Canonical Wnt signalling induces satellite-cell proliferation during adult skeletal muscle regeneration

Satellite cells represent the stem cell population of adult skeletal muscle. The molecular mechanisms that control the proliferation of satellite cells are not well understood. In this study, we show that in response to injury, myofibres activate Wnt ligand transcription and activate a reporter cell line that is sensitive to the canonical Wnt-signalling pathway. Activated satellite cells on isolated cultured myofibres show robust expression of activated-β-catenin (Act-β-Cat), a key downstream transcriptional coactivator of canonical Wnt signalling. We provide evidence that the Wnt family of secreted glycoproteins act on satellite cells in a ligand-specific manner. Overexpression of Wnt1, Wnt3a or Wnt5a protein causes a dramatic increase in satellite-cell proliferation. By contrast, exposure of satellite cells to Wnt4 or Wnt6 diminishes this process. Moreover, we show that the prolonged satellite-cell quiescence induced by inhibitory Wnt is reversible and exposing inhibited satellite cells to stimulatory Wnt signalling restores their proliferation rate. Stimulatory Wnt proteins induce premature satellite cell BrdU incorporation as well as nuclear translocation of Act-β-Cat. Finally, we provide evidence that the Act-β-Cat translocation observed in single fibres during in vitro culture also occurs in cases of acute and chronic skeletal muscle regeneration in rodents and humans. We propose that Wnt proteins may be key factors that regulate the rate of satellite-cell proliferation on adult muscle fibres during the wound-healing response.

Characterization of Grb2-binding proteins in human platelets activated by Fc gamma RIIA cross-linking.

Glutathione-S-transferase (GST)-Grb2 fusion proteins have been used to identify the potential role of Grb2-binding proteins in platelet activation by the platelet low-affinity IgG receptor, Fc gamma RIIA. Two tyrosine phosphoproteins of 38 and 63 kD bind to the SH2 domain of Grb2 following Fc gamma RIIA stimulation of platelets. Both are located in the particulate fraction following platelet activation and are also able to bind to a GST-construct containing the SH2 and SH3 domains of phospholipase C gamma 1. p38 also forms a complex with the tyrosine kinase csk in stimulated cells and is a substrate for the kinase. The SH3 domains of Grb2 form a stable complex with SOS1 and two proteins of 75 kD and 120 kD, which undergo tyrosine phosphorylation in Fc gamma RIIA stimulated cells. The 75-kD protein is recognized by antibodies to SLP-76, which has recently been isolated from T cells and sequenced. Tyrosine phosphorylation of p38 and p63 is also observed in platelets stimulated by the tyrosine kinase-linked receptor agonist collagen and by the G protein-coupled receptor agonist thrombin, although phosphorylation of SLP-76 is only observed in collagen-stimulated platelets. p38 and p63 may provide a docking site for Grb2, thereby linking Grb2 SH3-binding proteins SOS1, SLP-76, and p120 to downstream signalling events.

Glycogen synthase kinase 3 (GSK3) in the heart: a point of integration in hypertrophic signalling and a therapeutic target? A critical analysis

Glycogen synthase kinase 3 (GSK3, of which there are two isoforms, GSK3alpha and GSK3beta) was originally characterized in the context of regulation of glycogen metabolism, though it is now known to regulate many other cellular processes. Phosphorylation of GSK3alpha(Ser21) and GSK3beta(Ser9) inhibits their activity. In the heart, emphasis has been placed particularly on GSK3beta, rather than GSK3alpha. Importantly, catalytically-active GSK3 generally restrains gene expression and, in the heart, catalytically-active GSK3 has been implicated in anti-hypertrophic signalling. Inhibition of GSK3 results in changes in the activities of transcription and translation factors in the heart and promotes hypertrophic responses, and it is generally assumed that signal transduction from hypertrophic stimuli to GSK3 passes primarily through protein kinase B/Akt (PKB/Akt). However, recent data suggest that the situation is far more complex. We review evidence pertaining to the role of GSK3 in the myocardium and discuss effects of genetic manipulation of GSK3 activity in vivo. We also discuss the signalling pathways potentially regulating GSK3 activity and propose that, depending on the stimulus, phosphorylation of GSK3 is independent of PKB/Akt. Potential GSK3 substrates studied in relation to myocardial hypertrophy include nuclear factors of activated T cells, beta-catenin, GATA4, myocardin, CREB, and eukaryotic initiation factor 2Bvarepsilon. These and other transcription factor substrates putatively important in the heart are considered. We discuss whether cardiac pathologies could be treated by therapeutic intervention at the GSK3 level but conclude that any intervention would be premature without greater understanding of the precise role of GSK3 in cardiac processes.

