analyses were performed to assess the differences in expression and their clinical and pathological significance. In conclusion, PFN2 can be utilized as both a potential suppressor marker and a prognostic protein for OSCC. The function of PFN2 may be to regulate the N-WASP/Arp2/3 signaling pathway.
authors: Department of Oral and Maxillofacial Surgery, Ninth People's Hospital, College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, PR China.
authors: C Y
authors: CY
authors: Ma
authors: C P
authors: CP
authors: Zhang
authors: L P
authors: LP
authors: Zhong
authors: H Y
authors: HY
authors: Pan
authors: W T
authors: WT
authors: Chen
authors: L Z
authors: LZ
authors: Wang
authors: O W
authors: OW
authors: Andrew
authors: T
authors: T
authors: Ji
authors: W
authors: W
authors: Han
mesh_terms: D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D015815:Cell Adhesion Molecules / Q000096:biosynthesis / Q000235:genetics; D045744:Cell Line, Tumor; D002853:Chromatography, Liquid; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000096:biosynthesis / Q000235:genetics; D015536:Down-Regulation; D015180:Electrophoresis, Gel, Two-Dimensional; D005260:Female; D006801:Humans; D008297:Male; D008840:Microfilament Proteins / Q000096:biosynthesis / Q000235:genetics; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D010750:Phosphoproteins / Q000096:biosynthesis / Q000235:genetics; D051304:Profilins / Q000096:biosynthesis* / Q000235:genetics; D011379:Prognosis; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D053719:Tandem Mass Spectrometry; D014162:Transfection; D051317:Wiskott-Aldrich Syndrome Protein, Neuronal / Q000096:biosynthesis / Q000235:genetics; D000098662:Vasodilator-Stimulated Phosphoprotein
chemical_list: D015815:Cell Adhesion Molecules; D008840:Microfilament Proteins; C495738:PFN1 protein, human; C495741:PFN2 protein, human; D010750:Phosphoproteins; D051304:Profilins; D012333:RNA, Messenger; C495771:WASL protein, human; D051317:Wiskott-Aldrich Syndrome Protein, Neuronal; D000098662:Vasodilator-Stimulated Phosphoprotein; D050760:Cyclin-Dependent Kinase Inhibitor p27