scholarly journals Antimetastatic Potential of Rhodomyrtone on Human Chondrosarcoma SW1353 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Malatee Tayeh ◽  
Ramida Watanapokasin
Keyword(s):  
Cell Migration ◽  
Cell Viability ◽  
Cancer Metastasis ◽  
Gelatin Zymography ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Sw1353 Cell ◽  
Human Chondrosarcoma ◽  
Dose Dependent Fashion ◽  
Dose Dependent

Chondrosarcoma is primary bone cancer, with the forceful capacity to cause local invasion and distant metastasis, and has a poor prognosis. Cancer metastasis is a complication of most cancers; it is one of the leading causes of cancer-related death. Rhodomyrtone is a pure compound that has been shown to induce apoptosis and antimetastasis in skin cancer. However, the inhibitory effect of rhodomyrtone on human chondrosarcoma cell metastasis is largely unknown. Effect of rhodomyrtone on cell viability in SW1353 cell was determined by MTT assay. Antimigration, anti-invasion, and antiadhesion were carried out to investigate the antimetastatic potential of rhodomyrtone on SW1353 cells. Gelatin zymography was performed to determine matrix metalloproteinase-2 (MMP-2) and MMP-9 activities. The effect of rhodomyrtone on the underlying mechanisms was performed by Western blot analysis. The results demonstrated that rhodomyrtone reduced cell viability of SW1353 cells at the low concentration (<3 μg/mL); cell viability was >80%. Rhodomyrtone at the subcytotoxic concentrations (0.5, 1.5, and 3 μg/mL) significantly inhibited cell migration, invasion, and adhesion of SW1353 cells in a dose-dependent fashion. Protein expression of integrin αv, integrin β3, and the downstream migratory proteins including focal adhesion kinase (FAK) and the phosphorylation of serine/threonine AKT, Ras, RhoA, Rac1, and Cdc42 were inhibited after treatment with rhodomyrtone. Moreover, we found that rhodomyrtone decreased the protein level of MMP-2 and MMP-9 as well as the enzyme activity in SW1353 cells. Meanwhile, tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2 expression was increased in a dose-dependent fashion. Besides, rhodomyrtone dramatically inhibited the expression of growth factor receptor-bound protein-2 (GRB2) and the phosphorylated form of extracellular signal regulation kinase1/2 (ERK1/2) and c-Jun N-terminal kinase1/2 (JNK1/2). These results indicated that rhodomyrtone inhibited SW1353 cell migration, invasion, and metastasis by suppressing integrin αvβ3/FAK/AKT/small Rho GTPases pathway as well as downregulation of MMP-2/9 via ERK and JNK signal inhibition. These findings indicate that rhodomyrtone possessed the antimetastasis activity that may be used for antimetastasis therapy in the future.

MMP-2, MT1-MMP, and TIMP-2 are essential for the invasive capacity of human mesenchymal stem cells: differential regulation by inflammatory cytokines

Blood ◽  
2007 ◽  
Vol 109 (9) ◽  
pp. 4055-4063 ◽  
Author(s):  
Christian Ries ◽  
Virginia Egea ◽  
Marisa Karow ◽  
Helmut Kolb ◽  
Marianne Jochum ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Migration ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Human Mesenchymal Stem Cells ◽  
Basement Membranes ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Matrix Metalloproteinase 2

Abstract Human mesenchymal stem cells (hMSCs) represent promising tools in various clinical applications, including the regeneration of injured tissues by endogenous or transplanted hMSCs. The molecular mechanisms, however, that control hMSC mobilization and homing which require invasion through extracellular matrix (ECM) barriers are almost unknown. We have analyzed bone marrow–derivedhMSCs and detected strong expression and synthesis of matrix metalloproteinase 2 (MMP-2), membrane type 1 MMP (MT1-MMP), tissue inhibitor of metalloproteinase 1 (TIMP-1), and TIMP-2. The ability of hMSCs to traverse reconstituted human basement membranes was effectively blocked in the presence of synthetic MMP inhibitors. Detailed studies by RNA interference revealed that gene knock-down of MMP-2, MT1-MMP, or TIMP-2 substantially impaired hMSC invasion, whereas silencing of TIMP-1 enhanced cell migration, indicating opposing roles of both TIMPs in this process. Moreover, the inflammatory cytokines TGF-β1, IL-1β, and TNF-α up-regulated MMP-2, MT1-MMP, and/or MMP-9 production in these cells, resulting in a strong stimulation of chemotactic migration through ECM, whereas the chemokine SDF-1α exhibited minor effects on MMP/TIMP expression and cell invasion. Thus, induction of specific MMP activity in hMSCs by inflammatory cytokines promotes directed cell migration across reconstituted basement membranes in vitro providing a potential mechanism in hMSC recruitment and extravasation into injured tissues in vivo.

