OBJECTIVETo report two cases of glandular odontogenic cyst and examine its cytokeratin 18,19 expression.

METHODSTwo cases of glandular odontogenic cyst were reported and studied. The cytokeratin 18, 19 expression in these two cases were also investigated using immuno-histochemical staining as well as in the situ hybridization of the cyst epithelium.

RESULTSHisto-pathological examination revealed that ciliated columnar cells, squamous cells and low-columnar cells were found in the superficial layer of the lining epithelium. Several minor salivary glands, mainly composed of seromucous cells were observed near the satellite cyst. CK18 were expressed in all layers of the lining epithelium of varying intensity. CK18 was negative in lining epithelium of the daughter cyst, but CK19 was positive. CK18-mRNA was expressed in all the layers of the lining epithelium, the salivary glands and daughter cysts.

CONCLUSIONSHistological features and CK18 expression may be indicative of the possibility of salivary glandular and odontogenic differentiation.

Adolescent ; Adult ; Epithelium ; pathology ; Female ; Humans ; Keratin-18 ; metabolism ; Keratin-19 ; metabolism ; Male ; Odontogenic Cysts ; metabolism ; pathology

Adenoma, Sweat Gland ; metabolism ; Diagnosis, Differential ; Humans ; Keratin-14 ; metabolism ; Keratin-17 ; metabolism ; Keratin-18 ; metabolism ; Keratin-7 ; metabolism ; Keratins ; metabolism ; Papilloma ; metabolism ; Sebaceous Gland Neoplasms ; metabolism ; Skin Neoplasms ; metabolism ; Sweat Gland Neoplasms ; metabolism

OBJECTIVE: To identify the chaperone of polypyrimidine tractor-binding protein-associated splicing factor (PSF) in myeloid leukemia cells, and to explore the mechanism and redistributive pattern to cell surface of PSF in chemo-sensitive HL60 cells and resistant HL60/DOX cells. METHODS: The eukaryotic expression vector of PSF was transfected with liposomes transiently, then flow cytometry was used to detect the expression level of PSF on the cell surface 24 h, 48 h and 72 h after vector transfections. We constructed a chimeric expression vector, streptavidin binding peptide (SBP)-PSF, meanwhile this vector was transfected and made SBP-PSF fusion protein overexpress. In addition, we used streptavidin magnetic beads to precipitate the cellular chaperonin of PSF and then identified its chaperonin by mass spectrometry (MS). Lentiviral vectors containing cytokeratin18 (K18) interference sequences were transfected into 293T cells to prepare lentivirus. HL60 and HL60/DOX cells were infected with lentivirus to obtain stable interfering K18 cell lines. Next, flow cytometry was used to test the membrane relocation level of PSF. Together, these methods confirmed the similar or different mechanisms of the PSF redistributing to membrane synergistically mediated by K18 in HL60 and HL60/DOX cells. RESULTS: The expression of membrane relocated PSF was detected every day for three days (at the end of 24 h, 48 h and 72 h) after transient overexpression. The expressing rate of PSF on the cell surface was 22.4%±3.5%, 37.9%±6.0%, 58.3%±8.8%, respectively in sensitive HL60 cells, while that was 4.7%±0.5%, 3.9%±0.6%, 2.9%±0.6% , respectively in resistant HL60/DOX cells. The difference of expressing rate on each day was significant, P<0.01. We identified K18 detected by co-immunoprecipitation and mass spectrum assay which was the cellular chaperone of PSF. We found that K18 knockdown decreased the PSF expression level which redistributed on cell surface from 48.9%±5.4% to 6.2%±1.0% in sensitive HL60 cells, and from 9.11%±1.2% to 2.21%±0.51% in resistant HL60/DOX cells, respectively. CONCLUSION K18 is the intracellular chaperonin of PSF. The interaction of PSF and K18 mediates its redistribution to cell membrane in sensitive cells. While in resistant cells, PSF failed to relocate at the cell surface and accumulated in cells, which mediated resistance to chemotherapeutics.
Cell Membrane ; Doxorubicin ; Drug Resistance, Multiple ; Humans ; Keratin-18/metabolism* ; Leukemia, Myeloid

OBJECTIVETo study the mechanism of liver fibrogenesis and to find new non-invasive biomarkers.

METHODIn this study, we used subcellular proteomic technology to study the plasma membrane proteins related to immune or alcohol induced liver fibrosis. Rat liver fibrosis models were induced by pig serum or alcohol injection. The liver fibrogenesis were detected by James's staining in the rat models after 2, 4, 6 and 8 weeks of treatment. The liver plasma membrane (PM) of the 2- and 8-week treatment model rats were enriched by two-step sucrose density gradient centrifugation. The purity of PM was verified by western blotting, and the plasma membrane proteins were extracted and analyzed by 2 DE. The differentially expressed proteins were identified by LC-MS/MS. Cellular location and function of these identified differential protein were classified.

