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1.
Human placental lipid induces melanogenesis by increasing the expression of tyrosinase and its related proteins in vitro 总被引:4,自引:0,他引:4
Mallick S Singh SK Sarkar C Saha B Bhadra R 《Pigment cell research / sponsored by the European Society for Pigment Cell Research and the International Pigment Cell Society》2005,18(1):25-33
2.
Singh SK Sarkar C Mallick S Saha B Bera R Bhadra R 《Pigment cell research / sponsored by the European Society for Pigment Cell Research and the International Pigment Cell Society》2005,18(2):113-121
Melanogenesis is one of the characteristic functional activities of melanocyte/melanoma and is regulated via mitogen-activated protein kinase (MAPK) and Akt/protein kinase B (PKB) pathways. Placental total lipid fraction (PTLF), prepared from a hydroalcoholic extract of fresh term human placenta contains sphingolipids and was recently shown to stimulate melanogenesis via up-regulation of the key enzyme tyrosinase in B16F10 mouse melanoma cells. How such lipids mediate their effects on pigmentation and tyrosinase expression is a particularly important aspect of melanogenesis. To study the signaling that leads to tyrosinase expression, we have investigated the roles of the MAPK and Akt/PKB pathways in B16F10 melanoma cells in melanogenesis in response to PTLF. Treatment of cells with PTLF led to the time dependent phosphorylation of p38 MAPK. SB203580, a p38 MAPK inhibitor, completely blocked the PTLF-induced melanogenesis by inhibiting promoter activity and subsequent expression of tyrosinase. Phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002 a blocker of the Akt signaling pathway, or an inhibitor of MEK (MAPK/ERK Kinase), PD98059 when included along with PTLF was found to potentiate PTLF-induced phosphorylation of p38 MAPK together with tyrosinase expression and melanogenesis. The results suggest that the activation of p38 MAPK plays a crucial role in PTLF-induced B16F10 melanogenesis by up-regulating tyrosinase expression. 相似文献
3.
Ratha J Majumdar KN Mandal SK Bera R Sarkar C Saha B Mandal C Saha KD Bhadra R 《Molecular and cellular biochemistry》2006,290(1-2):113-123
Lipids, especially sphingolipids, are emerging as inducer of apoptosis in a wide range of immortal cells, potentiating their
therapeutic application in cancer. In the present study, a sphingolipid rich lipid fraction (denoted here as ALL), isolated
from an attenuated strain of Leishmania donovani promastigote, was tested for its tumoricidal activity taking melanoma, the dreaded form of skin cancer cells, as model. ALL was found
to induce chromatin condensation, internucleosomal DNA fragmentation and phosphatidylserine externalization with enhanced
cell population in sub-G1 region in both mouse and human melanoma systems, namely B16F10 and A375 respectively. These are
the hallmarks of cells undergoing apoptosis. Further analysis demonstrated that ALL treated melanoma cells showed significant
increase in ROS generation, mitochondrial membrane potential depolarization, release of cytochrome c, and caspase-3 activation,
which are the events closely involved in apoptosis. These findings indicate that one or more bioactive sphingolipid(s)/ceramide(s)
present in ALL could be the causative agent(s) for the induction of apoptosis in melanoma cells. Further studies are thus
necessary to identify these specific bioactive sphingolipid(s)/ceramide(s) and to establish their mechanism of action, in
order to explore their use as anticancer agents. 相似文献
4.
5.
6.
