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<p><b>OBJECTIVE</b>To detect protein expression of ERK(1), ERK(2), JNK(1), p38 and MEK(1), MEK(2) in human hepatocellular carcinoma and adjacent non-neoplastic liver.</p><p><b>METHODS</b>In 16 surgically resected hepatocellular carcinoma and para-carcinoma tissues, Western blotting was used to detect expression of ERK(1), ERK(2), JNK(1), p38 and MEK(1), MEK(2).</p><p><b>RESULTS</b>In all cases, ERK(1), ERK(2), p38 expression in hepatocellular carcinoma was significantly higher than that in para-carcinoma: integral optic density (IOD) of ERK(1) was 300 +/- 98 in carcinoma and 98 +/- 48 in para-carcinoma tissues (t = 2.519, P < 0.01); IOD of ERK(2) was 587 +/- 83 in carcinoma and 232 +/- 96 in para-carcinoma tissues (t = 2.745, P < 0.01); IOD of p38 was 270 +/- 85 in carcinoma and 107 +/- 88 in para-carcinoma tissues (t = 2.491, P < 0.01). JNK(1) expression in hepatocellular carcinoma was significantly lower than that in para-carcinoma; IOD of JNK(1) was 111 +/- 93 in carcinoma and 292 +/- 109 in para-carcinoma tissues (t = 2.473, P < 0.01). Protein levels of MEK(1) and MEK(2) in carcinoma were significantly higher than in para-carcinoma. IOD of MEK(1) was 1 418 +/- 244 in carcinoma and 806 +/- 90 in para-carcinoma tissues (t = 2.546, P < 0.01). IOD of MEK(2) was 1 041 +/- 122 in carcinoma and 468 +/- 40 in para-carcinoma tissues (t = 2.861, P < 0.01).</p><p><b>CONCLUSIONS</b>ERK(1), ERK(2), MEK(1) and MEK(2) in the signal transduction pathway for cell proliferation are significantly overexpressed and the expression of JNK(1) is lower in hepatocellular carcinoma. Their unbalance is one of the important reasons for the over growth and infinite proliferation of the hepatocellular carcinoma cell. The p38 and JNK(1) may be activated by different pathway.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Carcinoma, Hepatocellular , Enzyme Activation , JNK Mitogen-Activated Protein Kinases , Liver Neoplasms , MAP Kinase Kinase 1 , Mitogen-Activated Protein Kinase Kinases , Mitogen-Activated Protein Kinases , Metabolism , Protein Serine-Threonine KinasesABSTRACT
<p><b>OBJECTIVE</b>To investigate the prevalence of depressive disorder in patients undergoing general surgical operations.</p><p><b>METHODS</b>One hundred and four patients who had undergone general surgical operations were investigated. Each patient filled in the self rating depression scale (SDS) as the baseline data.</p><p><b>RESULTS</b>Among these patients 40.4% of them had depressive disorder. The major factors for the prevalence of depression were sex, educational background and malignant diseases.</p><p><b>CONCLUSIONS</b>A certain proportion of patients undergoing general surgical operations have depressive disorder. It is important to recognize and treat for this disorder.</p>
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Depressive Disorder , Epidemiology , Prevalence , Surgical Procedures, Operative , PsychologyABSTRACT
Objective To investigate the expression of a novel oncogene Stat3 in colorectal cancer. Methods Western blot analysis was performed on cancerous and normal colonic tissue of 45 patients with colorectal carcinoma. ResultsStat3 protein level increased in colorectal cancer compared with adjacent normal mucosa ( P
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Objective To clarify the role of a cell cycle regulator, cyclin D1 and CDK6 in patients with gastric carcinoma. Method Tissue samples from 48 patients with gastric carcinoma were included in the current study. Expression levels of cyclin Dl and CDK6 in samples of normal mucosa and tumor tissue were analyzed by Western blot. Result Overexpression of cyclin Dl and CDK6 protein were demonstrated in 58% and 69% of gastric cancer tissues, respectively. Several clinicopathologic parameters, including depth of tumor invasion, pathologic lymph node status and tumor stage ( P
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Objective To investigate the relationship between HPV infection and human colorectal carcinogenesis. Methods Colorectal carcinoma specimens from 72 Chinese patients were studied. DNA extracted from colorectal tissue was screened for HPV L1 by polymerase chain reaction (PCR), HPV subtype 6,11, 16, and 18 were detected by PCR using specific primers and in situ hybridization using specific probe. Results Twenty-four specimens out of 72 (33%) colorectal cancer were HPV L1 positive. The normal colorectal mucosa was HPV L1 negative. The location, infiltration and metastasis of colorectal carcinoma were all significantly related with HPV infection. The predominant HPV subtype was HPV 16,which was found in 58% of all HPV-positive colorectal carcinoma. Conclusion The presence of HPV DNA suggests that HPV may be involved in the carcinogenesis of colorectal carcinoma. HPV infection is closely related with the malignant potential of colorectal cancer.