RESULTSImmune or alcohol induced liver fibrosis rat models were successfully established. Liver plasma membrane was significantly enriched after sucrose density ultracentrifugation treatment. 87 differential protein spots were find out by 2DE combined with LC-MS/MS from the liver plasma membrane proteins of the 2- and 8-week treatment rat models, which corresponded to 30 non-redundant proteins including annexin A2, keratin 8 and keratin 18.

CONCLUSIONSA list of differentially expressed proteins relate to liver fibrosis were successfully identified. Differential proteins such as annexin A2, keratin 8 and keratin 18 could be new biomarkers for liver fibrosis diagnosis.

Alcohols ; adverse effects ; Animals ; Female ; Keratin-18 ; metabolism ; Keratin-8 ; metabolism ; Liver ; metabolism ; pathology ; Liver Cirrhosis ; chemically induced ; immunology ; metabolism ; pathology ; Male ; Proteome ; metabolism ; Rats ; Rats, Sprague-Dawley

Carcinoma, Renal Cell ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Humans ; Keratin-18 ; metabolism ; Keratin-19 ; metabolism ; Keratin-8 ; metabolism ; Kidney Neoplasms ; metabolism ; pathology ; surgery ; Male ; Middle Aged ; Nephrectomy ; Neprilysin ; metabolism ; Racemases and Epimerases ; metabolism

OBJECTIVETo investigate the expression of K18, Ser-33 and Ser-52 phosphorylated K18 in HBV infected human liver disease and its significance.

METHODSThe expression and localization of K18 and Ser-33, Ser-52 phosphorylated K18 in healthy liver tissue, in liver tissues of patients with post-HBV infection cirrhosis and severe chronic hepatitis were detected by histochemistry.

RESULTSK18, Ser-33 and Ser-52 phosphorylated K18 were expressed in normal liver cells, in liver tissues of cirrhosis patients and severe chronic hepatitis cases. The expression of K18 in the liver cells from the 3 different sources had no significant difference in levels. Ser-33 and Ser-52 phosphorylated K18 were expressed in normal liver cells, in liver tissues of cirrhosis patients chronicity HBV hepatitis and severe chronic hepatitis cases. Ser-33 and Ser-52 located around cytoplasmic membrane, diffused into cytoplasm and expressed at a higher levels in cirrhosis and severe chronic hepatitis.

CONCLUSIONThe expression levels of Ser-33 and Ser-52 phosphorylated K18 increased along with the progression of HBV infected human liver disease. The phosphorylation of K18 could be a marker of progression of HBV infected human liver disease.

Hepatitis B ; metabolism ; Humans ; Immunohistochemistry ; Keratin-18 ; metabolism ; Liver Cirrhosis ; metabolism ; pathology ; virology ; Liver Diseases ; metabolism ; pathology ; virology ; Phosphorylation ; Serine ; metabolism

Adenocarcinoma, Mucinous ; pathology ; Adenoma ; pathology ; Adolescent ; Breast Neoplasms, Male ; metabolism ; pathology ; secretion ; surgery ; Carcinoma ; metabolism ; pathology ; secretion ; surgery ; Diagnosis, Differential ; Humans ; Keratin-18 ; metabolism ; Keratin-8 ; metabolism ; Male ; Mastectomy, Modified Radical ; Proto-Oncogene Proteins c-kit ; metabolism ; S100 Proteins ; metabolism

OBJECTIVETo investigate the relationship between the expression of cytokeratin (CK)-18 and biological behavior of oral squamous cell carcinoma (OSCC).

METHODSTwenty-three patients with OSCC were investigated for the expression of CK-18-mRNA by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Correlations between clinical stages, pathological differentiation, lymphatic metastasis and the expression of CK-18-mRNA were evaluated. CK-18-mRNA expression of peripheral blood from the 23 patients and 23 healthy people were also examined. During follow-up after operation, the peripheral blood was collected again for the expression of CK-19-mRNA.

RESULTSExpression of CK-18-mRNA was found in 16 patients. The expression of CK-18-mRNA was significantly associated with clinical stages, tumor differentiation and lymphatic metastasis. CK-18-mRNA was positive in 4 of 23 blood specimens before operation, but during follow-up only 1 of 23 patients was still positive in peripheral blood.