Exposure to parabens at the concentration of maximal proliferative response increases migratory and invasive activity of human breast cancer cells in vitro

Alkyl esters of p–hydroxybenzoic acid (parabens) are widely used as preservatives in personal care products, foods and pharmaceuticals. Their oestrogenic activity, their measurement in human breast tissue and their ability to drive proliferation of oestrogen-responsive human breast cancer cells has opened a debate on their potential to influence breast cancer development. Since proliferation is not the only hallmark of cancer cells, we have investigated the effects of exposure to parabens at concentrations of maximal proliferative response on migratory and invasive properties using three oestrogen-responsive human breast cancer cell lines (MCF-7, T-47-D, ZR-75-1). Cells were maintained short-term (1 week) or long-term (20±2 weeks) in phenol-red-free medium containing 5% charcoal-stripped serum with no addition, 10-8M 17-oestradiol, 1-5x10-4M methylparaben, 10-5M n-propylparaben or 10-5M n-butylparaben. Long-term exposure (20±2 weeks) of MCF-7 cells to methylparaben, n-propylparaben or n-butylparaben increased migration as measured using a scratch assay, time-lapse microscopy and xCELLigence technology: invasive properties were found to increase in matrix degradation assays and migration through matrigel on xCELLigence. Western immunoblotting showed an associated downregulation of E-cadherin and -catenin in the long-term paraben-exposed cells which could be consistent with a mechanism involving epithelial to mesenchymal transition. Increased migratory activity was demonstrated also in long-term paraben-exposed T-47-D and ZR-75-1 cells using a scratch assay and time-lapse microscopy. This is the first report that in vitro, parabens can influence not only proliferation but also migratory and invasive properties of human breast cancer cells.

Glypican-3 regulates migration, adhesion and actin cytoskeleton organization in mammary tumor cells through Wnt signaling modulation

Glypican-3 (GPC3) is a proteoglycan involved in migration, proliferation and cell survival modulation in several tissues. There are many reports demonstrating a downregulation of GPC3 expression in some human tumors, including mesothelioma, ovarian and breast cancer. Previously, we determined that GPC3 reexpression in the murine mammary adenocarcinoma LM3 cells induced an impairment of their in vivo invasive and metastatic capacities together with a higher susceptibility to in vitro apoptosis. Currently, the signaling mechanism of GPC3 is not clear. First, it was speculated that GPC3 regulates the insulin-like growth factor (IGF) signaling system. This hypothesis, however, has been strongly challenged. Recently, several reports indicated that at least in some cell types GPC3 serves as a selective regulator of Wnt signaling. Here we provide new data demonstrating that GPC3 regulates Wnt pathway in the metastatic adenocarcinoma mammary LM3 cell line. We found that GPC3 is able to inhibit canonical Wnt signals involved in cell proliferation and survival, as well as it is able to activate non canonical pathway, which directs cell morphology and migration. This is the first report indicating that breast tumor cell malignant properties can be reverted, at least in part, by GPC3 modulation of Wnt signaling. Our results are consistent with the potential role of GPC3 as a metastasis suppressor.

Defining the role of common variation in the genomic and biological architecture of adult human height

Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated ∼2,000, ∼3,700 and ∼9,500 SNPs explained ∼21%, ∼24% and ∼29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/β-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.2014

Desenvolvimento ponderal de bubalinos da raça Murrah criados em pastagem de Brachiaria brizantha no Centro-Oeste do Estado de São Paulo, Brasil

