Comparative Analysis of Platelet-rich Plasma Effect on Tenocytes from Normal Human Rotator Cuff Tendon and Human Rotator Cuff Tendon with Degenerative Tears

BACKGROUND: Platelet-rich plasma (PRP) stimulates cell proliferation and enhances matrix gene expression and synthesis. However, there have been no comparative study of the PRP effect on the normal and degenerative tenocytes. The purpose of this study was to compare the effect of PRP on tenocytes from normal and degenerative tendon. METHODS: Tendon tissues were obtained from patients undergoing arthroscopic repair (n=9) and from healthy donors (n=3). Tenocytes were cultured with 10% (vol/vol) platelet-poor plasma, PRP activated with calcium, and PRP activated with calcium and thrombin. The total cell number was assessed at days 7 and 14. The expressions of type I and III collagen, decorin, tenascin-C, and scleraxis were evaluated by quantitative real-time reverse transcriptase polymerase chain reaction. The total collagen and glycosaminoglycan (GAG) synthesis was evaluated at days 7 and 14. RESULTS: No differences were observed between the groups at day 7, but cell proliferation was remarkably increased in tenocytes from the degenerative tendon at day 14. In both tenocyte groups, the gene expressions of type I and III collagen were up-regulated. GAG synthesis was greater in the normal tendon, whereas the expressions of decorin and tenascin-C were increased in tenocytes from the degenerative tendon. Tenocytes from the degenerative tendon had higher fold-change of GAG synthesis and a lower collagen III/I ratio than normal tenocytes. CONCLUSIONS: PRP promoted the cell proliferation and enhanced the synthesis of tendon matrix in both groups. PRP has a greater positive effect on cell proliferation, matrix gene expression and synthesis in tenocytes from degenerative tendon.

NecroX-5 exerts anti-inflammatory and anti-fibrotic effects via modulation of the TNFα/Dcn/TGFβ1/Smad2 pathway in hypoxia/reoxygenation-treated rat hearts

Inflammatory and fibrotic responses are accelerated during the reperfusion period, and excessive fibrosis and inflammation contribute to cardiac malfunction. NecroX compounds have been shown to protect the liver and heart from ischemia-reperfusion injury. The aim of this study was to further define the role and mechanism of action of NecroX-5 in regulating infl ammation and fi brosis responses in a model of hypoxia/reoxygenation (HR). We utilized HR-treated rat hearts and lipopolysaccharide (LPS)-treated H9C2 culture cells in the presence or absence of NecroX-5 (10 µmol/L) treatment as experimental models. Addition of NecroX-5 signifi cantly increased decorin (Dcn) expression levels in HR-treated hearts. In contrast, expression of transforming growth factor beta 1 (TGFβ1) and Smad2 phosphorylation (pSmad2) was strongly attenuated in NecroX-5-treated hearts. In addition, signifi cantly increased production of tumor necrosis factor alpha (TNFα), TGFβ1, and pSmad2, and markedly decreased Dcn expression levels, were observed in LPS-stimulated H9C2 cells. Interestingly, NecroX-5 supplementation effectively attenuated the increased expression levels of TNFα, TGFβ1, and pSmad2, as well as the decreased expression of Dcn. Thus, our data demonstrate potential antiinflammatory and anti-fibrotic effects of NecroX-5 against cardiac HR injuries via modulation of the TNFα/Dcn/TGFβ1/Smad2 pathway.

Advances in the research of modulation of dermal collagen fibrin assembly by decorin / 中华烧伤杂志

Formation of dermal collagen fiber is a complicated and sequential process with the progressive assembly of collagen. Collagen monomers form stepped and orderly protofibrils through longitudinal displacement. Subsequently, protofibrils or protofibrils and collagen are bonded by covalent bonds to form orderly lamellar structure of collagen fibers. Then collagen fibers are tightly wound into coarse collagen fiber bundles by covalent crosslinking. Decorin is a multifunctional small leucine-rich proteoglycan. It can prevent the aggregation of protofibrils by binding to the specific site of collagen with its core protein, and adjusting the spacing between the protofibrils with its glycosaminoglycan chain. Thus, by effecting the formation of collagen fibers with regulation of collagen assembly, decorin may help prevent scar formation and even promote regeneration.

