Epithelial-to-mesenchymal transition markers to predict response of Berberine in suppressing lung cancer invasion and metastasis

Qi, Hao; Xin, Ling-yan; Xu, Xin; Ji, Xianxiu; Fan, Lihong

doi:10.1186/1479-5876-12-22

Cited by 78 publications

(45 citation statements)

References 38 publications

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“…Ber has been reported to exhibit promising pharmacological activities including diarrhea, bellyache, and microbial infection 7 . In recent decades, much focus has been put on its significant anti-cancer activities [8][9][10] , especially in antihepatoma activities [11][12][13][14][15][16] . Despite the promising biological effects, Ber is poorly absorbed, resulting in low bioavailability after oral administration.…”

Section: Introductionmentioning

confidence: 99%

In vitroandin vivoantitumor efficacy of berberine-nanostructured lipid carriers against H22 tumor

Wang

Chen

et al. 2015

SPIE Proceedings

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Hepatocarcinoma, a malignant cancer, threaten human life badly. It is a current issue to seek the effective natural remedy from plant to treat cancer due to the resistance of the advanced hepatocarcinoma to chemotherapy. Berberine (Ber), an isoquinoline derivative alkaloid, has a wide range of pharmacological properties and is considered to have anti-hepatocarcinoma effects. However its low oral bioavailability restricts its wide application. In this report, Ber loaded nanostructured lipid carriers (Ber-NLC) was prepared by hot melting and then high pressure homogenization technique.Both in vitro and in vivo anti-hepatocarcinoma effects of Ber-NLC relative to efficacy of bulk Ber were evaluated. The particle size and zeta potential of Ber-NLC were 189.3 nm and −19.3 mV, respectively.MTT assay showed that Ber-NLC effectively inhibited the proliferation of H22 cells, and the corresponding IC 50 values were 6.3 µg/ml (22.1 µg/ml of bulk Ber). In vivo studies also showed higher antitumor efficacy, and inhibition rates was 68.3 % (41.4 % of bulk Ber) at 100 mg/kg intragastric administration in the H22 solid tumor bearing mice. These results suggest that the delivery of Ber-NLC is a promising approach for treating tumors.

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Section: Introductionmentioning

confidence: 99%

In vitroandin vivoantitumor efficacy of berberine-nanostructured lipid carriers against H22 tumor

Wang

Chen

et al. 2015

SPIE Proceedings

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“…BBR has an anti-tumor effect on many cancers including melanoma, neuroblastoma, lung cancer, colonic carcinoma, breast cancer, and HCC [7–12]. BBR acts both in vitro and in vivo to suppress human cancer cell growth via suppression of tumor cell proliferation, induction of tumor cell apoptosis, and inhibition of both invasion and metastasis [6, 13].…”

Section: Introductionmentioning

confidence: 99%

Berberine regulates the protein expression of multiple tumorigenesis-related genes in hepatocellular carcinoma cell lines

Chuang

Min

et al. 2017

Cancer Cell Int

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BackgroundHepatocellular carcinoma (HCC) is the seventh most common malignancy and the third leading cause of cancer-related death worldwide with an extremely grim prognosis. Berberine (BBR) has been found to inhibit proliferation of human HCC cells, although the underlying mechanism(s) are unclear.MethodsProtein expression was detected by Western blots. Cell viability was determined by using the CellTiter Assay kit.ResultsWe confirm that BBR treatment inhibits HepG2, Hep3B, and SNU-182 cell viability, and suggest that it regulates this proliferation via the modulation of multiple tumorigenesis-related genes protein expression. BBR treatment up-regulated protein expression of tumor suppressor genes, including Kruppel-like factor 6 (KLF6), activating transcription factor 3 (ATF3) and p21, while down-regulating the expression of selected oncogenes, including E2F transcription factor 1 (E2F1) and pituitary tumor transforming gene 1 (PTTG1). The specific extracellular signal–regulated kinases 1/2 (ERK1/2) inhibitor, PD98059, partially inhibited BBR effects including reduction of cell viability, and up-regulation of KLF6 and ATF3 expressions; although, PD98059 did not alter the down-regulation of E2F1 and PTTG1 expression by BBR.ConclusionsOur results suggest that BBR inhibits HCC cell viability by modulating multiple tumorigenesis-related genes, and that up-regulation of tumor suppressor genes by BBR is in part the result of ERK1/2 action. The results of this study augment our understanding of the mechanisms underlying the effect of BBR on hepatocellular cancers and provide further evidence as to the biological plausibility of this agent’s role in the treatment of these malignancies.Electronic supplementary materialThe online version of this article (doi:10.1186/s12935-017-0429-3) contains supplementary material, which is available to authorized users.

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“…As EMT is a critical step in the development of metastases, it is an attractive target for anticancer therapeutic strategies (33). In the present study, we first investigated the effect of leptin on EMT in A549 cells.…”

Section: Discussionmentioning

confidence: 98%

Leptin induces epithelial-to-mesenchymal transition via activation of the ERK signaling pathway in lung cancer cells

Cao²,

Li³

et al. 2018

Oncol Lett

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Abstract. Previous studies revealed that leptin induces the growth and proliferation and inhibits the apoptosis of lung cancer cells. However, the effect of leptin on epithelial-tomesenchymal transition (EMT) is not yet clear. In the present study, the effect of leptin on EMT was investigated as well as its underlying mechanisms in A549 cells. The ability of leptin to induce EMT was investigated by microscopic examination and western blotting. The impacts of leptin on cell migration, invasion and tumorigenesis were evaluated by wound healing, Transwell and colony formation assays, respectively. It was demonstrated that leptin induced EMT-associated morphological changes, namely a decrease in cell-cell contact and a more elongated morphological shape. Leptin decreased the expression levels of epithelial phenotype markers E-cadherin and keratin, increased the expression of mesenchymal phenotype marker Vimentin, and raised the expression of EMT-induced transcription factor ZEB-1. In addition, leptin activated the extracellular signal regulated kinase (ERK) signaling pathway and did not affect the activation of the protein kinase B signaling pathway in A549 cells. Leptin also promoted EMT-induced migration, invasion and tumorigenesis in vitro in A549 cells. The present study provides evidence that leptin induced EMT via the activation of the ERK signaling pathway and increased EMT-induced tumor phenotypes in lung cancer cells. These findings suggest that leptin may be a promising target for lung cancer treatment through the regulation of EMT.

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Epithelial-to-mesenchymal transition markers to predict response of Berberine in suppressing lung cancer invasion and metastasis

Cited by 78 publications

References 38 publications

In vitroandin vivoantitumor efficacy of berberine-nanostructured lipid carriers against H22 tumor

In vitroandin vivoantitumor efficacy of berberine-nanostructured lipid carriers against H22 tumor

Berberine regulates the protein expression of multiple tumorigenesis-related genes in hepatocellular carcinoma cell lines

Leptin induces epithelial-to-mesenchymal transition via activation of the ERK signaling pathway in lung cancer cells

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