The metabolites produced by Stigmatella WXNXJ-B inhibited the growth of tumor cells. The aims of this research were to evaluate the inhibition potency to different
tumor cell lines and to study the effects of ammonium, phosphate and iron salts on bacterial growth and production of bioactive
metabolites in Stigmatella WXNXJ-B fermentation. The results showed that the chloroform extract (CE-ME) showed the strongest growth inhibition bioactivity
on mouse melanoma cell line (B16), murine colon carcinoma cell line (CT-26), human liver carcinoma cell line (HepG2) and human
breast cancer cell line (MDA-MB231) in vitro and the IC50 values were 9.94, 7.33, 11.34 and 11.66 μg ml−1 respectively. The IC50 value was above 700 μg ml−1 on normal mouse spleen cells. Morphology happened changes in B16 cells treated with CE-ME. The anti-tumor metabolites were
mainly produced during the stationary phase of the bacterial growth. Cell growth was stimulated at the phosphate concentration
below 5 mM, but it was inhibited partly with 10 mM phosphate. The production of bioactive substances was inhibited by the
phosphate. Ammonium increased the cell growth by 250% at 5 mM addition. The inhibition rate to B16 cells was increased to
89% at the concentration of 40 mM ammonium. The bacteria showed the best growth with 4 mM iron. Iron had little effect on
the production at 2 mM, but bigger inhibition effect at higher iron concentration. 相似文献
7.
E. I. Yurlova K. A. Rubina V. Yu. Sysoeva G. V. Sharonov E. V. Semina E. V. Parfenova V. A. Tkachuk 《Russian Journal of Developmental Biology》2010,41(4):217-226
The influence of T-cadherin on the pigmentation and proliferation of mouse melanoma B16F10 cells in vitro and on the growth
and neovascularization of tumor cell masses formed by the B16F10 cells in a model of the chorioallantoic membrane of a chicken
embryo is studied. It is found that the proliferative activity of the cells decreases in the cell culture of mouse melanoma
upon the overexpression of T-cadherin in comparison with the cells in the control. It is shown in experiments in vitro that
the B16F10 cells with the overexpression of T-cadherin are rarely settling are to the chorioallantoic membrane than the control
cells. In addition, it is found that the control cells of mouse melanoma form tumors with area more 0.1 mm2 more often than the cells with the overexpression of T-cadherin and the amount of the vessels growing to tumor cell masses
formed by the cells with the overexpression of T-cadherin is significantly lower than the same index for the cells in the
control. Thus, the overexpression of T-cadherin in the B16F10 cells suppresses the proliferation of these cells in vitro and
the growth of the tumor masses formed by melanoma cells on the chorioallantoic membrane and their neovascularization in vivo. 相似文献
8.
1,3-Dichloro-2-propanol induces apoptosis via both calcium and ROS in mouse melanoma cells 总被引:1,自引:0,他引:1
We demonstrated that the apoptotic cell death of mouse melanoma cells exposed to 1,3-dichloro-2-propanol (DCP) was Ca2+ dependent. 1,3-DCP inhibited the growth of mouse melanoma cells in a concentration-dependent manner. Furthermore, a terminal
nick-end labeling of fragmented DNA (TUNEL) assay demonstrated that 1,3-DCP-induced apoptosis. Moreover, reactive oxygen species
and Ca2+, generated by mouse melanoma cells that were exposed to 1,3-DCP, resulted in the activation of NF-κB and MAPKs. Finally, treatment with BAPTA, an intracellular Ca2+ chelator, completely inhibited the apoptosis that was induced by 1,3-DCP treatment of B16F10 cells. 相似文献
9.
W. Lasek Wojciech Feleszko Jakub Goląb Tomasz Stokłosa Maria Marczak Anna Dąbrowska Magdalena Malejczyk Marek Jakóbisiak 《Cancer immunology, immunotherapy : CII》1997,45(2):100-108
There is strong evidence that antitumor activity of interleukin-12 (IL-12) in vivo is mediated, in part, through interferon
(IFNγ) produced by IL-12-stimulated natural killer and T cells. Since IFNγ and tumor necrosis factor α (TNFα) have been reported
to synergize in antitumor effects in a number of models, we decided to examine whether the combined treatment with recombinant
mouse IL-12 and recombinant human TNFα would produce similar effects. The efficacy of the combined IL-12/TNFα immunotherapy
was evaluated in three tumor models in mice: B16F10 melanoma, Lewis lung (LL/2) carcinoma and L1 sarcoma. Intratumoral daily
injections of 1 μg IL-12 in combination with 5 μg TNFα into B16F10-melanoma-bearing mice resulted in a significant retardation
of the tumor growth as compared with that in controls and in mice treated with either cytokine alone. Similar effects were
obtained using 0.1 μg IL-12 and 5 μg TNFα in LL/2 carcinoma and L1 sarcoma models. Antitumor activity against L1 sarcoma was
still preserved when TNFα at a low dose (1 μg) was combined with 0.1 μg IL-12 and applied for a prolonged time. Potentiation
of antitumor effects, which was observed in IL-12/TNFα-based immunotherapy, could result from at least three different mechanisms,
partly related to stimulation of IFNγ and TNFα production in treated mice: (a) direct cytostatic/cytotoxic effects on tumor
cells, (b) induction of antitumor activity of macrophages, and (c) inhibition of blood vessel formation in the tumor. Our
studies demonstrate that combination tumor immunotherapy with IL-12 and TNFα may be more effective than single-cytokine treatment,
and suggest possible mechanisms by which IL-12 and TNFα may exert potentiated therapeutic effects against locally growing
tumors.