Decorin accelerates the liver regeneration after partial hepatectomy in fibrotic mice / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Considering the existence of a large number of liver cell degeneration and necrosis in fibrotic liver, liver function was damaged severely and could not effectively regenerate after partial hepatectomy (PHx). The aim of this study was to investigate whether decorin (DCN) could promote the liver regeneration after PHx in fibrotic mice.</p><p><b>METHODS</b>Forty mice (5-week-old, Balb/c) were injected with CCl4 intraperitoneally and liver fibrosis model was established after 5 weeks. The survival mice were randomly divided into two groups: control group and DCN group. Then, we performed 70% PHx on all these mice and injected DCN or phosphate-buffered saline plus normal saline (NS) to each group, respectively, after surgery. Liver body weight ratio (LBR), quantitative real-time polymerase chain reaction, and immunohistochemistry were used to analyze liver regeneration and fibrosis degree in both groups, and to find out whether exogenous protein DCN could promote the regeneration of fibrosis liver after PHx.</p><p><b>RESULTS</b>Expressions of a-smooth muscle actin (SMA) mRNA and LBR had significant increases in the DCN group at postoperative Day 3 (POD 3, P < 0.05). The protein expressions of CD31, a-SMA, and tumor necrosis factor (TNF)-a were higher in the DCN group than those in the control group by immunohistochemistry at POD 3 (P < 0.05).</p><p><b>CONCLUSION</b>Exogenous protein DCN could promote liver regeneration after PHx in fibrotic mice.</p>

Decorin prevents the development of CCl₄-induced liver fibrosis in mice / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Liver fibrosis normally progresses to cirrhosis and destroys the normal architecture of the liver, resulting in liver dysfunction and irreversible cirrhosis. The aim of this study was to investigate the anti-fibrosis effect and the possible underlying mechanisms of decorin.</p><p><b>METHODS</b>The mice model of liver fibrosis was induced by intraperitoneal injection of 50% (v/v) of carbon tetrachloride (CCl4) diluted in olive oil (1 ml/kg body weight) once every 2 days for 5 weeks. Three weeks after injecting CCl4 intraperitoneally, mice were randomly divided into normal control with vehicles only (olive oil), mouse model given CCl4 only, and CCl4 plus decorin (DCN, 250 µg/kg). Two weeks later, all the mice were sacrificed and their liver tissues were analyzed for the expressions of genes related to liver fibrosis and under hematoxylin-eosin staining, Masson staining, and immunohistochemical staining of all groups. Aspartate transaminase, alanine transaminase, and total bilirubin of the serum were determined for evaluation of the liver function.</p><p><b>RESULTS</b>Exogenous protein decorin could reduce liver fibrosis induced by CCl4 in mice. The degree of fibrosis in the experimental group was alleviated, and the contents of collagen fibers were lower in the experimental group than those of the control group. In addition, expressions of transforming growth factor β1 and α-smooth muscle actin decreased in the experimental group.</p><p><b>CONCLUSIONS</b>Taking liver fibrosis model of mouse as the experimental target and by injecting exogenous protein decorin into the model, we confirmed that decorin could inhibit the expression of proteins related to fibrosis and reduce the formation of liver fibrosis in mice.</p>

Immunohistochemical expression of biglycan and decorin in the pulp tissue of human primary teeth during resorption

Primary teeth are interesting models that can be used to study physiological and pathological processes involving cells and extracellular matrices in hard and soft tissues. This study investigated the expression and distribution of biglycan and decorin-the non-collagenous components of the extracellular matrix-in primary teeth tissue, during physiological root resorption. Thirty healthy human primary teeth were grouped together according to root length: Group I - two-thirds root length, Group II - one-third root length, and Group III - teeth with no root. The streptavidin-biotin-peroxidase immunohistochemical method was used with antibodies against the previously named antigens. The proteoglycans studied were found in the pulp and dentin extracellular matrix in all groups without any differences in the proteins, among the groups. Biglycan was observed mainly in predentin and in pulp connective tissue in the resorption area. In addition, decorin was observed mainly in pulp connective tissue, but near the resorption area. Biglycan and decorin were distributed differentially in the dental tissues. The present immunohistocytochemical data, combined with previously reported data, suggest that these proteoglycans could be involved in regulating the physiological resorption process in healthy primary teeth.