Therapeutic Effects of Punicalagin Against Ovarian Carcinoma Cells in Association With β-Catenin Signaling Inhibition

2016 ◽  
Vol 26 (9) ◽  
pp. 1557-1563 ◽  
Author(s):  
Jian-ming Tang ◽  
Jie Min ◽  
Bing-shu Li ◽  
Sha-sha Hong ◽  
Cheng Liu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Migration ◽  
Cyclin D1 ◽  
Gelatin Zymography ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Cell Counting ◽  
Ovarian Cancer Cells ◽  
Therapeutic Effects ◽  
Dependent Manner

AimThe aim of this study was to investigate the effects of punicalagin, a polyphenol isolated from Punica granatum, on human A2780 ovarian cancer cells in vitro.MethodsThe viability of human A2780 ovarian cells was evaluated using Cell Counting Kit-8 assay. Cell cycle was detected with flow cytometry analysis. The protein expression levels of Bcl-2, Bax, β-catenin, cyclin D1, survivin, tissue inhibitor of metalloproteinase (TIMP)-2, and TIMP-3 were measured using Western blot analysis. Matrix metalloproteinase (MMP)-2 and MMP-9 activity was determined with gelatin zymography. Wound healing assay was used to determine cell migration.ResultsPunicalagin inhibited the cell viability of A2780 cells in a dose- and time-dependent manner, and the cell cycle of A2780 cells was arrested in G1/S phase transition. The treatment also induced apoptosis as shown by the up-regulation of Bax and down-regulation of Bcl-2. On the other hand, punicalagin treatment increased the expressions of TIMP-2 and TIMP-3, decreased the activities of MMP-2 and MMP-9, and inhibited cell migration. In addition, the β-catenin pathway was suppressed as shown by the down-regulations of β-catenin and its downstream factors including cyclin D1 and survivin.ConclusionsPunicalagin may have cancer-chemopreventive as well as cancer-chemotherapeutic effects against human ovarian cancer in humans through the inhibition of β-catenin signaling pathway.

CCR1 Inhibition Impairs Osteoclast Activity and Interaction with Myeloma Cells.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3494-3494
Author(s):  
Sonia Vallet ◽  
Noopur Raje ◽  
Kenji Ishitsuka ◽  
Teru Hideshima ◽  
Klaus Podar ◽  
...  
Keyword(s):  
Cell Migration ◽  
Fold Increase ◽  
Pit Formation ◽  
Inflammatory Protein ◽  
Healthy Donors ◽  
Direct Cytotoxicity ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Modest Effect