Foram analisados os dados de desempenho ponderal de bubalinos Murrah do Sistema de Produção de Leite da Universidade Estadual Paulista, Faculdade de Medicina Veterinária e Zootecnia, campus de Botucatu. Os pesos foram corrigidos às diversas idades-padrão e o modelo incluiu os efeitos de sexo (S), mês (M) e ano (A) de nascimento, classe de idade da búfala ao parto (C) e as interações S x M, S x A, S x C e M x A. As médias ajustadas e respectivos erros-padrão estimados para as características estudadas foram: Peso ao Nascer (PN): 37,71 ± 8,25kg; Peso aos 120 dias (P120): 102,08 ± 16,27kg; Peso aos 240 dias (P240): 169,84 ± 22,83kg; Peso aos 365 dias (P365): 250,59 ± 25,12kg; Peso aos 550 dias (P550): 326,13 ± 39,27kg e Peso aos 730 dias (P730): 389,80 ± 31,26kg. O efeito de sexo (S) foi significativo somente para PN e P365, sendo que machos tenderam a nascer mais pesados que fêmeas. O mês de nascimento (M) exerceu efeito sobre o PN, P120 e P730 sendo que animais nascidos em maio foram os mais pesados ao nascer, enquanto os nascidos em janeiro e maio, foram os mais pesados aos 120 e 730 dias, respectivamente. O efeito de ano de foi significativo sobre o PN, P120, P240 e P730. Os filhos de búfalas das classes de idade 1 (3 anos ou menos) e da classe 6 (10,11 e 12 anos) foram os mais leves e mais pesados ao nascer, respectivamente. O fato de a classe de idade da búfala não exercer efeito sobre os P365, P550 e P730 sugere que, em rebanhos comerciais possa ser feita a substituição de búfalas não gestantes por novilhas prenhes, apesar de esta prática reduzir a média de idade do rebanho de cria. Bubalinos da raça Murrah oriundos de rebanhos leiteiros podem ser utilizados para a produção de carne.

Análise da variabilidade genética aditiva de características de crescimento na raça Nelore

Foram utilizados dados de cinqüenta e um rebanhos participantes do Programa de Melhoramento Genético da Raça Nelore (PMGRN), distribuídos nos estados de Goiás (GO), Mato Grosso do Sul (MS), Mato Grosso (MT), Minas Gerais (MG), São Paulo (SP), Maranhão (MA) e Bahia (BA). Foram obtidas estimativas de parâmetros genéticos para os pesos padronizados aos 120 (P120), 455 (P455) e 550 (P550) dias de idade. Análises unicaráter e bicaráter foram realizadas por modelo animal usando o aplicativo MTDFREML. Para P120 foi utilizado um modelo que incluiu como efeitos fixos, grupo de contemporâneos e classe de idade da vaca ao parto, e como aleatórios, os efeitos genéticos direto, materno e de ambiente permanente da vaca. Para P455 e P550, o modelo utilizado incluiu os mesmos efeitos fixos e o efeito genético direto do animal. ANas análises unicaráter, as estimativas de herdabilidade direta foram 0,29, 0,51 e 0,47 para P120, P455 e P550, respectivamente. Nas análises bicaráter, observaram-se coeficientes de herdabilidade direta de 0,50 e 0,58 para P120, 0,50 e 0,53 para P455 e 0,44 e 0,49 para P550. As correlações genéticas estimadas entre P120 e P455, P120 e P550 e P455 e P550, foram 0,92, 0,93 e 0,96, respectivamente. As estimativas de herdabilidade obtidas para P455 e as correlações genéticas deste peso com P120 e P550 sugerem que a avaliação genética pode ser feita aos 15 meses de idade em substituição aos 18 meses.

Seleção para peso pós-desmama em um rebanho Gir. 2. Estimativas de variâncias e parâmetros genéticos dos efeitos direto e materno para características de crescimento

