| 1. |
- Zhang, Xiaoying, et al.
(författare)
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IL-6 Regulates MMP-10 Expression via JAK2/STAT3 Signaling Pathway in a Human Lung Adenocarcinoma Cell Line
- 2009
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Ingår i: Anticancer research. - 1791-7530. ; 29:11, s. 4497-4501
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Tidskriftsartikel (refereegranskat)abstract
- We previously reported that matrix metalloproteinase (MMP)-10 mRNA levels were significantly lower in tumor tissues than in adjacent normal tissues in human non-small cell lung cancer (NSCLC), whereas protein levels of MMP-10 were higher in the tumor tissues than the adjacent tissues. The mechanism of this divergence is still unknown. In the present stud), the role of Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) on interleukin (IL)-6 mediated regulation of MMP-10 expression was investigated in a human lung adenocarcinoma cell line (A549 cells) and the molecular regulatory mechanism of MMP-10 expression was explored. A549 cells were stimulated by different concentrations of IL-6 with or without AG490, a specific JAK2 inhibitor. It was demonstrated that IL-6 moderately reduced the MMP-10 mRNA levels, whereas it significantly enhanced the MMP-10 protein mass in the A549 cells. This phenomenon mimicked the divergence of mRNA level and protein mass of MMP-10 in human NSCLC. Moreover, the present study indicated that IL-6 regulation of MMP-10 expression was via the JAK2/STAT3 pathway. STAT3 mRNA levels were significantly increased when the cells were treated with IL-6, whereas when AG490 (50 mu M) was added to the cell cultures, IL-6-induced increase of STAT3 mRNA levels was abolished. Meanwhile, AG490 blocked the IL-6-induced inhibition of MMP-10 mRNA as well as blocking the IL-6-induced increase of MMP-10 protein mass in the A549 cells. Neither IL-6 nor AG490 influenced JAK2 mRNA levels in the A549 cell cultures. It is concluded that the JAK2/STAT3 pathway is involved in the IL-6-mediated regulation of MMP-10, and IL-6 can moderately reduce MMP-10 mRNA levels and strongly increase MMP-10 protein mass in human lung adenocarcinoma A549 cells. Contrasting effects of IL-6 on MMP-10 mRNA level and protein concentration in A549 cells may partially explain the divergence of MMP-10 mRNA level and protein mass in human NSCLC.
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| 2. |
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| 3. |
- Chen, Lujun, et al.
(författare)
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Immunolocalisation of tissue factor in esophageal cancer is correlated with intratumoral angiogenesis and prognosis of the patient
- 2010
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Ingår i: Acta Histochemica. - : Elsevier BV. - 0065-1281. ; 112:3, s. 233-239
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Tidskriftsartikel (refereegranskat)abstract
- It has been demonstrated that tissue factor (TF) may be involved in the tumor-derived procoagulatory status and angiogenic modulation in certain solid tumors. In the present study, we examined immunohistochemical localisation of TF in esophageal squamous cell carcinomas (ESCC) from 103 patients. TF immunopositivity was found in 91.3% of all tumor sections, while normal esophageal tissues were immunonegative. Patients were divided into a low TF immunoreactivity group (9 cases of negative and 48 cases of weak positive) and a high TF immunoreactivity group (35 cases of moderate positive and 11 cases of strong positive). TF immunoreactivity was significantly correlated to the presence of distant metastasis (P = 0.0014), while it was not correlated to patient's gender, age, tumor size, depth of tumor invasion or lymph node metastasis. Survival analysis revealed that the overall survival rate in the patients that had high TF immunoreactivity was significantly poorer than those with low TF immunoreactivity (P = 0.0094). Univariate analysis demonstrated that tumor size (P = 0.0095), depth of tumor invasion (P = 0.0050), lymph node metastasis (P = 0.0045) and distant metastasis (P < 0.0001) were effective predictors of prognosis in patients. However, only distant metastasis could independently predict patients' outcomes by the analysis of multivariate proportional hazards regression (P = 0.0043). Furthermore, the intratumoral microvessel density (MVD), evaluated by CD34 immunolabeling, indicated that MVD was positively correlated to the TF immunoreactivity (P = 0.0056). It is concluded that TF immunopositivity in ESCC tissues is strongly correlated to the intratumoral angiogenesis and to poor patient prognosis. (C) 2009 Elsevier GmbH. All rights reserved.
