Berbamine induces SMMC-7721 cell apoptosis via upregulating p53, downregulating survivin expression and activating mitochondria signaling pathway

Cao, Jianbo; Yu, Bin; Wang, Shusheng; Liu, Huan; Li, Tao; Sun, Wanping

doi:10.3892/etm.2017.5637

Cited by 14 publications

(20 citation statements)

References 37 publications

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“…As reported here, BBM is effective in inhibiting the growth of cancer cells with induction of the apoptosis of cancer cells. 12 , 20 Moreover, BBM shows significant potential to sensitize cancer cells to radiation therapy, which suggests that BBM maybe a novel radiosensitizer for the treatment of cancer. Previous studies reported the anticancer effect of BBM against a series of tumors including solid tumors and leukemia.…”

Section: Discussionmentioning

confidence: 99%

In vitro and in vivo superior radiosensitizing effect of berbamine for head and neck squamous cell carcinoma

Zhu

Ruan

Feng

et al. 2018

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BackgroundBerbamine (BBM), one of the bis-benzylisoquinoline products isolated from Berberis amurensis, has been demonstrated for its anticancer effect against leukemia, breast cancer, liver cancer, etc. There are some studies focusing on the chemosensitization effect of BBM. However, there is no report about whether BBM could enhance the anticancer effect of radiation, which made us to explore the possible radiosensitization effect of BBM.Materials and methodsHere, in vitro cytotoxicity of BBM was evaluated on two kinds of head and neck squamous cancer cell lines. Clonogenic assay was performed to study the radiosensitization effect of BBM. Western blot was utilized to elucidate the possible mechanism underlying the radiosensitization effect.ResultsBBM effectively inhibited the growth of two kinds of cancer cells in a time- and dose-dependent manner. Radiation plus BBM led to significantly more reduction of the colony-forming ability of cancer cells when compared with radiation alone. BBM plus radiation led to the most reduction of STAT3 phosphorylation, followed by the significant decrease of the ratio of Bax/Bcl-2. In vivo study demonstrated that the combinational administration of BBM and radiation generated the most significant tumor-delaying effect among all of the treatment regimens.ConclusionWe reported, in the current study, the potential role of BBM in not only treating cancer by itself but also offering a promising way to improve the efficacy of radiotherapy by inhibiting the activation of STAT3 and subsequently inducing the apoptosis of cancer.

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Section: Discussionmentioning

confidence: 99%

In vitro and in vivo superior radiosensitizing effect of berbamine for head and neck squamous cell carcinoma

Zhu

Ruan

Feng

et al. 2018

OTT

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“…Previous studies have demonstrated that the antitumor effects of BBM in a variety of tumors, including breast cancer [19], myeloma [7,20], hepatoma [9,21], prostatic neoplasms [9], pancreatic carcinoma [22] and lung cancer [23]. Jin [22] con rmed that BBM signi cantly downregulated the expression of the antiapoptotic proteins such as Bcl-2 and Bcl-xL and inhibited proliferation in pancreatic carcinoma cells.…”

Section: Discussionmentioning

confidence: 97%

“…It has been reported to possess the effects of anti-oxidation, immunoregulation, and anti-arrhythmia in recent studies [4][5][6][7]. BBM was also revealed to have potential function of antitumor [8][9][10]. However, there were few studies on the anti-tumor effect of BBM in lung cancer,and the in vitro studies just evaluated the cell activity and migration, and the mechanism involved was just Bcl-2/Bax.…”

Section: Introductionmentioning

confidence: 99%

Berbamine Inhibits Cell Proliferation, Migration, and Invasion and Induces Cell Apoptosis of A549 Cells Via Regulating C-Maf, PI3K/Akt and MDM2-P53 Pathways