Componentes de variância e parâmetros genéticos para características de crescimento foram estimados usando diferentes modelos em um rebanho da raça Gir. Utilizou-se o método da máxima verossimilhança restrita sob modelo animal univariado. Os modelos de análise incluíram os efeitos fixos de mês de nascimento, grupo contemporâneo e idade da vaca. Cinco modelos diferindo quanto aos efeitos aleatórios foram testados. Para todas as características da fase pré-desmama, o teste de razão de verossimilhança (LRT) indicou o modelo com efeito genético aditivo direto e efeitos maternos (genético e de ambiente permanente) como o de melhor ajuste. As estimativas de herdabilidade direta para peso ao nascer (PN), peso aos quatro meses corrigido para 120 dias (P120), peso à desmama corrigido para 210 dias (P210) e ganho diário na fase pré-desmama (GPRE) foram, respectivamente, 0,31± 0,07; 0,14 ± 0,06; 0,23 ± 0,07 e 0,22 ± 0,07. Para as características da fase pós-desmama, o modelo que forneceu o melhor ajuste aos dados incluiu apenas o efeito genético aditivo direto. As estimativas de herdabilidade direta para peso de machos ao final da prova de ganho de peso (P378), peso de fêmeas corrigido para 550 dias (P550), ganho diário na prova de ganho de peso (G112), altura aos 378 dias em machos (AM) e altura aos 550 dias, em fêmeas (AF) foram, respectivamente: 0,45 ± 0,11; 0,29 ± 0,11; 0,37 ± 0,11; 0,79 ± 0,13 e 0,36 ± 0,0. Os efeitos maternos, tanto o genético quanto o de ambiente permanente, foram fontes de variação importantes para as características da fase pré-desmama, não sendo verificada influência desses efeitos sobre as características da fase pós-desmama.

Estimativas de parâmetros genéticos de características de crescimento em um rebanho Caracu selecionado para peso ao sobreano

Foram analisados registros de 1.698 animais de um rebanho Caracu selecionado para peso pós-desmame entre os anos 1979 e 2002 com o objetivo de verificar a existência de variabilidade genética aditiva nas características de crescimento e suas interpretações. As características analisadas foram: peso ao nascer (PN), peso padronizado aos 120 dias (P120), peso ao desmame padronizado aos 210 dias (P210), peso de machos ao final da prova de ganho de peso (P378) e ganhos diários do nascimento ao desmame (GND), dos machos na prova de ganho de peso (G112), do desmame ao sobreano em machos (GDSm), peso de fêmeas padronizado aos 550 dias (P550) e ganhos das fêmeas em pastagem do desmame ao sobreano (GDSf), além da altura da garupa a um ano em machos (ALTm) e ao sobreano em fêmeas (ALTf). Os componentes de (co) variâncias, as herdabilidades e as correlações genéticas foram estimados por máxima verossimilhança restrita não-derivativa utilizando-se o software MTDFREML. As estimativas de herdabilidade e os erros-padrão foram iguais a 0,34±0,06; 0,11±0,05; 0,13±0,05; 0,11±0,05; 0,35±0,09; 0,42±0,09; 0,31±0,09; 0,13±0,06; 0,21±0,08; 0,55±0,11; 0,51±0,09 para PN, P120, P210, GND, P378, P550, GDSm, GDSf, G112, ALTm e ALTf, respectivamente. As correlações genéticas entre as características foram de moderadas a altas e positivas, com exceção de algumas correlações com a característica GDSf e o PN. A seleção com base no desempenho do próprio indivíduo, como tem sido realizada, proporciona progresso genético nas características de seleção direta, assim como em algumas características com alta correlação genética.

Efeito da seleção para peso pós-desmama sobre indicadores da eficiência produtiva de vacas da raça Nelore

O objetivo deste estudo foi avaliar indicadores da eficiência produtiva de vacas Nelore selecionadas para peso pós-desmama, enfocados nas relações peso bezerro e peso da vaca, nos rebanhos controle (NeC), não-selecionados para peso pós-desmama, seleção (NeS) e tradicional (NeT). As análises envolveram 3929 e 3906 pesos dos bezerros aos 120 (P120) e 210 (P210) dias de idade, respectivamente. Os pesos das vacas àquelas idades também foram considerados, obtendo-se 3824 (PV120) e 3777 (PV210) registros, respectivamente, para 120 e 210 dias. A análise incluiu 183, 375 e 554 vacas dos rebanhos NeC, NeS e NeT, respectivamente. Para as análises utilizou-se o procedimento GLM/SAS, em modelos que incluíram os efeitos fixos de rebanho, ano e mês de nascimento, sexo do bezerro, idade da vaca ao parto e as interações rebanho x ano de nascimento e ano x mês de nascimento. Todos os efeitos foram significativos. Os resultados mostraram respostas correlacionadas positivas na seleção para peso pós-desmama nos pesos dos bezerros e, em menor magnitude, no peso das vacas. As relações peso bezerro e peso da vaca apresentaram valores médios ajustados de 249,0±2,1; 253,7±1,6; e 255,8±1,2 g/kg para R120 e 362,9±2,8; 368,5±2,1; e 374,6±1,7 para NeC, NeS e NeT em R210, respectivamente, indicando que, nas duas idades, os rebanhos NeS e NeT produziram mais quilogramas de bezerro por quilogramas de vaca, quando comparados ao NeC.