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Objective To explore the mechanism of HPV infection in carcinogenesis and progression of colon cancer. Methods Human colon cancer cells, HCT116 (with wild-type p53) and SW480 (with mutant-type p53), were transfected by HPV16 E6E7 oncogenes using a recombinant adeno-associated virus vector system. The transfection efficiency was determined by flow cytometry. The expression of HPV16 E6 genes was determined by Western blot. The cell proliferation and cell cycle was studied by MTT method and flow cytometry. Results Western blot confirmed the expression of E6 gene in colon cells that were infected by rAAV-E6E7. The population doubling time of HCT116 cell, which was more than 48 hours at control group, decreased to 33 hours. HPV16 E6E7 increased cell percentage of S phase and decreased cell percentage of G0/G1. The population doubling time of SW480 cell was 77.06% decreased and the OD540 was 47.18% increased with interference of HPV16 E6E7 gene. Conclusion HPV16 E6E7 oncogene precipitates the proliferation and positively controls cell cycle of HCT116 and SW480 human colon cancer cells. HPV infection may closely relate to the carcinogenesis and progression of colon cancer.
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Objective To explore the effect of EBV infection on proliferation and invasiveness of gastric cancer cell. Method BGC823, an EBV-negative human gastric cancer cell line, was infected by EBV. The cell proliferation and ability of invasion were studied by MTT method and in vitro invasive assay, respectively. Cell cycle was investigated by flow cytometry. RT-PCR was used to detect the EBNAs, LMP1 and EBER1 in the infected cell. Result The A ratio of EBV-infected cells increased by 34. 34% and the population of invasive cells increased by 28.72%. The cell percentage of S phase, which was 36. 7% at control group cell, was increased to 41. 9% while the cell percentage of G0/G1 was decreased. EBNA1 and EBER1 were detected in EBV infected gastric cancer cells while EBNA2 and LMP1 were both negative. Conclusion Epstein-Barr virus infection promoted proliferation and upregulated invasion of human gastric cancer cell. EBV infection may play an important role in the carcinogenesis and progression of human gastric cancer.
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AIM: The purpose of the study was to examine colon cancer cell lines to determine whether Stat5b/Survivin plays an important role in the process of apoptosis in colon cancer cells. METHODS: Protein lysates were extracted from colon cancer cells. Human colon cancer cell line HT29 was transfected with Stat5b antisense oligonucleotide mediated by liposome. MTT assay was used to measure the proliferation. Flow cytometry was applied to analyze the cell cycle and apoptosis. EMSA was used to detect the activity of Stat5. Western blotting was applied to measure the expression of Stat5, p-Stat5, cyclin D1, Survivin, Bcl-2 and Bcl-xL. RESULTS: Targeting of Stat5 using antisense oligonucleotide against the translation site resulted in apoptosis and downregulaed the expressions of Stat5, p-Stat5, cyclin D1 and Survivin, but not Bcl-2 and Bcl-xL. CONCLUSION: Constitutive activation of Stat5 is associated with the carcinogenesis of colon cancer cells. Blocking of Stat5 signaling inhibits the expression of Survivin and induces apoptosis in colon cancer cells.