Human decorin regulates proliferation and migration of human lung cancer A549 cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Decorin is a small leucine-rich proteoglycan and it plays an important role in regulation of cell growth and migration in various tumor cell lines. Decorin was found down-regulated in non-small cell lung cancer tissue and may be involved in regulation of lung cancer development.</p><p><b>METHODS</b>In this study, lentivirus-mediated RNA interference and over expression were employed to change the expression levels of decorin in lung cancer A549 cells. We tested the cell cycle of A549 cells and the expression of transforming growth factor (TGF)-β, cyclin D1, epidermal growth factor receptor (EGFR), P53, and P21.</p><p><b>RESULTS</b>We found that up-regulation of decorin could inhibit proliferation, block cell cycle at G1 and decrease invasive activity of A549 cells. Moreover, we also show that up-regulation of decorin induced significant decreases of TGF-β1, cyclin D1 expression, phosphorylation of EGFR, and increases of P53 and P21 expression. Opposite results were observed in A549 cells with down-regulation of decorin.</p><p><b>CONCLUSION</b>Our results suggest that decorin is a key regulator involved in proliferation and migration of A549 cells.</p>

Biological functions of decorin in cancer / 癌症

Decorin is a member of the extracellular matrix small leucine-rich proteoglycans family that exists and functions in stromal and epithelial cells. Accumulating evidence suggests that decorin affects the biology of various types of cancer by directly or indirectly targeting the signaling molecules involved in cell growth, survival, metastasis, and angiogenesis. More recent studies show that decorin plays important roles during tumor development and progression and is a potential cancer therapeutic agent. In this article, we summarize recent studies of decorin in cancer and discuss decorin's therapeutic and prognostic value.

Decorin and TGF-beta Expression after Partial Myotomy of the Extraocular Muscle in Rat

PURPOSE: To report the expression of decorin and TGF-beta in partial myotomy of the extraocular muscle in rats. METHODS: Partial myotomy of the superior rectus muscle was performed on the right eye of 10 Sprague-Dawley rats followed by exposure of the left superior rectus muscle and a simple suture of the conjunctiva. The bilateral superior rectus muscle was obtained from all rats at 2 weeks postoperatively. The tissues were observed under light microscopy with hematoxylin-eosin, Masson's trichrome staining and immunohistochemistry. RESULTS: Histological examinations of the surgical area at 2 weeks after postoperatively showed irregularly concentrated fibrosis on light microscopy with hematoxylin-eosin and Masson's trichrome staining of the experimental eyes. Immnohistochemistry showed that expression of decorin was in the same location as TGF-beta in the experimental group. CONCLUSIONS: The expression of decorin was found in the healing process after partial myotomy of the extraocular muscle in rats. Immunohistochemistry showed that expression of decorin was in the same location as with TGF-beta.

A Novel Decorin Gene Mutation in Congenital Hereditary Stromal Dystrophy: A Korean Family

A 43-year-old man developed decreased vision in the right eye that had persisted for seven years. Under slit lamp examination, corneal clouding was noted with normal endothelium and ocular structure. From the clinical evidence, we suspected that the patient had congenital hereditary stromal dystrophy (CHSD). He and his family underwent a genetic analysis. Penetrating keratoplasty was conducted, and the corneal button was investigated for histopathologic confirmation via both light and electron microscopy. The histopathologic results revealed mildly loosened stromal structures, which exhibited an almost normal arrangement and differed slightly from the previous findings of CHSD cases. With regard to the genetic aspects, the patient and his mother harbored a novel point mutation of the decorin gene. This genetic mutation is also distinct from previously described deletion mutations of the decorin gene. This case involved delayed penetration of mild clinical symptoms with the histological feature of a loosened fiber arrangement in the corneal stroma. We concluded that this condition was a mild form of CHSD. However, from another perspective, this case could be considered as "decorin gene-associated corneal dystrophy," which is distinct from CHSD. Further evaluation will be required for appropriate clinical, histopathologic and genetic approaches for such cases.

Mechanisms of decorin inhibiting epithelial-to-mesenchymal transition induced by transforming growth factor beta1 in renal tubular epithelial cells / 中华儿科杂志