Abstract Multiple Myeloma (MM) is characterized by increased osteoclasts (OC) activity leading to severe bone disease. Several inducers of OC number and activity have been identified, including several key chemokines. In particular, macrophage inflammatory protein-1α (MIP-1α) and RANTES activate CCR1 and CCR5, resulting in increased osteoclastogenesis (Oba et al. Exp Hematol. 2005) and increased OC motility (Yu X. J Bone Miner Res. 2004) These studies underscore the role of CCR1 in promoting osteoclastogenesis. Here we demonstrate the effects of inhibition of CCR1 with a specific receptor antagonist (MLN3897, Millenium Pharmaceuticals) on normal mature OC. Mature OC were obtained by stimulating PBMC of healthy donors with RANKL and MCSF (50 ng/ml) for three weeks. OC expressed high levels of CCR1 and secreted both MIP-1α (1 ng/ml +/− 1.8) and RANTES (12 pg/ml +/− 0.66), suggesting an autocrine effect of these chemokines. Analyzing the bone resorptive ability with a pit formation assay, we observed that MLN3897 impaired OC function in a dose-dependent fashion (at 10 nM: 20% of reduction in resorbed area, at 100 nM: 50% of reduction). We then studied the effects of CCR1 inhibition on OC viability by analyzing nuclear integrity with Hoechst33258 staining. After 12 hours of cytokine-deprivation, MLN3897 enhanced OC nuclear fragmentation and condensation, suggesting a role for CCR1 ligands in OC survival. We next studied the interactions between OC and MM cells. Because OC secrete several chemoattractants, we studied their ability to stimulate RPMI8226 MM cell migration. We first confirmed high expression levels of CCR1 on RPMI8226 MM cells by flow cytometry (86% compared to isotype control). Inhibition of CCR1 with MLN3897 did not induce any direct cytotoxicity or growth arrest of these cells. We then studied the effects of OC on RPMI8226 MM cells. We observed that OC potently stimulated migration of RPMI8226 MM cells (8-fold increase), which was almost completely blocked by treatment with MLN3897. In contrast, MIP-1α alone induced only a modest effect on migration: the highest effective concentration (0.5 ng/ml) induced only a 2-fold increase. Neutralizing MIP-1α antibody partially reversed these effects, suggesting that other factors may contribute to this migratory effect. Our data therefore demonstrate that CCR1 inhibition by MLN3897 impairs mature OC survival and activity. Although MLN3897 does not have any direct antiMM activity, it affects MM-OC interactions and inhibits MM cell migration to OC. Ongoing studies are further characterizing the effects of CCR1 inhibition on MM-OC interactions in order to provide the framework for its clinical evaluation in MM.

Inhibition of the Jak/Stat Pathway Downregulates Immunoglobulin Production and Induces Cell Death in Waldenström Macroglobulinemia.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1691-1691
Author(s):  
Stephen M Ansell ◽  
Deanna Grote ◽  
Sherine F. Elsawa ◽  
Mamta Gupta ◽  
Steven C Ziesmer ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cell Line ◽  
Conflicts Of Interest ◽  
Thymidine Uptake ◽  
Complete Suppression ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Stat Pathway

Abstract Abstract 1691 Poster Board I-717 Waldenström macroglobulinemia (WM) is a B-cell malignancy that is characterized by the production of a monoclonal IgM protein and a lymphoplasmacytic infiltrate in the bone marrow. The aberrant production of the monoclonal IgM can result in serum hyperviscosity that can cause significant morbidity in patients with this disease. In previous work, we have shown that IL-6 significantly upregulates IgM secretion by WM cells and that IL-6 secretion is regulated by CCL5 (Rantes). We have also shown that IL-6 mediated IgM secretion in WM requires phosphorylation of Stat1 and Stat3. Because IL-6 induced signaling involves the Jak/Stat pathway, we tested whether the use of a Jak/Stat inhibitor, TG101348, would result in down regulation of CCL5, IL-6 and IgM production and inhibit cell proliferation and viability in WM. First, we determined whether TG101348 could inhibit the production of CCL5 because other Jak inhibitors have been shown to inhibit cytokine production. Using the BCWM.1 cell line as well CD19+ malignant cells from bone marrow specimens from WM patients, we measured CCL5 by ELISA in the culture supernatant 24 hours after treatment with increasing concentrations of the inhibitor. We found that CCL5 secretion was decreased by 50% at a concentration of TG101348 of 250nM and was completely inhibited at 2μM. Next, we measured IL-6 production after treatment with TG101348. We had previously shown that stromal cells are the primary source of IL-6 and therefore used the stromal cell line HS-5 to measure IL-6 by ELISA after treatment with the inhibitor. Our previous work had also shown that IL-6 secretion was mediated by GLI (a member of the Hedgehog pathway) rather than the Jak/Stat pathway. Interestingly, we found that IL-6 secretion was inhibited in a dose dependent fashion but required higher doses for complete suppression (8μM). We then measured IgM production by malignant B-cells 24 hours after treatment with TG101348. Our previous work had shown that IL-6 mediated IgM secretion was dependent on the Jak/Stat pathway. We found that IgM production was inhibited by 50% at 500nM and completely suppressed at 2μM. Finally, we measured the effect of TG101348 on cell proliferation and survival. Using the BCWM.1 cell line, we found that cell proliferation as determined by tritiated thymidine uptake was inhibited in a dose dependent fashion with 50% inhibition at 1μM. Inhibition of cell viability as measured by Annexin V/propidium iodide staining, however, required higher concentrations and cell viability was inhibited with an IC50 of 8μM. These data confirm the role of Jak/Stat signaling in the CCL5-IL-6-IgM axis in WM. We found that TG101348 generally suppressed the signaling and growth of WM cells but that pathways that were known to be Jak/Stat dependent required significantly lower doses to be completely inhibited. These data provide a strong rationale for the use of inhibitors of this pathway, such as TG101348, in the treatment of patients with WM. Disclosures No relevant conflicts of interest to declare.

