CpG Oligodeoxynucleotides Induces Apoptosis of Human Bladder Cancer Cells via Caspase-3-Bax/Bcl-2-p53 Axis

Luo, Yan; Fu, Xiaoyi; Ru, Ruizhen; Han, Bin; Zhang, Fafu; Yuan, Lihong; Men, Hongsheng; Zhang, Shulin; Tian, Shaomin; Dong, Bin; Mei, Meng

doi:10.1016/j.arcmed.2020.02.005

Cited by 20 publications

(16 citation statements)

References 40 publications

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“…In many instances, apoptosis is involved in tissue damage, and Bax, Bcl-2 and caspase-3 have been confirmed to be important apoptosis-regulating proteins [13]. As shown in Figure 4, CTN significantly increased Bax/Bcl-2 and cleaved-caspase-3/pro-caspase-3 ratios in a dose-dependent manner (p < 0.01) (Figure 4), suggesting that CTN induced hepatocyte apoptosis.…”

Section: The Effects Of Ctn On Hepatocyte Apoptosismentioning

confidence: 84%

Citrinin-Induced Hepatotoxicity in Mice Is Regulated by the Ca2+/Endoplasmic Reticulum Stress Signaling Pathway

Yang

et al. 2022

Toxins

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Citrinin (CTN) is a mycotoxin found in crops and agricultural products and poses a serious threat to human and animal health. The aim of this study is to investigate the hepatotoxicity of CTN in mice and analyze its mechanisms from Ca2+-dependent endoplasmic reticulum (ER) stress perspective. We showed that CTN induced histopathological damage, caused ultrastructural changes in liver cells, and induced abnormal values of biochemical laboratory tests of some liver functions in mice. Treatment with CTN could induce nitric oxide (NO), malondialdehyde (MDA), and reactive oxygen species (ROS) accumulation in mice, accompanied with losses of activities of superoxide dismutase (SOD) and catalase (CAT), levels of glutathione (GSH), and capacities of total antioxidant (T-AOC), resulting in oxidative stress in mice. Furthermore, CTN treatment significantly increased Ca2+ accumulation, upregulated protein expressions of ER stress-mediated apoptosis signal protein (glucose regulated protein 78 (GRP78/BIP), C/EBP-homologous protein (CHOP), Caspase-12, and Caspase-3), and induced hepatocyte apoptosis. These adverse effects were counteracted by 4-phenylbutyric acid (4-PBA), an ER stress inhibitor. In summary, our results showed a possible underlying molecular mechanism for CTN that induced hepatocyte apoptosis in mice by the regulation of the Ca2+/ER stress signaling pathway.

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Section: The Effects Of Ctn On Hepatocyte Apoptosismentioning

confidence: 84%

Citrinin-Induced Hepatotoxicity in Mice Is Regulated by the Ca2+/Endoplasmic Reticulum Stress Signaling Pathway

Yang

et al. 2022

Toxins

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“…P53 inhibition in pancreatic cancer cells could enhance MDM2 expression and reduce BAX, caspase 3, caspase 9, and cyclin-dependent kinase inhibitor 1A (p21) . Bai et al found that cytosine-phosphorothioate-guanine oligodeoxynucleotides could induce apoptosis in human bladder cancer cells by enhanced expressions of pro-apoptotic-related factors caspase 3, BAX, and p53, as well as reduced BCL2 expression . Cytochrome c (Cyt- c ) is one of the key mediators of the mitochondrial-mediated endogenous apoptotic pathway, which can be released from the mitochondria into the cytoplasm under oxidative stress. , Li et al found that the expression levels of Cyt- c and caspase 3 in human multiple myeloma cells exposed to zinc oxide nanoparticles were significantly higher than those in the control group .…”

Section: Results and Discussionmentioning

confidence: 99%

Hormesis Effect of Methyl Triclosan on Cell Proliferation and Migration in Human Hepatocyte L02 Cells

