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Vol. 54. Num. 3.March 2018
Pages 115-174
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Vol. 54. Num. 3.March 2018
Pages 115-174
Original article
DOI: 10.1016/j.arbr.2017.09.012
Esculetin Attenuates the Growth of Lung Cancer by Downregulating Wnt Targeted Genes and Suppressing NF-κB
La esculetina atenúa el crecimiento del cáncer de pulmón por downregulation de los genes diana de Wnt y supresión de NF-κB
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Xiangyun Zhu, Jiaping Gu, Hongxian Qian
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qianhongxianwuxi@126.com

Corresponding author.
Department of Respiratory Medicine, The Second People's Hospital of Wuxi, No. 68 Zhongshan Road, Wuxi 214002, China
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Abstract
Introduction

Esculetin was identified to inhibit cell proliferation and induce apoptosis or cell cycle arrest in several cancer cell lines. However, the effect of esculetin on lung cancer remains elusive.

Methods

The anti-proliferative role of esculetin in murine Lewis lung carcinoma (LLC) cells was evaluated by 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) and colony formation assays. BALB/c mice were subcutaneously injected with LLC cells to investigate the inhibitory effect of esculetin on the growth of lung cancer xenograft. Invasive ability was detected in esculetin treated and untreated LLC cells by transwell assay. The association between esculetin and Wnt/β-catenin signaling, as well as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), was confirmed by testing the expression of c-myc, Cyclin D1 and NF-κB using Western blot.

Results

Esculetin treatment in LLC cells led to significant decrease of cell proliferation in a time- and dose-dependent manner. After injection of LLC cells into mice, reduced size and weight of tumors were observed in esculetin treated mice compared to untreated mice. However, no difference in cell invasion was observed between the treated and untreated LLC cells. Notably decreased expression of c-myc, Cyclin D1 and NF-κB were observed in LLC cells with esculetin treatment compared to untreated cells.

Conclusion

Esculetin plays an inhibitory role in the growth of lung cancer by down-regulating c-myc, Cyclin D1 and NF-κB.

Keywords:
Esculetin
Lung cancer
Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)
C-myc
Cyclin D1
Resumen
Introducción

Se ha determinado que la esculetina inhibe la proliferación celular e induce la apoptosis o la detención del ciclo celular en varias líneas celulares de cáncer. Sin embargo, su efecto sobre el cáncer de pulmón es todavía desconocido.

Métodos

Se estudió el papel antiproliferativo de la esculetina en células murinas de carcinoma pulmonar de Lewis (LLC) mediante ensayos de bromuro de 3-(4,5-dimetil-2-tiazolil)-2,5-difenil-2H-tetrazolio (MTT) y de formación de colonias. Se inyectaron subcutáneamente células LLC a ratones BALB/c para investigar el efecto inhibidor de la esculetina sobre el crecimiento del xenoinjerto de cáncer de pulmón. La capacidad invasiva en células LLC tratadas o no tratadas con esculetina se evaluó mediante el ensayo transwell. La asociación entre la señalización de la esculetina y la de Wnt/β-catenina, y con el factor nuclear potenciador de las cadenas ligeras kappa de células B activadas (NF-κB) se confirmó midiendo la expresión de c-myc, de ciclina D1 y NF- κB usando Western blot.

Resultados

El tratamiento con esculetina de las células LLC disminuyó significativamente la proliferación celular de una manera dependiente del tiempo y de la dosis. Tras la inyección de células LLC en ratones, se observó que los tumores de los ratones tratados con esculetina eran de menor tamaño y peso que los de los ratones no tratados. Sin embargo, no se observó diferencia en la invasividad celular entre las células LLC tratadas y las no tratadas. Se destacó la disminución de la expresión de c-myc, ciclina D1 y NF-κB en células LLC tratadas con esculetina en comparación con células no tratadas.

Conclusión

La esculetina desempeña un papel inhibitorio en el crecimiento del cáncer de pulmón a través de la regulación de c-myc, ciclina D1 y NF-κ B.

Palabras clave:
Esculetina
Cáncer de pulmón
Factor nuclear potenciador de las cadenas ligeras kappa de células B activadas (NF-κB)
C-myc
Ciclina D1

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