The alteration of the mucin profile have been known to play a role in colorectal carcinogenesis. MUC1 is up-regulated and MUC2 is down-regulated in colorectalcarcinomas. Overexpression of p53 is frequently noted in colorectal carcinomas with deep invasion or lymph node metastasis. However, there have been few reports about the association between MUC1, MUC2, and p53 expression with respect to the metastatic potential. This study was aimed to investigate the relationship of MUC1, MUC2, and protein p53 expressions with clinicopathological factors in colorectal carcinomas. Expressions of MUC1, MUC2, and p53 protein were examined immunohistochemically. Of total 97 cancers, 44 (45%) were MUC1 positive, 39 (40%) were MUC2 positive and 58 (59%) showed a p53 overexpression. Coexpression of MUC1 with p53 and dual expression of MUC1 with MUC2 were associated with a higher frequency of lymph node metastasis (p<0.05). The right colon showed a higher MUC1 positivity and frequent lymph node metastasis than the left colon (p<0.05). These results suggest that the coexpression of MUC 1 with p53 or MUC2 are involved in regional lymph node metastasis in colorectal carcinomas. The high expression of MUC1 in the right colon cancer was revealed to relate with lymph node metastasis.
Adult ; Aged ; Aged, 80 and over ; Colorectal Neoplasms/*metabolism/pathology ; Female ; Humans ; Lymph Nodes ; Lymphatic Metastasis ; Male ; Middle Aged ; Mucin-1/*biosynthesis ; Mucin-2 ; Mucins/*biosynthesis ; Tumor Suppressor Protein p53/*biosynthesis

OBJECTIVETo study the expression of Mucin1 gene and tumor infiltrating dendritic cells(TIDC) in the tissues of benign prostatic hyperplasia (BPH) and prostate cancer.

METHODSMucin1 and TIDC were detected in 20 specimens of BPH and 30 specimens of prostate cancer by immunohistochemistry SP method.

RESULTSMUC1 expressed in both prostate cancer and BPH. The staining patterns were significantly associated with tumor pathological grade (P < 0.001). The number of TIDC was negatively correlated with tumor pathological grade, the higher the grade, the smaller the number of TIDC (P < 0.001).

CONCLUSIONSThe expression pattern of MUC1 and the number of TIDC could be considered as useful markers to evaluate the malignant degree and prognosis of prostate cancer. The decrease of TIDC plays an important role in tumor immune evasion and immune tolerance. Highly expressed MUC1 could lead to the failure of hormonal treatment for prostate cancer, and contribute much to tumor infiltration and metastasis.

Antigens, Neoplasm ; biosynthesis ; Dendritic Cells ; immunology ; Humans ; Immunohistochemistry ; Lymphocytes, Tumor-Infiltrating ; immunology ; Male ; Mucin-1 ; Mucins ; biosynthesis ; Prostatic Hyperplasia ; immunology ; metabolism ; pathology ; Prostatic Neoplasms ; immunology ; metabolism ; pathology

OBJECTIVE: To explore the therapeutic effects and mechanisms of the combination of traditional Chinese medicine and western medicine on patients with peptic ulcers. METHODS: One hundred and twenty patients were randomly divided into 6 groups. Another 10 patients as the control group were confirmed with no peptic ulcers by endoscope, but had digestive tract symptoms. The clinical effects were compared among each group after the one month treatment. RESULTS: The clinical effects of the combination of Jianweiyuyang granules and ranitidine capsules were better than those of western medicine, with improvement in symptoms and syndrome (P < 0.01 to 0.05), but there was not significant difference with the rate of ulcer healing and the Hp clearance among the combination of Jianweiyuyang granules and ranitidine capsules, Jianweiyuyang granules, and ranitidine capsules (P > 0.05). The combination of Jianweiyuyang granules and ranitidine capsules could significantly upregulate the expression of MUCSAC mRNA (P < 0.01), while downregulate the expression of ETAR mRNA (P < 0.01). CONCLUSION There is obvious advantage in treating peptic ulcers by the combination of Jianweiyuyang granules and ranitidine capsules, and its mechanisms may be to protect the gastric mucosal barrier by up-regulating the expression of MUCSAC mRNA and to improve the gastric mucosal blood flow by down-regulating the expression of ETAR mRNA.
Adult ; Capsules ; Drug Therapy, Combination ; Drugs, Chinese Herbal ; therapeutic use ; Endothelin-1 ; biosynthesis ; genetics ; Female ; Gastric Mucosa ; metabolism ; Humans ; Male ; Middle Aged ; Mucin 5AC ; Mucins ; biosynthesis ; genetics ; Peptic Ulcer ; drug therapy ; Phytotherapy ; RNA, Messenger ; biosynthesis ; genetics ; Ranitidine ; therapeutic use ; Receptors, Endothelin ; biosynthesis ; genetics

Interleukin 1 beta (IL-1 beta), a proinflammatory cytokine, is related with inflammatory diseases and it up-regulates MUC2 gene expression and mucin secretion. This study was designed to investigate the signal transduction pathway of the IL-1 beta-mediated MUC2 gene expression and mucin secretion in human airway epithelial cells. In cultured human airway NCI-H292 epithelial cells, the steady state of the mRNA level of MUC2 gene expression and mucin secretion induced by IL-1 were determined by reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme immunoassay, and immunoblot analysis. To observe the signal pathway of the IL-1 beta-mediated MUC2 gene expression and mucin secretion, we used several specific inhibitors. PD98059 (MEK/ERK inhibitor) suppressed IL-1 beta-mediated MUC2 gene expression and mucin secretion, while SB203580 (p38 inhibitor) did not. Ro31-8220 (PKC inhibitor) inhibited IL-1 beta-mediated MUC2 gene expression and mucin secretion. It inhibited ERK phosphorylation, but did not inhibit p38 phosphorylation. LY294002 (PI3K inhibitor) also suppressed MUC2 expression, but did not inhibit any MAPKs phosphorylation. These results suggest that the IL-1 -mediated MUC2 gene expression and mucin secretion in NCI-H292 cells are regulated through activation of the PKC-MEK/ERK pathway, and that PI3K is also involved in the IL-1 beta-mediated MUC2 gene expression and mucin secretion.
1-Phosphatidylinositol 3-Kinase/*metabolism ; Cell Line ; Chromones/pharmacology ; Dose-Response Relationship, Drug ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Epithelium/*enzymology ; Flavonoids/pharmacology ; Humans ; Imidazoles/pharmacology ; Immunoassay ; Immunoblotting ; Indoles/pharmacology ; Interleukin-1/metabolism/*physiology ; Lung/cytology/*metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/*metabolism ; Morpholines/pharmacology ; Mucin-2 ; Mucins/*biosynthesis/metabolism ; Phosphorylation ; Protein Kinase C/*metabolism ; Protein Structure, Tertiary ; Pyridines/pharmacology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Time Factors