Yao

Tang

et al. 2021

ACS Omega

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Methyl triclosan (mTCS) is a methylated derivative of triclosan (TCS), which is extensively used as an antimicrobial component of various nursing products and disinfectants. Current research studies of mTCS mainly focused on the environmental persistence and bioaccumulation potential. Knowledge regarding the toxicity and carcinogenicity of mTCS is limited until now. In this study, the human hepatocyte L02 cells were used to investigate the cellular effects of mTCS under different concentrations (0.1–60 μM). The hormesis effect was observed where a low dose of mTCS (≤5 μM) exposure stimulated the cell proliferation ability, while high-dose exposure (≥20 μM) inhibited cell proliferation. In the same time, low doses of mTCS (0.5 and 1 μM) induced enhanced anchorage-independent proliferation ability and cell migration ability, indicating a positive effect on malignant transformation in L02 cells. Moreover, reactive oxygen species productions were significantly increased after mTCS exposure (≥1 μM), as compared with the control group. Furthermore, expressions of tumor-related genes, mouse double minute 2 (MDM2), matrix metalloproteinase 9 (MMP9), and proliferating cell nuclear antigen (PCNA), and proto-oncogene MYC (c-Myc), Jun, and FosB were significantly upregulated, while no significant changes were observed on expressions of apoptosis-related and cell cycle-related genes in L02 cells after exposure of low-dose mTCS. In conclusion, these results indicated that a low dose of mTCS had a hormesis effect in L02 cells on cell proliferation and malignant transformation in vitro, which might be mediated through oxidative stress response.

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“…In order to detect the immunohistochemical features of apoptosis, 3,3′-diaminobenzidine (DAB) staining was performed to detect caspase-3 (a well-known marker for apoptosis (Luo et al, 2020)) on the porcine urinary bladder tissues. The tissues from the ex-vivo model were sectioned and mounted on slides as above.…”

Section: Immunohistochemistry Of Caspase-3mentioning

confidence: 99%

P2X7 Receptor Blockade Protects Against Acrolein-Induced Bladder Damage: A Potential New Therapeutic Approach for the Treatment of Bladder Inflammatory Diseases

et al. 2021

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Inflammatory conditions of the urinary bladder have been shown to be associated with urothelial damage and loss of function. The purinergic P2X7 receptor has been implicated in several inflammatory conditions. The aim of this study was to investigate the role of the P2X7 receptor in acrolein-induced inflammatory damage using the porcine urinary bladder. For this purpose, an ex-vivo model of porcine urothelial damage induced by direct instillation of acrolein into the whole bladder lumen was used. To determine the role of the P2X7 receptor, the bladders were pre-incubated with a selective P2X7 receptor antagonist, A804598 (10 μM), for 1 h. The effects of the acrolein-induced urothelial damage on the bladder’s function were assessed by examining the bladder wall contractile response, structure changes, apoptosis, and oxidative stress in the bladder tissues. The acrolein treatment led to significant damage to the urothelium histology, tight junction expression, and contractile responses. Acrolein also induced apoptosis in the mucosa layer. All these acrolein-induced responses were attenuated by pre-treatment with the P2X7 receptor antagonist A804598. Acrolein also significantly induced DNA oxidation in the submucosal layer; however, the P2X7 receptor antagonism did not show any protective effect towards the acrolein-induced oxidative stress. These findings suggested that the P2X7 receptor is involved in the acrolein-induced damage to the urothelium; therefore, the P2X7 receptor antagonists may be a new therapeutic option for the treatment of bladder inflammation.

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CpG Oligodeoxynucleotides Induces Apoptosis of Human Bladder Cancer Cells via Caspase-3-Bax/Bcl-2-p53 Axis

Cited by 20 publications

References 40 publications

Citrinin-Induced Hepatotoxicity in Mice Is Regulated by the Ca2+/Endoplasmic Reticulum Stress Signaling Pathway

Citrinin-Induced Hepatotoxicity in Mice Is Regulated by the Ca2+/Endoplasmic Reticulum Stress Signaling Pathway

Hormesis Effect of Methyl Triclosan on Cell Proliferation and Migration in Human Hepatocyte L02 Cells

P2X7 Receptor Blockade Protects Against Acrolein-Induced Bladder Damage: A Potential New Therapeutic Approach for the Treatment of Bladder Inflammatory Diseases

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