| 651. |
- 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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| 652. |
- 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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| 653. |
- Zheng, Biying, et al.
(författare)
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Genetic polymorphism of chemokine receptors CCR2 and CCR5 in Swedish cervical cancer patients
- 2006
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Ingår i: Anticancer research. - 1791-7530. ; 26:5B, s. 3669-3674
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Tidskriftsartikel (refereegranskat)abstract
- Chemokines are chemotactic cytokines that orchestrate leukocyte trafficking in tissues, thus, playing an important role in regulation of immunological processes. The aim of this study was to investigate the association of human papillomavirus (HPV) infection and cervical cancer with two DNA polymorphisms of the chemokine receptors CCR5-Delta 32 and CCR2-64L The study material consisted of 50 cervical intraepithelial neoplasia (CIN) cases and 50 of age and sampling-date matched controls, 100 invasive cervix cancer cases and 100 of their corresponding matched disease-free controls. Pyrosequencing (TM) was employed to genotype the CCR2-64I polymorphism. CCR5-Delta 32 was genotyped using standard PCR fragment length analysis. The frequencies of CCR2 and CCR5 genotypes from 150 patients and 150 healthy controls were representative of the general population according to the Hardy-Weinberg equilibrium analysis. Risk association was computed with conditional logistic regression analysis. HPV-positive individuals with the rare CCR5 Delta 32/Delta 32 genotype have a risk of 4.58 (CI=0.40-52.64, p-valite=0.045) compare to HPV negative group. The Delta-32 mutation on the CCR locus is imperceptibly associated with increased risk of HPV infection. In total, cervical neoplasia was not associated with genetic polymorphism of CCR2 and CCR5.
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| 654. |
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| 655. |
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| 656. |
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| 657. |
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| 658. |
- Öhman, Jenny, et al.
(författare)
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Presence of CD3-Positive T-Cells in Oral Premalignant Leukoplakia Indicates Prevention of Cancer Transformation
- 2015
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Ingår i: Anticancer Research. - 0250-7005. ; 35:1, s. 311-317
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Tidskriftsartikel (refereegranskat)abstract
- Aim: Leukoplakias (LPLs) are lesions in the oral mucosa that have a potential to transform into oral squamous cell carcinoma (OSCC). As the degree of immunosurveillance may be important for this transformation to occur, the aim of this study was to determine the presence of immune cells in LPLs with dysplasia in relation to later development of OSCC. Materials and Methods: Biopsies from 16 patients with clinical diagnosis of LPL and histopathological diagnosis of hyperkeratosis with dysplasia were immunostained with antibodies to detect CD3(+) T cells, CD1a(+) LCs, Ki-67(+) and p53-expressing cells. Patients were divided into two groups: LPL with dysplasia that transformed into OSCC (LPL-dys) and that which did not (LPL-ca). Results: Quantitative analyses showed significantly lower numbers of CD3+ T-cells in LPL-ca than in LPL-dys. No significant differences were detected when comparing LPL-dys and LPL-ca regarding CD1a(+), p53(+) and Ki-67(+) cells. Conclusion: The number of CD3-expressing T-cells may be important for preventing malignant transformation of LPL.
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