<p><b>OBJECTIVE</b>To investigate the mechanisms of decorin inhibiting epithelial-to-mesenchymal transition (EMT) induced by transforming growth factor beta1 (TGF-beta1) in renal tubular epithelial cells.</p><p><b>METHOD</b>HK-2 cells in vitro were divided into 4 groups: (1) negative control group; (2) decorin group, added with decorin 100 ng/ml ; (3) TGF-beta1 group, added with TGF-beta1 10 ng/ml; (4) decorin and TGF-beta1 group, added with decorin 100 ng/ml and TGF-beta1 10 ng/ml. The protein level of phosphor-ERK, phosphor-PI3K, phosphor-Smad(3) and beta-catenin was detected by Western blotting method. The snail mRNA level was tested by real time-PCR, while the lymphoid enhancer factor-1 (LEF-1) mRNA level was measured by RT-PCR.</p><p><b>RESULTS</b>The snail (2.59 +/- 0.70:1.02 +/- 0.13) and LEF-1 mRNA (1.85 +/- 0.08:0.30 +/- 0.11) were significantly up-regulated, meanwhile the protein level of phosphor-ERK (1.11 +/- 0.09:0.47 +/- 0.07), phosphor-PI3K (14.79 +/- 1.02:2.48 +/- 0.06), phosphor-Smad(3) (0.95 +/- 0.02:0.08 +/- 0.01) and beta-catenin (1.46 +/- 0.20:0.49 +/- 0.05) were significantly increased in TGF-beta1 group compared to control group, while there were no statistically significant difference in all figures between control group and decorin group. The phosphor-ERK protein level (0.58 +/- 0.08) and the snail mRNA level (1.24 +/- 0.03) were significantly down-regulated in TGF-beta1 and decorin group compared to TGF-beta1 group, however there were no statistically significant differences in the level of phosphor-PI3K (15.84 +/- 1.64), phosphor-Smad(3) (0.90 +/- 0.04) and beta-catenin (1.42 +/- 0.09) between these two groups.</p><p><b>CONCLUSION</b>Decorin inhibited EMT induced by TGF-beta1 which may be through blocking the ERK signal transduction pathway.</p>

Pro-apoptotic effect of decorin on rat mesangial cells in vitro / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the effects of over-expression of decorin (DCN) gene on apoptosis of cultured rat mesangial cells (MsC).</p><p><b>METHODS</b>PcDNA3.1A-DCN plasmid was transfected into cultured rat MsC by the induction of liposome and positive clones were selected by treating the cells with G418. The MsC clones stably expressing DCN (MsC/DCN) were confirmed by cellular immunofluorescence, reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot. The DCN-siRNA was used for blocking DCN expression in MsC/DCN, and was confirmed by Western blot. The apoptosis of MsC was assayed by flow cytometry and Hoechst staining. Expression of Caspase-3 was assayed by Western blot.</p><p><b>RESULTS</b>Positive clones with DCN over-expression were established. The apoptotic rate in MsC/DCN was (20.40 +/- 8.01)% and was much higher than the (2.07 +/- 0.99)% in MsC (P < 0.01). Some of the MsC/DCN cells showed typical morphologic changes of apoptosis. The protein expression of active Caspase-3 was also significantly increased in MsC/DCN compared to MsC (P < 0.01). DCN-siRNA transfection not only significantly blocked the expression of DCN and reduced the rate of apoptotic cells, but also down-regulated the expression of active Caspase-3.</p><p><b>CONCLUSIONS</b>Over-expression of DCN induces apoptosis of cultured rat MsC in vitro. This effect of DCN inducing apoptosis suggests a novel strategy for regulating the proliferation of MsC in glomerular diseases.</p>

Adhering effect of Leptospira interrongan to major extracellular matrix molecules / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To determine the adhering ability of Leptospira interrogans to extracellular matrix molecules (ECM) of host cells and its diversity.</p><p><b>METHODS</b>The infection models of L. interrogans serogroup Icterohaemorrhagiae serovar lai strain 56601 to J774A.1, L929 and Vero cells were established. Fontana silver impregnation method was applied to demonstrate the adhering effect of microbes to extracellular matrix (ECM) of the cells. ELISA methods were established to detect the adhering effects of L. interrogans to ECM molecules laminin (LN), fibronectin (FN), decorin (DEN) and collagen1, 2, 4 (COL1, 2, 4). A competitive inhibition test was performed to verify the results.</p><p><b>RESULT</b>L. interrogans strain 56601 adhered the ECMs of L929, J774A.1 and Vero cells with its one or two sites. L. interrogans strain 56601 adhered all six ECM molecules; the adhering effects to COL1, LN, COL4 were relatively stronger. The adhering effects were markedly decreased after the microbes were pre-incubated with corresponding ECM molecules.</p><p><b>CONCLUSION</b>L. interrogans adheres to host cells through ECM molecules; LN, FN, DEN, COL1, COL2 and COL4 are the receptor molecules with different adhesion intensity.</p>