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| 4. |
- Feng, Yue Hua, et al.
(författare)
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Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes
- 2018
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Ingår i: Lipids in Health and Disease. - : Springer Science and Business Media LLC. - 1476-511X. ; 17:1
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Tidskriftsartikel (refereegranskat)abstract
- Background: Scavenger receptor BI (SR-BI) is a classic high-density lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C). Apolipoprotein M (ApoM), as a component of HDL particles, could influence preβ-HDL formation and cholesterol efflux. The aim of this study was to determine whether SR-BI deficiency influenced the expression of ApoM. Methods: Blood samples and liver tissues were collected from SR-BI gene knockout mice, and serum lipid parameters, including total cholesterol (TC), triglyceride (TG), high and low-density lipoprotein cholesterol (HDL-C and LDL-C) and ApoM were measured. Hepatic ApoM and ApoAI mRNA levels were also determined. In addition, BLT-1, an inhibitor of SR-BI, was added to HepG2 cells cultured with cholesterol and HDL, under serum or serum-free conditions. The mRNA and protein expression levels of ApoM were detected by RT-PCR and western blot. Results: We found that increased serum ApoM protein levels corresponded with high hepatic ApoM mRNA levels in both male and female SR-BI-/- mice. Besides, serum TC and HDL-C were also significantly increased. Treatment of HepG2 hepatoma cells with SR-BI specific inhibitor, BLT-1, could up-regulate ApoM expression in serum-containing medium but not in serum-free medium, even in the presence of HDL-C and cholesterol. Conclusions: Results suggested that SR-BI deficiency promoted ApoM expression, but the increased ApoM might be independent from HDL-mediated cholesterol uptake in hepatocytes.
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| 5. |
- Luo, Guanghua, et al.
(författare)
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Expression and localization of apolipoprotein M in human colorectal tissues
- 2010
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Ingår i: Lipids in Health and Disease. - 1476-511X. ; 9
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Tidskriftsartikel (refereegranskat)abstract
- Background: It has been well documented that apolipoprotein M (apoM) is principally expressed in the liver and kidney. However we found that there was weak apoM expression in other tissues or organs too, which could not be ignored. In the present study, we therefore examined apoM expression in human colorectal tissues including cancer tissues, cancer adjacent normal tissues, polyp tissues and normal mucosa as well as inflammatory mucosa. Methods: Tissue samples were collected from patients who underwent surgical resection or endoscopic examination. ApoM mRNA levels were determined by the real-time RT-PCR and apoM protein mass were examined by the immunohistochemistry. Results: ApoM protein can be detected in all colorectal tissues. However, apoM protein mass were significantly lower in the cancer tissues than its matched adjacent normal tissues, polyp tissues, normal mucosa and inflammatory mucosa. In parallel, apoM mRNA levels in the colorectal cancer tissues (0.0536 +/- 0.0131) were also significantly lower than those in their adjacent normal tissues (0.1907 +/- 0.0563) (P = 0.033). Interestingly, apoM mRNA levels in colorectal cancer tissues were statistic significant higher in the patients with lymph node metastasis than the patients without lymph node metastasis (P = 0.008). Patients under Dukes' C and D stages had much higher apoM mRNA levels than patients under Dukes' A and B stages (P = 0.034). Conclusion: It is concluded that apoM could also be expressed in human colorectal tissues besides liver and kidney. ApoM mRNA levels in the colorectal cancer tissues were significantly increased in the patients with lymph node metastasis. Whether increased apoM expression in the patients with lymph node metastasis being related to patients' prognosis and the physiopathological importance of apoM expression in colorectal tissues need further investigation.