Received: 17 February 1997 / Accepted: 5 August 1997 相似文献
10.
Debasish Maiti Ashish Kumar Singha Chaitali Sarkar Soham Sarkar Indrajit Sil Sarma Kuntal Manna Biswanath Dinda 《Cytotechnology》2018,70(4):1111-1120
Melanoma is a predominant cause of skin cancer-related deaths. It was reported that, the methanolic extract of Pouzolzia Indica (P. indica) on chromatography gave five compounds (1-hentriacontanyl palmitate, myricyl alcohol, 6,7-dimethoxycoumarin, trichadonic acid and friedelane), which inhibited the acute promyelocytic leukemia cell lines, NB4, and HT93A. Friedelane was extracted as active compound from methanolic extract of P. indica. In this study, friedelane was tested on murine metastatic B16F10 and B16BL6 melanoma cell lines. To achieve the target, the cell viability using trypan blue exclusion, acridine orange/EtBr staining and cell cytotoxicity were tested using MTT assay. Caspase-3, caspase-9, Cyt-c, BAD and Bax protein were assayed to evidence the apoptosis induction. The compound friedelane shows potent cytotoxic effect against metastatic melanoma mouse cell lines in 10 µg/ml concentration. 相似文献
11.
Toshihiro Fujimoto Michael A. O’Donnell Akos Szilvasi H. Yang R. B. Duda 《Cancer immunology, immunotherapy : CII》1996,42(5):280-284
Although immunotherapy with bacillus Calmette Guérin (BCG) is an established adjuvant treatment for malignant melanoma, the
mechanism of its role in this process is unclear. To investigate the possible contribution of tumor-inhibitory cytokines induced
by BCG, B16F10 melanoma cell growth in culture was assessed in response to purified cytokines and conditioned media of BCG-stimulated
splenocytes. Interferon-γ (IFNγ) was the most potent single agent (IC50≈50 pg/ml). Tumor necrosis factor α was substantially weaker (IC50>10 ng/ml) but provided synergy with IFNγ. None of the other
cytokines such as interleukin-2 (IL-2), IL-4, IL-6, IL-10, IL-12, or granulocyte/macrophage-colony-stimulating factor had
direct antitumor activity against B16F10 melanoma cells. However, when IL-2 and/or GM-CSF were combined with BCG either by
exogenous addition or through endogenous production by novel cytokine-secreting recombinant BCG (rBCG), a substantial increase
in INFγ production by splenocytes was observed. Antitumor activity of this conditioned medium directly correlated with IFNγ
concentration and was completely blocked by neutralizing antibody to IFNγ. These results suggest that BCG may exert part of
its antitumor action on melanoma through the induction of IFNγ, which can be greatly enhanced through the concomitant addition
of IL-2 and/or GM-CSF. Furthermore, by utilizing rBCG that secrete these cytokines, it may be possible to potentiate the antitumor
effect of BCG directly at the site of BCG inoculation.
Received: 29 January 1996 / Accepted: 9 April 1996 相似文献
12.