Liu

Zhang²,

et al. 2020

Preprint

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Background To investigate the influences of berbamine (BBM) on the cell viability, proliferation, and migration of A549 cells in vitro and in vivo, and explore the possible mechanisms.MethodsAfter the A549 cells were treated with BBM, the cell viability and proliferation of the cancer cells were detected by MTT assay, EdU assay, and colony formation assay. Migration and invasion of cancer cells were illustrated through wound scratch assay and transwell assay. Apoptosis of cancer cells was evaluated by trypan blue dye exclusion assay and elisa assay. Beside, the expression of PI3K/Akt signal pathway-related proteins and c-Maf were detected employing western blotting assay. Xenografted model of NSCLC was used to detect the effect of BBM on tumor growth and metastasis in vivo.ResultsMTT assay showed that BBM inhibited the viability of A549 cells in a concentration-dependent manner and time-dependent manner. The results from the colony formation assay and EdU assay revealed that BBM (10 µM) could significantly inhibit the proliferation of A549 cells (P＜0.001). And BBM (10 µM) significantly inhibited the migration and invasion in the wound scratch assay and transwell assay (P＜0.05). Trypan blue assay and elisa assay indicated that BBM (20 µM) significantly induced apoptosis of A549 cells. The nude mice assay manifested the tumor volume was significantly shrank by BBM (20 mg/kg) (P＜0.05). Western blotting assay showed that the PI3K/Akt and MDM2-p53 signaling pathways were inhibited by BBM, and the expression of c-Maf was downregulated by BBM. ConclusionsBBM could inhibit the proliferation and metastasis, and induce apoptosis of A549 cells in vitro and in vivo, these effects may be achieved by reducing the expression of c-Maf and regulating the PI3K/Akt and MDM2-p53 pathways.

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“…Berbamine can also lead to the loss of MMP in human hepatocellular carcinoma cells (SMMC‐7721). Moreover, berbamine can aggravate the release of Cyt‐c into the cytoplasm by upregulating the level of p53 and bax in cells . Mitochondrial dysfunction is a very important link and target in the toxic mechanism of MC‐LR.…”

Section: Discussionmentioning

confidence: 99%

p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

Liu

Huang

et al. 2019

Environmental Toxicology

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Microcystin‐LR (MC‐LR), a potent endotoxin, can induce reproductive toxicity. In order to investigate the role and mechanisms of apoptosis (p53‐dependent and mitochondrial pathways) of germ cells induced by MC‐LR, the co‐cultured primary Sertoli‐germ cells from Sprague‐Dawley rats were used for the experiments. Expression levels of proteins, genes, and mitochondrial membrane potential (MMP) were obtained after exposing co‐cultured Sertoli‐germ cells to MC‐LR with or without the addition of the p53 inhibitor, pifithrin‐α (PFT‐α), and MMP inhibitor, cyclosporin A (CsA). Results indicated that MC‐LR could activate p53‐dependent pathway‐associated proteins in Sertoli‐germ cells, leading to a decrease in MMP (indicating the opening of mitochondrial permeability transition pore [mPTP] and the release of Cytochrome‐c [Cyt‐c]) from the mitochondria into the cytoplasm and eventually the induction of apoptosis. PFT‐α inhibited the expression ofp53, ameliorated the MMP of the co‐cultured Sertoli‐germ cells, and prevented the release of Cyt‐c from the mitochondria into the cytoplasm, which reduces the occurrence of apoptosis. Similarly, the decreased release of Cyt‐c from the mitochondria into the cytoplasm and the declined level of apoptosis in Sertoli‐germ cells induced by MC‐LR were observed after the addition of CsA. These results indicated that the apoptosis of the co‐cultured Sertoli‐germ cells induced by MC‐LR was mediated by the p53‐dependent pathway, with the involvement of the opening of mPTP.

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Berbamine induces SMMC-7721 cell apoptosis via upregulating p53, downregulating survivin expression and activating mitochondria signaling pathway

Cited by 14 publications

References 37 publications

In vitro and in vivo superior radiosensitizing effect of berbamine for head and neck squamous cell carcinoma

In vitro and in vivo superior radiosensitizing effect of berbamine for head and neck squamous cell carcinoma

Berbamine Inhibits Cell Proliferation, Migration, and Invasion and Induces Cell Apoptosis of A549 Cells Via Regulating C-Maf, PI3K/Akt and MDM2-P53 Pathways

p53‐Dependent pathway and the opening of mPTP mediate the apoptosis of co‐cultured Sertoli‐germ cells induced by microcystin‐LR

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