scholarly journals Tissue inhibitor of metalloproteinase 1 expression and secretion are induced by β-adrenergic stimulation in 3T3-L1 adipocytes

2006 ◽  
Vol 189 (3) ◽  
pp. 665-670 ◽  
Author(s):  
S Kralisch ◽  
U Lossner ◽  
M Bluher ◽  
R Paschke ◽  
M Stumvoll ◽  
...  
Keyword(s):  
Tissue Inhibitor Of Metalloproteinase ◽  
Adrenergic Stimulation ◽  
Tissue Inhibitor ◽  
Dose Dependent Fashion ◽  
Adipose Tissue Development ◽  
Gs Protein ◽  
Β Adrenergic Receptors ◽  
The Impact ◽  
Camp Levels ◽  
Dose Dependent

Tissue inhibitor of metalloproteinase (TIMP)-1 is an adipocytokine upregulated in obesity which might promote adipose tissue development. In the current study, the impact of the β-adrenergic agonist isoproterenol on TIMP-1 gene expression and secretion was determined in 3T3-L1 adipocytes. Interestingly, isoproterenol increased TIMP-1 secretion 2.7-fold. Furthermore, isoproterenol induced TIMP-1 mRNA in a time- and dose-dependent fashion with significant effects observed as early as 1 h after effector addition and at concentrations as low as 1 μM isoproterenol. Significant isoproterenol-induced upregulation of TIMP-1 mRNA could also be found in immortalized brown adipocytes. Inhibitor experiments confirmed that the positive effect of isoproterenol on TIMP-1 is mediated via β-adrenergic receptors and protein kinase A. Moreover, increasing cAMP levels with forskolin or dibutyryl-cAMP was sufficient to stimulate TIMP-1 synthesis. Insulin induced basal TIMP-1 mRNA, but did not significantly influence forskolin-induced TIMP-1 expression. Taken together, we demonstrate that TIMP-1 expression and secretion are selectively upregulated in adipocytes by β-adrenergic agonists via a classic Gs-protein-coupled pathway.

Matrix metalloproteinase-2 activity, protein, mRNA, and tissue inhibitors in small arteries from pregnant and relaxin-treated nonpregnant rats

2006 ◽  
Vol 100 (6) ◽  
pp. 1955-1963 ◽  
Author(s):  
Arundhathi Jeyabalan ◽  
Laurie J. Kerchner ◽  
Michelle C. Fisher ◽  
Jonathan T. McGuane ◽  
Ketah D. Doty ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Gelatin Zymography ◽  
Renal Arteries ◽  
Mesenteric Arteries ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Pregnant Rats ◽  
Gelatinase Activity ◽  
Small Arteries ◽  
Major Factors

