Cadmium induces apoptotic program imbalance and cell cycle inhibitor expression in cultured human astrocytes

Ospondpant, Dusadee; Phuagkhaopong, Suttinee; Suknuntha, Kran; Sangpairoj, Kant; Kasemsuk, Thitima; Srimaroeng, Chutima; Vivithanaporn, Pornpun

doi:10.1016/j.etap.2018.12.001

Cited by 29 publications

(10 citation statements)

References 34 publications

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“…Taken together, these results indicate Ca 2+ as a fundamental mediator of Cd 2+ in its negative neuronal effect. The effect on glia, in particular on astrocytes, has been tested by Ospondpant et al [59], demonstrating how intracellular Cd 2+ increase, decrease the glutathione levels, increase Ca 2+ content, altering mitochondrial membrane state end activate the JNK and PI3k/Akt pathways, to induce astrocyte apoptosis. The ability of Cd 2+ to induce apoptosis and cell cycle arrest is analyzed in this study, and the authors observed that Cd 2+ concentrations > 20 μM induce DNA fragmentation, Bcl2 downregulation, and Bax upregulation and the promotion of p53, p27, and p21 [59].…”

Section: Cellular Implication Of Cadmium In Als Modelsmentioning

confidence: 99%

“…The effect on glia, in particular on astrocytes, has been tested by Ospondpant et al [59], demonstrating how intracellular Cd 2+ increase, decrease the glutathione levels, increase Ca 2+ content, altering mitochondrial membrane state end activate the JNK and PI3k/Akt pathways, to induce astrocyte apoptosis. The ability of Cd 2+ to induce apoptosis and cell cycle arrest is analyzed in this study, and the authors observed that Cd 2+ concentrations > 20 μM induce DNA fragmentation, Bcl2 downregulation, and Bax upregulation and the promotion of p53, p27, and p21 [59]. In conclusion, the idea of an involvement of Cd among the behavioral components implicated in the ALS insurgence seems to be supported by the literature of in vitro models, with different mechanisms such as alteration of antioxidants, cell cycle, and cell fate system, to induce motor neuron cell death (Fig.…”

Section: Cellular Implication Of Cadmium In Als Modelsmentioning

confidence: 99%

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An overview on amyotrophic lateral sclerosis and cadmium

et al. 2020

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The present review represents an update about the knowledge of the possible role of Cadmium (Cd) in amyotrophic lateral sclerosis (ALS) initiation and its progression. ALS is a neurodegenerative disease that occurs in adulthood; its etiology is unknown and leads to death within a few years from its appearance. Among the various possible causes that can favor the development of the disease, heavy metals cannot be excluded. Cadmium is a heavy metal that does not play a biological role, but its neurotoxicity is well known. Numerous in vitro studies on cell and animal models confirm the toxicity of the metal on the nervous system, but these data are not accompanied by an epidemiological evidence, and, thus, an unclear correlation between Cd and the onset of the disease can be pointed out. On the other hand, a possible multifactorial and synergic mechanism in which Cd may have a role can explain the ALS onset. More efforts in new clinical, biochemical, and epidemiological studies are necessary to better elucidate the involvement of Cd in this lethal disease.

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Section: Cellular Implication Of Cadmium In Als Modelsmentioning

confidence: 99%

Section: Cellular Implication Of Cadmium In Als Modelsmentioning

confidence: 99%

An overview on amyotrophic lateral sclerosis and cadmium

et al. 2020

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“…More recently, an alternative hypothesis has emerged in which the primary injury to the BEC is cytopathic, with altered expression of self-antigen (pyruvate dehydrogenase) as a consequence of injury. [36] Cadmium is cytopathic, inducing apoptosis, cell senescence and epithelial to mesenchymal transition; [37] all cardinal features of the BEC response to injury in PBC. [32][ [38][39][40] The observation of PSC being more common in rural, affluent areas raises questions regarding the inter-play between environmental entities in the landscape and socio-economic status.…”

Section: Discussionmentioning

confidence: 99%

Geo-epidemiology and environmental co-variate mapping of primary biliary cholangitis and primary sclerosing cholangitis

et al. 2021

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…28 Bax and Bcl-2 imbalance is key to the regulation of cell apoptosis. 29 Next, we measured the expression levels of Bax and Bcl-2. Western blotting results showed that a significant up-regulation of Bax level was detected in cells after ROS1 knockdown, whereas Bcl-2 was down-regulated.…”

Section: Discussionmentioning

confidence: 99%

<p>Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway</p>

Jian¹,

Sun³

et al. 2019

OTT

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Objectives: Gastric cancer ranks the fourth most common cancer and the third leading cause of cancer mortality in the world. ROS proto-oncogene 1 (ROS1) is an oncogene and ROS1 rearrangement has been reported in many cancers. Our study aimed to investigate the potential function and the precise mechanisms of ROS1 in gastric cancer. Methods: In our study, the analysis of ROS1 expression and clinical pathologic factors of gastric cancer in gastric cancer using TCGA database demonstrated that ROS1 expression was elevated in gastric cancer and related to T, N, M and TNM staging. High expression of ROS1 predicted poor survival in patients with gastric cancer. Then, we measured ROS1 expression in four human gastric cancer cell lines and knocked down ROS1 expression in BGC-823 and SGC-7901 cells by specific shRNA transfection via Lipofectamine 2000. The effect of ROS1 knockdown on cell proliferation, cell cycle distribution, cell apoptosis and metastasis in vitro was evaluated by MTT, colony formation, flow cytometric analysis, wound healing and Transwell invasion assays. The levels of apoptosis-related proteins, EMT markers and the PI3K/Akt signaling pathway members were measured by Western blotting. Results: We demonstrated that shROS1 transfection markedly downregulated ROS1 expression in BGC-823 and SGC-7901 cells. Knockdown of ROS1 inhibited cell survival, clonogenic growth, migration, invasion and epithelial-mesenchymal transition (EMT), as well as induced cell cycle arrest and apoptosis in gastric cancer cells. Furthermore, ROS1 knockdown inhibited the phosphorylation of PI3K and Akt. Conclusion: Collectively, our data suggest that ROS1 may serve as a promising therapeutic target in gastric cancer treatment.

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Cadmium induces apoptotic program imbalance and cell cycle inhibitor expression in cultured human astrocytes

Cited by 29 publications

References 34 publications

An overview on amyotrophic lateral sclerosis and cadmium

An overview on amyotrophic lateral sclerosis and cadmium

Geo-epidemiology and environmental co-variate mapping of primary biliary cholangitis and primary sclerosing cholangitis

<p>Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway</p>

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