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| 6. |
- Shi, Yuanping, et al.
(författare)
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Expression of Zinc Finger 23 Gene in Human Hepatocellular Carcinoma
- 2011
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Ingår i: Anticancer research. - 1791-7530. ; 31:10, s. 3595-3599
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to investigate the relationship between human zinc finger 23 (ZNF23) expression and clinico-pathological characteristics in patients suffering from hepatocellular carcinoma (HCC), and to investigate ZNF23 expression in relation to cell apoptosis. Patients and Methods: Thirty-seven HCC samples were collected and ZFP23 mRNA levels were determined by real-time reverse transcription-polymerase chain reaction (RTPCR). Correlation between ZNF23 expression and patients' clinical characteristics was analyzed. For determining the effect of ZNF23 on cell apoptosis, HepG2 cells were exposed to cisplatin at different concentrations and ZNF23 mRNA assayed. Results: Median relative mRNA levels of ZNF23 mRNA in HCC tissues and adjacent tissues were 8.84 (3.59-15.05) and 22.20 (13.85-42.90), respectively (U=259.5, p<0.01). Median mRNA levels of ZNF23 in patients with Edmondson stage I+II disease [12.80 (4.80-19.50)] were much higher than those of patients with stage III+IV disease [5.01 (2.88-11.68), U=99.00, p<0.05]. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay demonstrated that cisplatin significantly inhibited cell proliferation of HepG2 cells in a dose-dependent manner, which was positively correlated to cell apoptosis (F=27.89, p<0.01), and in response to increasing cisplatin concentrations, ZNF23 mRNA levels increased in the cells. Conclusion: Cisplatin-induced apoptotic effect in HepG2 cells may be mediated via the up-regulation of ZNF23, which suggests that the ZNF23 gene could play an important role in the development of hepatocellular carcinoma.
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| 7. |
- Zhang, Xiaoying, et al.
(författare)
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Expression of MMP-10 in lung cancer
- 2007
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Ingår i: Anticancer research. - 1791-7530. ; 27:4C, s. 2791-2795
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Tidskriftsartikel (refereegranskat)abstract
- Background: Matrix metalloproteinase (MMP)-mediated degradation of the extracellular matrix is a key point in tumor development and expansion. MMP-10 is one of the most important and well-characterized members of the MMP family. In the present study, we examined MMP-10 mRNA and protein levels in non-small cell lung cancer (NSCLC). Patients and Methods: Three endogenous reference genes including GAPDH, beta-actin and 18S rRNA, and MMP-10 mRNA levels were determined using real-time RT-PCR. Immunohistochemical staining was applied to examine MMP-10 protein levels. Both tumor and adjacent normal lung tissues were collected from 32 NSCLC patients. The mRNA levels of GAPDH, beta-actin and 18S rRNA exhibited great differences in tumor tissues and in the adjacent normal tissues. The ratio of mRNA levels in the tumor tissues compared to the adjacent normal tissues followed the pattern GAPDH > beta-actin > 18S rRNA. Thereafter, we chose 18S rRNA as the reference gene for MMP-10 mRNA level determinations. MMP-10 mRNA levels in tumor tissues were significantly lower than those in the adjacent normal tissues (p = 0.0423). However, the MMP- 10 protein levels were higher in the tumor tissues than in the adjacent normal tissues (p=0.0055). The MMP-10 mRNA level was positively-correlated to the MMP-10 protein level in tumor tissues (r=0.4672, p=0.0161), but this correlation was not seen in the adjacent normal tissues (r=-0.0030, p=0.9891). Conclusion: There were no statistical differences in MMP-10 mRNA levels and protein levels in relation to patient's gender, age, tumor stages, tumor size, lymph node metastasis or tumor histological type.
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