Estimativas de parâmetros genéticos para altura do posterior, peso e circunferência escrotal em bovinos da raça Nelore

Visando estimar parâmetros genéticos em bovinos, foram utilizados registros de pesos padronizados aos 120, 210, 365, 450 e 550 dias de idade (P120, P210, P365, P450 e P550), altura do posterior mensurada próxima ao sobreano (ALT) e circunferências escrotais (CE) padronizadas aos 365, 450 e 550 dias de idade (CE365, CE450 e CE550). Os dados foram provenientes de animais machos e fêmeas, nascidos entre 1998 e 2003 em dez fazendas de seis estados brasileiros. Os componentes de (co)variância foram estimados pela metodologia REML em análises uni, bi e trivariadas, utilizando-se modelos animal. As estimativas de herdabilidade do efeito direto com os respectivos erros-padrão foram: ALT 0,63 (0,09), P120 0,25 (0,03), P210 0,34 (0,03), P365 0,45 (0,04), P450 0,48 (0,04), P550 0,49 (0,04), CE365 0,48 (0,04), CE450 0,53 (0,04) e CE550 0,42 (0,09). As correlações genéticas entre a ALT e as variáveis P120, P210, P365, P450 e P550 foram de 0,68; 0,64; 0,53; 0,58 e 0,59, respectivamente. As associações genéticas do P120 com as CE ajustadas para peso e idade foram próximas de zero, entretanto, essas correlações foram positivas e moderadas, quando as CE foram ajustadas somente pela idade. As correlações genéticas da ALT com as CE, quando ajustadas para peso e idade, foram: -0,19 (CE365), -0,24 (CE450) e 0,00 (CE550). Utilizando um modelo que não incluiu o peso do animal como covariável, as correlações genéticas das CE com a ALT foram: 0,21 (CE365), 0,12 (CE450) e 0,39 (CE550). Essas estimativas indicam que as características de crescimento e CE apresentam variabilidade genética na raça Nelore, podendo ser incluídas em programas de melhoramento genético, e a seleção para peso em qualquer idade deve acarretar aumento na estatura dos animais. Desta forma, para obtenção de animais com tamanho e peso adequados ao sistema de produção, faz-se necessária a utilização de um índice de seleção aliando estas características.

Alterações nos genes da E-caderina e β-catenina em adenoma pleomórfico e carcinoma adenóide cístico: estudo molecular e imuno-histoquímico

Pleomorphic adenoma and adenoid cystic carcinoma represent a benign and malignant salivary gland neoplasm, respectively, that shares the same histological origin, however with distinct biological behavior. The aim of the present study was identify the -160 C/A polymorphism in the gene CDH1, mutational analysis of CTNNB1 gene and evaluation the expression of the E-cadherin and β-catenin in pleomorphic adenomas and adenoid cystic carcinomas. Furthermore, it was proposed correlate the immunochemistry staining patterns with the polymorphism and mutations. Twenty-four pleomorphic adenomas and 24 adenoid cystic carcinomas were retrieved. The polymorphism analysis was performed by restriction fragment length polymorphism (RFLP), using the restriction enzymes HphI or AflIII and the mutational screening was performed by PCR-single strand conformational polymorphism (PCR-SSCP). The immunohistochemical analysis was taken by the counting of cells, recorded as the Hscore index, and considering the presence or absence, intensity, distribution and localization of proteins expression. Comparing the two neoplasms, the results demonstrated statistically significant difference for the E-cadherin and β-catenin expression, with pleomorphic adenoma presenting weaker immunostaining. Was observed statistical correlation between E-cadherin and β-catenin expression. CDH1 heterozigotic polymorphism was seen in two cases and 13 cases displayed abnormal mobility electrophoretic shifts, suggesting CTNNB1 gene mutation. The immunohistochemical expression was not statistically correlated with the polymorphism or suggested mutations. In conclusion this study supports that the E-cadherin/β-catenin complex immunohistochemical expression might be related with the myoepithelial component amount and differentiation neither the tumor biological behavior. The cases that showed E-cadherin gene polymorphism presented reduced protein expression and, moreover, CTNNB1 suggested mutations seem not influence in the β-catenin protein expression