Vascular gelatinase activity is essential for pregnancy- and relaxin (Rlx)-induced renal vasodilation and hyperfiltration in rats. The objective of this study was to further elucidate the mechanisms for the increase in vascular matrix metalloproteinase (MMP)-2 activity caused by pregnancy and Rlx. We first corroborated our earlier work by showing that pro- and active forms of MMP-2 were increased in small renal arteries from pregnant compared with virgin rats and Rlx-treated compared with vehicle-treated nonpregnant rats. We next investigated other artery types and showed that MMP-2 activity was upregulated in mesenteric arteries from pregnant rats (pro-MMP-2 by 50% and active MMP-2 by 40%, both P < 0.05) and from Rlx-treated nonpregnant rats (pro-MMP-2 by 50% and active MMP-2 by 90%, both P < 0.005) compared with their respective controls. To corroborate these results obtained by gelatin zymography, pro-MMP-2 protein was determined by Western analysis in the same small arteries. Pro-MMP-2 protein was increased in small renal arteries from pregnant compared with virgin rats and from Rlx- compared with vehicle-treated nonpregnant rats: pro-MMP-2-to-β-actin ratio = 0.29 vs. 0.21 ( P < 0.01) and 0.43 vs. 0.32 ( P < 0.005). Findings were similar for mesenteric arteries. MMP-2 mRNA as measured by real-time PCR was increased in small renal arteries from pregnant and Rlx-treated nonpregnant rats compared with their respective controls. There were no significant differences in tissue inhibitor of metalloproteinase (TIMP-1 or TIMP-2) activity by reverse zymography in small renal arteries. Thus increases in MMP-2 mRNA and protein expression are major factors contributing to increased MMP-2 activity in small arteries from pregnant and Rlx-treated nonpregnant rats.

Antiangiogenesis Is Produced by Nontoxic Doses of Vinblastine

Blood ◽  
1999 ◽  
Vol 94 (12) ◽  
pp. 4143-4155 ◽  
Author(s):  
Angelo Vacca ◽  
Monica Iurlaro ◽  
Domenico Ribatti ◽  
Monica Minischetti ◽  
Beatrice Nico ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Wide Spectrum ◽  
Chorioallantoic Membrane ◽  
Ultrastructural Level ◽  
Matrix Metalloproteinase 2 ◽  
Cell Functions ◽  
Dose Dependent Fashion ◽  
Dose Dependent

Abstract The effects of vinblastine (VBL) on endothelial cell functions involved in angiogenesis, namely proliferation, chemotaxis, spreading on fibronectin (FN), secretion of matrix-metalloproteinase-2 (MMP-2) and MMP-9, and morphogenesis on Matrigel were tested in vitro, whereas its effects on angiogenesis were studied in vivo by using the chick embryo chorioallantoic membrane (CAM) model. In vitro, at noncytotoxic doses (0.1, 0.25, 0.5, 0.75, and 1 pmol/L), VBL impacted all these functions, except secretion of MMPs, in a dose-dependent fashion. By contrast, proliferation of other primary cells such as fibroblasts and lymphoid tumor cells was not impacted. In vivo, VBL at 0.5, 0.75, and 1 pmol/L again displayed a dose-dependent antiangiogenic activity. Lack of cytotoxicity in vitro and in vivo was shown both morphologically, and also because the antiangiogenic effects were rapidly abolished when VBL was removed. Apoptosis was not induced. At the ultrastructural level, impairment of cell functions in vitro was associated with thin disturbance of the cytoskeleton, in the form of slight depolymerization and accumulation of microfilaments, which was equally reversible. Results suggest that VBL has an antiangiogenic component at very low, noncytotoxic doses, and that antiangiogenesis by VBL could be used to treat a wide spectrum of angiogenesis-dependent diseases, including certain chronic inflammatory diseases, Kaposi's sarcoma, and cancer.

scholarly journals Dose-dependent green tea effect on decrease of inflammation in human oral gingival epithelial keratinocytes: in vitro study

2019 ◽  
Vol 24 (7) ◽  
pp. 2375-2383 ◽  
Author(s):  
Ana Hagiu ◽  
Thomas Attin ◽  
Patrick R. Schmidlin ◽  
Liza L. Ramenzoni
Keyword(s):  
Gene Expression ◽  
Wound Healing ◽  
Cell Migration ◽  
Cell Viability ◽  
Green Tea ◽  
In Vitro Study ◽  
Vitro Study ◽  
Anti Inflammatory ◽  
Dose Dependent