M Edward J A Gold R M MacKie 《Biochemical and biophysical research communications》1988,155(2):773-778
The effect of retinoic acid on murine B16 melanoma cell growth, tyrosinase activity and melanin synthesis was investigated. Retinoic acid inhibited the growth of B16F1, B16F10 and B16BL6 melanoma cells, but enhanced melanin synthesis only in the B16F1 cells. The B16F10 and B16BL6 cells exhibited retinoic acid-induced suppression of tyrosinase activity and melanin synthesis, which was most apparent in the B16F10 cell variant. For comparison, Cloudman S91 melanoma cells proved to be particularly sensitive to retinoic acid-induced growth inhibition and stimulation of the expression of their melanotic phenotype. These results suggest considerable heterogeneity in the B16 melanoma with respect to their response to retinoic acid. 相似文献
13.
Ratha J Majumdar KN Dhara K Singh SK Saha KD Bhadra R 《Molecular and cellular biochemistry》2007,304(1-2):143-154
A fraction of attenuated Leishmanial lipid (ALL) rich in sphingolipids, previously shown to have apoptosis inducing activity
in mouse melanoma (B16F10) and human melanoma (A375) cells, was resolved to isolate the bioactive sphingolipid. The mechanism
of apoptosis induction by this bioactive attenuated Leishmanial sphingolipid (ALSL) was studied in A375 cells. Apoptosis induced
by ALSL in A375 cells was found to be dose and time-dependent. Exposure of cells to ALSL resulted in a rapid increase in reactive
oxygen species generation. Pretreatment of cells with the antioxidant N-acetyl-cystein reduced ROS generation and attenuated apoptosis induced by ALSL. Again, ALSL sensitization resulted in the
activation of caspase-3 and -9 but not caspase-8. However, inhibitors of these caspases could not protect the cells completely
from ALSL-induced apoptosis. N-acetyl-cystein pretreatment was again found to attenuate the activation of caspase-3 and -9. ALSL treatment also resulted
in the alteration of mitochondrial membrane potential, and release of pro-apoptotic factors such as cytochrome c and apoptosis
inducing factor (AIF) from mitochondria. Furthermore, c-Jun N-terminal kinase was activated that resulted in apoptosis of A375 cells, whereas p38 MAPK was activated to counteract the
stress generated in cells in response to ALSL treatment. Taken together, our results indicate that ALSL-induced apoptosis
of A375 cells is mediated by both mitochondrial caspase-dependent and -independent pathways and it involves ROS and JNK activation
in the mitogen-activated protein kinase cascade. 相似文献
14.
Cancer associated gene (CAGE) regulates expression of epithelial-mesenchymal transition (EMT)-related proteins through extracellular
regulated kinase (ERK), Akt and nuclear factor κB (NF-kB) in mouse B16F10 melanoma cells. Snail, a EMT-related protein, mediates
the effect of CAGE on the induction of matrix metalloproteinase-2 (MMP-2) and cancer cell motility. C-Flice inhibitory protein
mediates the effect of CAGE on the induction of MMP-2 and cell motility by the induction of Snail. CAGE was shown to protect
cells against celastrol, an anti-cancer agent. Celastrol-resistant B16F10 melanoma cells had a higher expression level of
c-FLIPL and Snail as compared with a sensitive cell line.
Youngmi Kim and Hyunmi Park contributed equally to this work. 相似文献
15.
Objectives: Poor therapeutic results have been reported for treatment of malignant melanoma; therefore in this study we have investigated inhibitory capacity of ethyl acetate, chloroform (Chl) and methanol extracts from Moricandia arvensis on mouse melanoma (B16‐F0) and human keratinocyte (HaCaT) cell proliferation. Influence of Chl extract on percentage distribution in cell cycle phases and melanogenesis was also studied. Material and methods: Cell viability was determined at various periods using the MTT assay, and flow cytometry was used to analyse effects of Chl extract on progression through the cell cycle and apoptosis. In addition, amounts of melanin and tyrosinase were measured spectrophotometrically at 475 nm. Results: Chl extract exhibited significant anti‐proliferative activity after incubation with the two types of tumour skin cells. Morphological changes in B16‐F0 cells, accompanied by increase of tyrosinase activity, and of melanin synthesis were observed, which are markers of differentiation of malignant melanoma cells. Furthermore, cell cycle analysis revealed that B16‐F0 cells treated with Chl extract were arrested predominantly in G1 phase. Conclusion: Chl extract had the ability to reverse malignant melanoma cells from proliferative to differentiated state, thus providing a new perspective in developing novel strategies for prevention and treatment of malignant melanoma, possibly through consumption of the extract in an appropriate cancer prevention diet. Moreover, there is scope for the extract being introduced into cosmetic products as a natural tanning agent. 相似文献
16.