The effect of basic fibroblast growth factor on the gene expression of decorin by periodontal ligament fibroblasts in culture / 华西口腔医学杂志

<p><b>OBJECTIVE</b>To study the effect of basic fibroblast growth factor (bFGF) on the gene expression of decorin by periodontal ligament fibroblasts (PLFs) in culture, and discuss the effect of bFGF in periodontal regeneration.</p><p><b>METHODS</b>Human PLFs were cultured and stimulated by exogenous bFGF. Gene expression of decorin was assessed by semi-quantitive RT-PCR.</p><p><b>RESULTS</b>The mRNA expression of decorin was suppressed by bFGF and the effect was dose-dependent. When the dose of bFGF increased, the inhibitive effect decreased.</p><p><b>CONCLUSION</b>Decorin has many biological effects. The inhibitive effect may be one of important factors which participate in the healing process of periodontitis, and provide partly theoretical basis of bFGF in periodontal regeneration.</p>

The action of decorin in anti-fibrosis and anti-cancer / 生物医学工程学杂志

Decorin (DCN) is a member of the small leucine-rich proteoglycan gene family. Many studies indicated that DCN inhibited fibrosis and scar-formation by neutralization of TGF-P and interfering the binding of TGF-beta with its receptor, which induced ectopic deposition of extracellular matrix. Additionally, DCN can prevent the proliferation and metastasis of tumor cells by activating EGFR/MAPK/p21 signal pathway and inhibiting the cell proliferation pathway mediated by EGF-EGFR. It is suggested that the recombinant DCN had potential pharmaceutical potency in treatment of chronic fibrosis and neoplasm for its critical biological activities and low immunogenicity.

The antagonistic effect of recombinant human decorin on TGF-beta1 stimulation of fibroblasts in collagen lattices / 中华烧伤杂志

<p><b>OBJECTIVE</b>To mimic contact pattern between decorin and TGF-beta1, in vivo, and investigate the antagonistic effect of recombinant human decorin on TGF-beta1 stimulation of hypertrophic scar fibroblasts in collagen lattices.</p><p><b>METHODS</b>Fibroblasts populated collagen lattices (FPCL) model was adopted in the study, and they were divided into control group, decorin group [2mg/L recombinant human decorin (rh-decorin) was administered to FPCL], TGF-beta1 group (5 microg/LTGF-beta1 was administered to the culture medium), and TGF-beta1 + decorin group (2mg/L rh-decorin was administered to FPCL, then culture medium containing 5 microg/L TGF-beta1 was added into FPCL). Changes in PAI-1 and alpha-SMA protein expression in scar fibroblasts in collagen lattices were detected with Western blotting at 12 post-administration hour (PAH), 24 PAH, 48 PAH, and 72 PAH, and expressions of PAI-1 and alpha-SMA mRNA were concomitantly examined by RT-PCR.</p><p><b>RESULTS</b>The contraction of FPCL at each time-point in control group was obviously attenuated compared with that in decorin group, but it was significantly intensified compared with that in TGF-beta1 group. The expression of PAI-1 and alpha-SMA mRNA and protein in TGF-beta1 group (3482 +/- 211, 4320 +/- 272, 0.89 +/- 0.15, 0.56 +/- 0. 11) were markedly increased than those in control group (1764 +/- 147, 1699 +/- 146, 0.29 +/- 0.06, 0.21 +/- 0.06, P < 0.01), while no obvious difference of them was found between control and other two groups.</p><p><b>CONCLUSION</b>Stimulation of scar fibroblasts by TGF-beta1, can be suppressed when rh-decorin is blended into collagen lattices, indicating that decorin is effective in neutralizing TGF-beta1 in vitro. The pathogenesis of hypertrophic scar might be related to up-regulation of TGF-beta1 with the lack of decorin after cutaneous injury.</p>

Screening differentially expressed genes in human bone marrow stromal cells at defined stage of differentiation / 生理学报

To screen differentially expressed genes involved in osteogenic differentiation of human bone marrow stromal cells (BMSCs) at defined stages, subtractive cDNA library was established by means of suppression subtractive hybridization. The BMSCs cultured for 12 and 21 d were used as driver and tester, respectively. A subtract library was successfully constructed and five positive clones were selected from the library. Sequencing analysis and homology comparison showed that the five clones differentially expressed in BMSCs cultured for 21 d were at least 90% homologous with the known genes in human GenBank. It was interestingly found that the osteogenic BMSCs cultured for 21 d differentially expressed decorin and Bax inhibitor 1. RT-PCR was performed to confirm the differentially expressed genes. The results showed that the expression of Bax inhibitor 1 was significantly higher in the cells of 21-day than that of 12-day, while the expression of decorin was only detected in the cells of 21-day.