Expressão imuno-histoquímica da e-caderina e da ß-catenina em carcinoma epidermóide oral com e sem metástase nodal

The adhesion molecules E-cadherin and β-catenin have been studied as possible markers to distinguish carcinomas with and without metastatic potential. The objective of this research was to study the imunohistochemistry expression of the E-cadherin and β-catenin in oral squamous cell carcinoma (OSCC), aiming to contribute for the better understanding of the biological behavior of this lesion. The sample consisted of 30 cases of OSCC, being 15 of tongue and 15 of lower lip. The profile and intensity of labeling and semi quantitative analysis of the percentage of immunopositive tumoral cells in membrane for E-cadherin and β-catenin had been related with the anatomical localization of the lesion, the presence or not of nodal metastasis and the histological grade of malignancy in the invasive front area of the tumor. It was registered the presence or not of cytoplasmic and nuclear labeling of the β-catenin. The results had been submitted to the statistical analysis, being used the Mann-Whitney Test, the Fisher Test and the Spearman Correlation Coefficient (α=0, 05). The results showed that the expression in membrane for E-cadherin and β-catenin was, predominantly, the heterogeneous profile in the lower lip and tongue carcinomas, as well as in the cases with and without nodal metastasis. It was not observed significant statistical difference between expression profile and amount of immunopositive cells for E-cadherin, β-catenin and the anatomical localization of the lesion and for the presence or not of nodal metastasis. However, there was significant difference of the reduced expression of these proteins with the high score of malignancy. It was verified that the expression of the β-catenin in cytoplasm was present in 22 (73.33%) of the 30 analyzed cases, and 6 cases (20%) showed nuclear expression. The statistical analysis detected significant association between the expression of the β-catenin in the cytoplasm with the histological grade of malignancy, being this molecule more frequently present in the cytoplasm in the cases of high score of malignancy. It was concluded that the reduced immunoexpression of these proteins in membrane can be related with the lowest cellular differentiation, as well as with the pattern of invasion in nests and isolated cells, demonstrated in the cases of OSCC with high histological grade of malignancy

Efeitos da laserterapia na atividade biológica de células de carcinoma epidermóide de língua humano

The low level laser therapy (LLLT) has shown to be effective in promoting the proliferation of different cells in vitro, including keratinocytes, osteoblasts, endothelial cells and stem cells. It has been speculated that the biostimulatory effect of LLLT could cause undesirable enhancement of tumor growth in neoplastic diseases, since the malignant cells are more susceptible to proliferative stimuli. Within this context, this study evaluated the effect of LLLT on epidermoid carcinoma of the tongue cell line (SCC25) proliferation and invasion. Cultured cells were irradiated with an InGaAIP diode laser, 660nm, 30mW using two energy densities (0.5J/cm2 and 1.0J/cm2). Proliferative activity was assessed through trypan blue staining method and through cell cycle analysis using flow cytometry. The invasive potential was measured through cell invasion assay using matrigel. Cyclin D1, E-cadherin, -catenin and MMP-9 expressions were analyzed by immunofluorescence and flow cytometry and related to the investigated biological activities. Proliferation curve demonstrated that SCC25 irradiated with 1.0J/cm2 had the highest proliferative rate when compared to the control group and the group irradiated with 0.5J/cm2 (p<0.05). LLLT affected cell cycle distribution and energy density of 1.0 J/cm2 promoted a higher percentage of cells in S/G2/M phases, with statistically significant differences at 24h interval (p<0.05). LLLT, mainly with 1.0J/cm2, revealed significantly higher potential for invasion and influenced the expression of cyclin D1, E-cadherin, -catenin and MMP-9, promoting the malignant phenotype. In conclusion, our results indicate that LLLT has an important stimulatory effect on proliferation and invasion of SCC25 cells, likely due to altered expression of proteins associated with these processes