Matsuda H Yoshida K Miyagawa K Nemoto Y Asao Y Yoshikawa M 《Bioorganic & medicinal chemistry letters》2006,16(6):1567-1573
The methanolic extract and its alkaloid fraction from the rhizomes of Nuphar pumilum showed cytotoxic effects on human leukemia cell (U937), mouse melanoma cell (B16F10), and human fibroblast (HT1080). Dimeric sesquiterpene thioalkaloids with the 6-hydroxyl group (6-hydroxythiobinupharidine, 6,6'-dihydroxythiobinupharidine, 6-hydroxythionuphlutine B) showed substantial cytotoxic activity at a concentration of 10 microM, but dimeric sesquiterpene thioalkaloids lacking the 6-hydroxyl group (thiobinupharidine, thionuphlutine B, 6'-hydroxythionuphlutine B, neothiobinupharidine, thionuphlutine B beta-sulfoxide, and neothiobinupharidine beta-sulfoxide) and monomeric sesquiterpene alkaloids (nupharidine, 7-epideoxynupharidine, and nupharolutine) showed weak activity. Next, apoptosis-inducing activity of a principal active constituent, 6-hydroxythiobinupharidine, on U937 was examined using morphological observation and DNA fragmentation assay (TUNEL method). Apoptosis of U937 was immediately observed within 1 h after treatment of 6-hydroxythiobinupharidine at 2.5-10 microM. 相似文献
17.
目的: 观察双基因联合干扰MMP-9和FAK对小鼠黑色素瘤高转移细胞B16F10体外侵袭、迁移能力的影响。方法:分别构建pGV102-MMP9-siRNA,pGV102-FAK-siRNA重组质粒载体,脂质体TM2000介导转染小鼠黑色素瘤B16F10细胞,实验分为空白对照组、Anti-MMP-9组,Anti-FAK组、Anti-MMP-9 &FAK组、阴性对照组。经G418筛选GFP+克隆,流式细胞仪分析阳性率,激光共聚焦观察转染后细胞形态,半定量RT-PCR检测各组B16F10细胞MMP-9和FAK基因的mRNA转录水平,Transwell侵袭、迁移实验测定各组B16F10细胞体外侵袭、迁移能力。结果: 经G418筛选,3个转染组阳性率分别为92.41±1.64%,95.72±0.21%,91.52±0.11%,且转染后细胞形态良好;与空白对照组相比,3个转染组的MMP-9,FAK mRNA转录水平下降明显(P<0.01),迁移、侵袭能力明显降低(P<0.01),但Anti-MMP-9 &FAK组细胞侵袭迁移能力显著低于Anti-MMP-9 组和Anti-FAK组(P<0.01)。结论: 相比单独沉默MMP-9 或FAK,联合沉默MMP-9 和FAK可明显降低小鼠黑色素瘤B16F10细胞体外迁移、侵袭能力。 相似文献
18.