Immunohistochemical localization of leucine-rich proteoglycans in the developing periodontal tissues of mice / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To study the distribution and expression of fibromodulin, decorin and biglycan in developing normal periodontal tissues, so as to understand its role in periodontal tissue formation.</p><p><b>METHODS</b>Thirty six BALB/c mice in different developing stages were killed and their bilateral mandibular first molars with surrounding alveolar bones and gingival tissues were taken out, Power Vision two steps immunohistochemical method with anti-fibromodulin, anti-decorin and anti-biglycan was used to detect the tissue distribution and cellular localization of fibromodulin and related proteoglycans, decorin and biglycan.</p><p><b>RESULTS</b>Fibromodulin was strongly expressed in the subcutaneous gingival connective tissue, periodontal ligament, mainly in gingival and periodontal fibroblasts as well as their matrices. Strong expression was also noted in the area close to the interfaces of periodontal ligament-alveolar bone and periodontal ligament-cementum. Decorin was strongly expressed in the area of gingival connective tissue, periodontal ligament and the surface of alveolar bone, while biglycan was stained evidently in gingival connective tissue throughout the period of investigation, but negative in the surface of alveolar bone and osteoblasts.</p><p><b>CONCLUSIONS</b>Fibromodulin may interact with decorin and biglycan to regulate the network formation of gingival connective tissues and periodontal collagen fibers, and may be involved in mineralization of the alveolar bone and cementum.</p>

The content of decorin and its mRNA expression in normal human skin and hyperplastic scars / 中华烧伤杂志

<p><b>OBJECTIVE</b>To investigate the content of decorin and its mRNA expression in normal human skin and hyperplastic scars at different stages, so as to explore the relationship between the change of decorin and its synthesis.</p><p><b>METHODS</b>Scar tissue samples from 22 patients undergoing scar excision and 10 specimens of normal skin or prepuce were obtained. The content and distribution of decorin in the tissue samples were determined with immunohistochemistry and Western blot, and the expression of decorin mRNA was detected by in situ hybridization.</p><p><b>RESULTS</b>The content of decorin was rich in the normal skin dermis with lower expression of the mRNA. In contrast, the decorin content was scarce in hyperplastic scars (HS) within 6 months, but increased gradually beginning from 7 to 12 months, and increased continuously for 13 to 36 months. There was no difference between the decorin content in normal skin and that in HS after 36 months (P > 0.05). Furthermore, the mRNA expression level in HS tissue was lower than that in normal skin within 6 months, but increased from 7 to 12 months. The mRNA expression continuously increased during 13 to 36 months and then returned to the level similar to that in normal skin thereafter.</p><p><b>CONCLUSION</b>The decrease of decorin in hyperplastic scar was resulted primarily from reduced synthesis. The increase in decorin level coincided with the time of scar tissue stabilization, which implied that the delayed appearance was correlated with the formation of HS.</p>

DNA chip analysis of gene expression patterns in poorly-differentiated human stage I lung adenocarcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To screen genes with abnormal expression in poorly-differentiated human lung adenocarcinoma at stage I with cDNA chip.</p><p><b>METHODS</b>The mRNA was extracted from cancer tissue and matched normal lung tissue, and was labeled by Cy5-dUTP or Cy3-dUTP as probes. Subsequently, the mixed probes were hybridized to the cDNA chip containing 8192 genes. The information was obtained by managing the cDNA chip with ScanArray4000 scanner and GenePix3.0 software.</p><p><b>RESULTS</b>Five hundred and eighty genes were differentially expressed between cancer and normal lung tissue. Compared with normal lung tissue, 405 genes were up-regulated and 175 genes were down-regulated in cancer tissue. These genes are involved in different cell activities such as growth regulation and signal transduction. Among the 66 genes with remarkable differential expression between the two tissues, 39 were up-regulated and 27 down-regulated.</p><p><b>CONCLUSION</b>Many different kinds of genes are possibly involved in the initiation and progression of human lung adenocarcinoma. cDNA chip technique might be a useful method in screening lung cancer implicated genes.</p>