Abstract Objectives This in vitro study aimed to analyze the anti-inflammatory and wound healing potential of green tea extract (GTE) in human gingival epithelial keratinocytes (HGEK) treated with lipopolysaccharides (LPS). Materials and methods A cell viability assay was conducted using MTT to determine nontoxic levels of GTE on immortalized HGEK. Cells were concomitantly treated with LPS (1 μg/ml) and GTE (1 mg/ml, 2.5 mg/ml, 5 mg/ml, and 10 mg/ml) to assess inflammation. Gene expression levels of inflammatory markers IL-β1, IL-6, and TNFα were measured by RT-PCR and their protein production was assessed by ELISA. The scratch wound healing assay was used to investigate the effects of different concentrations of GTE on cell migration. We also explored the effect of GTE on the induction of the Nrf2/HO-1 pathway in the cells with or without LPS. Results GTE at concentrations of 2.5 mg/ml, 5 mg/ml, and 10 mg/ml significantly enhanced cell viability (p < 0.05). And IL-β1, IL-6, and TNFα gene expression presented up to 10-fold decrease compared with LPS-treated cells, which was also similarly found on the protein levels. At the same concentrations, cell migration increased. Conclusions The mechanism results showed that GTE produced the anti-inflammatory response by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway and increasing the level of anti-oxidant protein heme oxygenase-1 (HO-1). Clinical relevance GTE may be potentially used as oral rinse anti-inflammatory drug for treatment and prevention of oral inflammatory diseases, which is shown here by the ability to reduce the inflammation and increase in cell migration in a dose-dependent manner.

scholarly journals Ethanol Extracts of Fruiting Bodies ofAntrodia cinnamomeaSuppress CL1-5 Human Lung Adenocarcinoma Cells Migration by Inhibiting Matrix Metalloproteinase-2/9 through ERK, JNK, p38, and PI3K/Akt Signaling Pathways

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Ying-Yi Chen ◽  
Fon-Chang Liu ◽  
Pei-Yu Chou ◽  
Yi-Chung Chien ◽  
Wun-Shaing Wayne Chang ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Lung Adenocarcinoma ◽  
Cancer Metastasis ◽  
Human Lung ◽  
Gelatin Zymography ◽  
Matrix Metalloproteinase 2 ◽  
Dependent Manner ◽  
Fruiting Bodies ◽  
Anticancer Activities ◽  
Human Lung Adenocarcinoma

Cancer metastasis is a primary cause of cancer death.Antrodia cinnamomea(A. cinnamomea), a medicinal mushroom in Taiwan, has shown antioxidant and anticancer activities. In this study, we first observed that ethanol extract of fruiting bodies ofA. cinnamomea(EEAC) exerted a concentration-dependent inhibitory effect on migration and motility of the highly metastatic CL1-5 cells in the absence of cytotoxicity. The results of a gelatin zymography assay showed thatA. cinnamomeasuppressed the activities of matrix metalloproteinase-(MMP-) 2 and MMP-9 in a concentration-dependent manner. Western blot results demonstrated that treatment withA. cinnamomeadecreased the expression of MMP-9 and MMP-2; while the expression of the endogenous inhibitors of these proteins, that is, tissue inhibitors of MMP (TIMP-1 and TIMP-2) increased. Further investigation revealed thatA. cinnamomeasuppressed the phosphorylation of ERK1/2, p38, and JNK1/2.A. cinnamomeaalso suppressed the expressions of PI3K and phosphorylation of Akt. Furthermore, treatment of CL1-5 cells with inhibitors specific for PI3K (LY 294002), ERK1/2 (PD98059), JNK (SP600125), and p38 MAPK (SB203580) decreased the expression of MMP-2 and MMP-9. This is the first paper confirming the antimigration activity of this potentially beneficial mushroom against human lung adenocarcinoma CL1-5 cancer cells.

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