DuBok Choi Sang-Shin Park Ji-Lu Ding Wol-Suk Cha 《Biotechnology and Bioprocess Engineering》2007,12(5):516-524
We investigated the effects ofFomitopsis pinicola extract on biological activity by examining the antioxidant and antitumor activityin vitro andin vivo. When theF. pinicola extract concentration was raised from 60 to 120 μg/mL, the DPPH scavenging rate increased from 50.3 to 88.2% and the superoxide
anion radical scavenging rate increased from 45.2 to 85.3% when theF. pinicola extract concentration was raised from 500 to 700 μg/mL. After incubatingF. pinicola extract for 12 h, the linoleic acid scavenging rate increased from 35.5 to 90.5%. A similar finding was observed for butylated
hydroxytoluene. The total phenolic content of theF. pinicola extracts were approximately 10- to 16-fold higher than what was observed in theP. nebrodensis andA. camphorate extracts. The glutathione production, using decoctions prepared fromF. pinicola, was 20.0 μM/g of liver, which corresponded to approximately 4.0-fold higher than the control. The glutathione peroxidase
activity was 8.3 U/mg of protein, which was approximately 2.8-fold higher than the activity level observed in the control
rat livers. The cell viability rates of all the human cancer cells, when 100 μg/mL of ethanol extract was used for the different
types of cancer cells, decreased with increasing extract concentrations in comparison to the hot water extract. In particular,
when HeLa and Hep3B cells were incubated with 1.000 μg/mL of methanol extract, the cell viability rates were 20 and 25%, respectively,
which was approximately 3.0-fold higher than what was observed for the hot water extract.
The first two authors contributed equally to this work. 相似文献
19.
Reactive oxygen species (ROS) generation is linked to dynamic actin cytoskeleton reorganization, which is involved in tumor
cell motility and metastasis. Thus, inhibition of ROS generation and actin polymerization in tumor cells may represent an
effective anticancer strategy. However, the molecular basis of this signaling pathway is currently unknown. Here, we show
that the Ecklonia cava-derived antioxidant dieckol downregulates the Rac1/ROS signaling pathway and inhibits Wiskott-Aldrich syndrome protein (WASP)-family
verprolin-homologous protein 2 (WAVE2)-mediated invasive migration of B16 mouse melanoma cells. Steady-state intracellular
ROS levels were higher in malignant B16F10 cells than in parental, nonmetastatic B16F0 cells. Elevation of ROS by H2O2 treatment increased migration and invasion ability of B16F0 cells to level similar to that of B16F10 cells, suggesting that
intracellular ROS signaling mediates the prometastatic properties of B16 mouse melanoma cells. ROS levels and the cell migration
and invasion ability of B16 melanoma cells correlated with Rac1 activation and WAVE2 expression. Overexpression of dominant
negative Rac1 and depletion of WAVE2 by siRNA suppressed H2O2-induced cell invasion of B16F0 and B16F10 cells. Similarly, dieckol attenuates the ROS-mediated Rac1 activation and WAVE2
expression, resulting in decreased migration and invasion of B16 melanoma cells. In addition, we found that dieckol decreases
association between WAVE2 and NADPH oxidase subunit p47phox. Therefore, this finding suggests that WAVE2 acts to couple intracellular Rac1/ROS signaling to the invasive migration of
B16 melanoma cells, which is inhibited by dieckol. 相似文献
20.
The matricellular protein connective tissue growth factor (CTGF, CCN2) is overexpressed in several forms of cancer and may
represent a novel target in anti-cancer therapy. However, whether CCN2 is expressed in melanoma cells is unknown. The highly
metastatic murine melanoma cell line B16(F10) was used for our studies. Real time polymerase chain reaction analysis was used
to detect mRNA expression of CCN1, CCN2, CCN3 and CCN4 in Western blot and immunofluorescence analyses were used to detect
CCN2 protein. Inhibitors of signal transduction cascades were used to probe the mechanism underlying CCN2 expression in B16(F10)
cells. CCN2 was expressed in B16(F10) cells, and was reduced by the FAK/src inhibitor PP2 and the MEK/ERK inhibitor U0126
indicating that CCN2 acts downstream of these pathways in B16(F10) murine melanoma cells. Expression of CCN1, CCN3 and CCN4
was not reduced by PP2 or U0126; in fact, expression of CCN4 mRNA was elevated by PP2 or U0126 treatment. To our surprise,
CCN2 protein was detected in the nuclei of B16(F10) cells, and was undetectable in the cytoplasm. CCN2 was expressed in B16(F10)
melanoma cells, adding to the list of cancer cells in which CCN2 is expressed. Of the CCN family members tested, only CCN2
is downstream of the highly oncogenic MEK/ERK pathway. CCN2 should be further evaluated for a possible role in melanoma growth
and progression. 相似文献