CONCLUSIONSCK-18 may provide additional information in forecasting the metastasis of OSCC and serve as a reference in monitoring recurrence.

Adult ; Aged ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Case-Control Studies ; Female ; Humans ; Keratin-18 ; genetics ; metabolism ; Male ; Middle Aged ; Mouth Neoplasms ; metabolism ; pathology ; Neoplasm Metastasis ; RNA, Messenger ; genetics

OBJECTIVETo study the cytokeratin 18 and 13 and their gene (CK) expression in post-operation maxillary cyst linings with metaplastic epithelium.

METHODSCK expressions were examined with immunohistochemistry in 46 post-operative maxillary cyst (POMC) which were lined with pseudostriated columnar cells only (13 cases), both kinds of columnar and squamous cells (30 cases) and squamous cells only (3 cases).

RESULTSThe expressions of CK8, CK13 and CK18 were observed in 39, 9 and all of the 43 columnar epithelial linings, respectively. Metaplastic squamous epithelia expressed more CK13 and less CK18 and CK8. Of the 33 metaplastic linings, 24 expressed CK8, 23 CK13 and 26 linings expressed CK18. The expression of CK13- and CK18-mRNA was generally correlated with the protein expression level. By in situ hybridization, CK18-mRNA expression was observed not only in 26 metaplastic linings which were positive for CK18 protein but also in five of the seven metaplastic linings which did not express CK18 protein. In addition, RT-PCR revealed an expression of CK18-mRNA in all metaplastic squamous linings although the expression level was weaker than that in the columnar epithelial linings. The CK13-mRNA was expressed in a fashion inverse to the CK18-mRNA.

CONCLUSIONSThese results indicate that CK18-mRNA is preserved through metaplasia although the protein expression decreases and metaplastic squamous cells differentiate with a decrease of CK18 and an increase of CK13 expression.

Epithelial Cells ; metabolism ; pathology ; Humans ; Jaw Cysts ; etiology ; metabolism ; pathology ; Keratin-13 ; biosynthesis ; genetics ; Keratin-18 ; biosynthesis ; genetics ; Maxillary Diseases ; etiology ; metabolism ; pathology ; Metaplasia ; metabolism ; pathology ; Postoperative Complications ; RNA, Messenger ; genetics

OBJECTIVETo evaluate the value of application of cellular protein markers stained by immunocytochemistry in combination with ThinPrep bronchial brush cytology in classification of lung cancer subtypes.

METHODSRemaining bronchial brush cytology samples from 206 lung cancer patients with positive cytological diagnosis and 45 fine needle aspiration samples of resected lung carcinomas were collected. The expressions of CK10/13, CK7, CK18, CD56 and SYN in those samples were detected by immunocytochemistry (ICC) using corresponding antibodies.

RESULTSThe sensitivity and specificity of CK10/13 were 94.7% and 72.0%, respectively, in diagnosis of squamous cell carcinoma. The sensitivity and specificity of CK7 were 98.6% and 61.5%, and those of CK18 were 98.6% and 37.5%, respectively, in diagnosis of adenocarcinoma. The sensitivity and specificity of CD56 were 86.3% and 82.9%, and those of SYN were 81.6% and 93.5%, respectively, in diagnosis of small cell lung cancer. No significant difference was found in the expressions of CK10/13, CK7 and CK18 protein markers among differently differentiated lung squamous cell carcinomas and adenocarcinomas (P > 0.05). The classification rate of cytology in combination with ICC in differential diagnosis for 44 cases of unclassified lung cancer reached 90.0% for squamous cell carcinoma, 96.3% for adenocarcinoma, and 100.0% for small cell lung carcinoma.

CONCLUSIONApplication of cellular protein markers in combination with ThinPrep bronchial brush cytology is helpful to improve the differential diagnosis of lung cancer subtypes, and may become a supplementary diagnostic method in subclassification of lung cancer.

Adenocarcinoma ; diagnosis ; metabolism ; Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor ; metabolism ; Biopsy, Fine-Needle ; Bronchi ; pathology ; Bronchoscopy ; CD56 Antigen ; metabolism ; Carcinoma, Squamous Cell ; diagnosis ; metabolism ; Cytodiagnosis ; methods ; Cytological Techniques ; Diagnosis, Differential ; Female ; Humans ; Immunohistochemistry ; Keratin-13 ; metabolism ; Keratin-18 ; metabolism ; Keratin-7 ; metabolism ; Lung Neoplasms ; classification ; diagnosis ; metabolism ; Male ; Middle Aged ; Sensitivity and Specificity ; Small Cell Lung Carcinoma ; diagnosis ; metabolism ; Synaptophysin ; metabolism