Toad skin extract cinobufatini inhibits migration of human breast carcinoma MDA-MB-231 cells into a model stromal tissue

Nakata, Munehiro; Mori, Shuya; Kamoshida, Yo; Kawaguchi, Shota; Fujita‐Yamaguchi, Yoko; Gao, Bo; Tang, Wei

doi:10.5582/bst.2015.01109

Cited by 16 publications

(11 citation statements)

References 21 publications

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“…Generally, metastasis is the primary failure factor in cancer treatment, contributing to approximately 90% of all cancer deaths . Reagents that can suppress invasion and metastasis of breast cancer are urgently needed . As an efficient DNA replication origin, MCM10 promotes the proliferation and differentiation of tumor cells.…”

Section: Discussionmentioning

confidence: 98%

MCM10 facilitates the invaded/migrated potentials of breast cancer cells via Wnt/β‐catenin signaling and is positively interlinked with poor prognosis in breast carcinoma

Yang

Wang

2019

J Biochem & Molecular Tox

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The minichromosome maintenance protein 10 (MCM10) is one of the MCM proteins that initiate DNA replication by interacting with CDC45-MCM2-7. It has been reported that MCM10 has a role in breast cancer progression. However, MCM10 in breast cancer is still not comprehensively studied and further research is needed. This study was aimed at investigating the potential effects of MCM10 on metastasis, the prognosis of breast carcinoma, and its underlying mechanisms. Using the ONCOMINE database and the Kaplan-Meier Plotter, MCM10 was significantly overexpressed in cancers, and high expression of MCM10 was involved in the poor prognosis of breast carcinoma. MCM10 can promote the proliferation, migration, and invasion of MDA-MB-231 cells. MCM10 knockdown brought about a radical reversal in cell behaviors.Meanwhile, decreased expression of β-catenin and cyclin Dl was detected in MCM10 short hairpin RNA cells, implying that MCM10 might induce breast cancer metastasis via the Wnt/β-catenin pathway. MCM10 can be defined as a potential diagnostic tool and a promising target for breast carcinoma.

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Section: Discussionmentioning

confidence: 98%

MCM10 facilitates the invaded/migrated potentials of breast cancer cells via Wnt/β‐catenin signaling and is positively interlinked with poor prognosis in breast carcinoma

Yang

Wang

2019

J Biochem & Molecular Tox

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“…The antitumor effects of cinobufacini mainly include inhibiting cancer cell proliferation and differentiation, inducing apoptosis, and enhancing immune responses against cancer (24). Recently, an experimental study showed cinobufacini could prevent cell migration and invasion of human breast carcinoma MDA-MB-231 cells into a model stromal tissue, which indicated cinobufacini might possess cancer cell migration preventing activity in addition to cell toxicity such as apoptosis-inducing activity (25). However, there are few studies about the effects of cinobufacini on inhibiting HCC cells invasion and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Cinobufacini inhibits epithelial-mesenchymal transition of human hepatocellular carcinoma cells through c-Met/ERK signaling pathway

Wang

Zhao

et al. 2018

BST

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Cinobufacini, an aqueous extract from the skins and parotid venom glands of the toad Bufo bufo gargarizans Cantor, is a well known traditional Chinese medicine widely used in clinical cancer therapy in China. Its therapeutic effect is especially pronounced in liver cancer. However, the precise mechanisms induced by cinobufacini in human hepatocellular carcinoma (HCC) cells are still not very clear. Here, we investigated the effects and mechanisms of cinobufacini on inhibiting HepG2 cells invasion and metastasis. Epithelial-mesenchymal transition (EMT) is identified as an important initiation step for HCC metastasis. After the HepG2 cells were treated with different concentrations of cinobufacini, the expression of EMT related E-cadherin was increased while N-cadherin and Vimentin were decreased, and the expression of EMT related transcription factors Snail and Twist were decreased. Moreover, the phosphorylation of c-Met was inhibited by cinobufacini, and the expression of MEK1/2 and ERK1/2, the downstream kinase of the signal transduction pathway activated by c-Met, also decreased in a dose-dependent manner with cinobufacini. In addition, after the cells were treated with different concentrations of cinobufacini, there was a significant decrease in MMP-2 and MMP-9 expression in HepG2 cells. In conclusion, the current study suggested cinobufacini could prevent HepG2 cells migration and invasion via inhibiting EMT through c-Met/ERK signaling pathway, which might provide experimental evidence for cinobufacini treatment of HCC.

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“…Toad venom (Venenum Bufonis, also called Chan'su), extracted from the dried skin secretions of giant toads (Bufo gargarizans Cantor), has now been widely used as a traditional Chinese medicine for the therapy of various kinds of cancers. [10][11][12][13][14] In traditional Chinese medicine, amphibian skin extract has been used for the treatments of several diseases. 15,16 Many studies have reported that toad skin extract and its components enabled to inhibit cancer cell growth, migration and invasion via different mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Cinobufagin, a bufadienolide, activates ROS-mediated pathways to trigger human lung cancer cell apoptosis in vivo

Peng

Cai

et al. 2017

RSC Adv.

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Toad skin extract cinobufatini inhibits migration of human breast carcinoma MDA-MB-231 cells into a model stromal tissue

Cited by 16 publications

References 21 publications

MCM10 facilitates the invaded/migrated potentials of breast cancer cells via Wnt/β‐catenin signaling and is positively interlinked with poor prognosis in breast carcinoma

MCM10 facilitates the invaded/migrated potentials of breast cancer cells via Wnt/β‐catenin signaling and is positively interlinked with poor prognosis in breast carcinoma

Cinobufacini inhibits epithelial-mesenchymal transition of human hepatocellular carcinoma cells through c-Met/ERK signaling pathway

Cinobufagin, a bufadienolide, activates ROS-mediated pathways to trigger human lung cancer cell apoptosis in vivo

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