Epirubicin induces apoptosis in osteoblasts through death-receptor and mitochondrial pathways

Huang, Tzu-Ching; Chiu, Pu-Rong; Chang, Wai Hoong; Hsieh, Bau-Shan; Huang, Yu‐Chi; Cheng, Hsiao-Ling; Huang, Liwen; Hu, Yue; Chang, Kee-Lung

doi:10.1007/s10495-018-1450-2

Cited by 28 publications

(15 citation statements)

References 29 publications

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“…In the present study, McAb blocked extracellular 15-kDa-ALR without influencing 23-kDa-ALR, which may be the reason for the inconsistent results with previous studies. Therefore, epirubicin, a traditional chemotherapy drug used to induce apoptosis (40), was employed in the present study. When the injury factor was present, apoptosis was increased as expected.…”

Section: Discussionmentioning

confidence: 99%

Blocking the short isoform of augmenter of liver regeneration inhibits proliferation of human multiple myeloma U266 cells via the MAPK/STAT3/cell cycle signaling pathway

Huang

Sun

et al. 2021

Oncol Lett

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Multiple myeloma (MM) is the second most common haematological malignancy and remains an incurable disease, with most patients relapsing and requiring further treatment. Augmenter of liver regeneration (ALR) is a vital protein affecting fundamental processes such as energy transduction, cell survival and regeneration. Silencing ALR inhibits cell proliferation and triggers apoptosis in human MM U266 cells. However, little is known about the role of 15-kDa-ALR on MM. In the present study, the role of 15-kDa-ALR in human MM cells was investigated. Blocking extracellular 15-kDa-ALR with an anti-ALR monoclonal antibody (McAb) decreased the proliferation and viability of U266 cells. However, the results of flow cytometry revealed no changes in apoptosis, and the expression levels of Bax, Bcl-2, caspase-3 and cleaved caspase-3 were not affected. However, combined treatment with anti-ALR McAb and epirubicin increased the apoptosis of U266 cells. RNA sequencing results indicated that the ERK1/2, JNK-MAPK and STAT3 signaling pathways, as well as the cell cycle, were associated with the mechanism of action of the anti-ALR McAb, and PCR, western blotting and cell cycle analysis confirmed these results. The present findings suggested that blocking extracellular 15-kDa-ALR in U266 cells with an anti-ALR McAb decreased cell proliferation via the MAPK, STAT3 and cell cycle signaling pathways without increasing apoptosis. Thus, 15-kDa-ALR may be a new therapeutic target for myeloma.

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Section: Discussionmentioning

confidence: 99%

Blocking the short isoform of augmenter of liver regeneration inhibits proliferation of human multiple myeloma U266 cells via the MAPK/STAT3/cell cycle signaling pathway

Huang

Sun

et al. 2021

Oncol Lett

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“…There are two pathways in caspase-dependent cell apoptosis: the death receptor-mediated exogenous pathway and the mitochondrial-mediated endogenous pathway [ 27 ]. The common induction of apoptosis involves one of the apoptotic modes [ 28 , 29 , 30 ]; studies on triggering endogenous and exogenous apoptosis are widely available [ 31 , 32 , 33 ]. Exogenous pathways are caspase cascades triggered by the binding of death receptor Fas or TFN-α with its extracellular ligands.…”

Section: Discussionmentioning

confidence: 99%

N6-(2-hydroxyethyl)-Adenosine Induces Apoptosis via ER Stress and Autophagy of Gastric Carcinoma Cells In Vitro and In Vivo

Xie

Yang

et al. 2020

IJMS

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Gastric cancer is the most common malignant tumor of the digestive tract and is great challenge in clinical treatment. N6-(2-Hydroxyethyl)-adenosine (HEA), widely present in various fungi, is a natural adenosine derivative with many biological and pharmacological activities. Here, we assessed the antineoplastic effect of HEA on gastric carcinoma. HEA exerted cytotoxic effects against gastric carcinoma cells (SGC-7901 and AGS) in a dose and time-dependent manner. Additionally, we found that HEA induced reactive oxygen species production and mitochondrial membrane potential depolarization. Moreover, it could trigger caspase-dependent apoptosis, promoting intracellular Ca2+-related endoplasmic reticulum (ER) stress and autophagy. On the other hand, HEA could significantly inhibit the growth of transplanted tumors in nude mice and induce apoptosis of tumor tissues cells in vivo. In conclusion, HEA induced apoptosis of gastric carcinoma cells in vitro and in vivo, demonstrating that HEA is a potential chemotherapeutic agent for gastric carcinoma.

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“…Studies have found that epirubicin can increase the expression of FasL and FADD, the extrinsic apoptotic pathway‐related factors in primary cultured osteosarcoma cells. These factors then upregulate the content of ROS, Bax, and Cyt‐c in cells, inducing apoptosis through the mitochondrial‐dependent pathway . Berbamine can also lead to the loss of MMP in human hepatocellular carcinoma cells (SMMC‐7721).…”

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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Epirubicin induces apoptosis in osteoblasts through death-receptor and mitochondrial pathways

Cited by 28 publications

References 29 publications

Blocking the short isoform of augmenter of liver regeneration inhibits proliferation of human multiple myeloma U266 cells via the MAPK/STAT3/cell cycle signaling pathway

Blocking the short isoform of augmenter of liver regeneration inhibits proliferation of human multiple myeloma U266 cells via the MAPK/STAT3/cell cycle signaling pathway

N6-(2-hydroxyethyl)-Adenosine Induces Apoptosis via ER Stress and Autophagy of Gastric Carcinoma Cells In Vitro and In Vivo

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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