Arsenic compounds activate <scp>MAPK</scp> and inhibit Akt pathways to induce apoptosis in <scp>MA</scp>‐10 mouse Leydig tumor cells

Juan, W.; Mu, Yi-Fen; Wang, Chia‐Yih; So, Edmund Cheung; Lee, Yi-Ping; Lin, Shio‐Jean; Huang, Bu‐Miin

doi:10.1002/cam4.5068

Cited by 3 publications

(4 citation statements)

References 61 publications

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“…Studies have shown MAPK signaling pathways are involved to regulate cell survival, differentiation, gene expression, proliferation, mitosis and/or apoptosis ( 21 – 24 ). To test if MAPK pathways were associated with apoptosis induced by arsenic compounds in OC3 cells, JNK, ERK1/2 and p38 phosphorylation was analyzed with western blotting.…”

Section: Resultsmentioning

confidence: 99%

“…Apoptotic cascades are regulated by a number of cellular signal transduction pathways and the MAPK signaling pathway is one associated with cellular stress ( 15 , 16 , 21 – 24 ). It has been shown that MAPK signaling pathways can enhance cell survival or promote sensitivity to apoptosis, which depends on different stimuli, cell types and activation latency ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

“…Conventional MAPKs include three members: ERK, p38 and JNK ( 22 ), which regulate cell mitosis, survival, gene expression, proliferation, differentiation and apoptosis ( 23 ). According to different cell types and stimuli, MAPKs can promote cells to survive and/or to undergo cell death ( 20 , 21 , 24 ). In fact, ATO can induce p38 and JNK phosphorylation, which result in human cervical cancer cell death through mitochondrial apoptotic cascade death ( 25 ).…”

Section: Introductionmentioning

confidence: 99%

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Sodium arsenite and dimethylarsenic acid induces apoptosis in OC3 oral cavity cancer cells

Lan

Chu

et al. 2022

Mol Med Rep

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although arsenic is an environmental toxicant, arsenic trioxide (aTo) is used to treat acute promyelocytic leukemia (aPl) with anticancer effects. Studies have demonstrated oral cancer is in the top 10 cancers in Taiwan. High rate of oral cancers is linked to various behaviors, such as excessive alcohol consumption and tobacco use. Similarly, betel chewing is a strong risk factor in oral cancer. in the present study, oral squamous carcinoma oc3 cells were investigated with the treatments of sodium arsenite (naaso 2 ) and dimethylarsenic acid (dMa), respectively, to examine if arsenic compounds have anti-cancer efforts. it was found that 1 µM naaso 2 and 1 mM dMa for 24 h induced rounded contours with membrane blebbing phenomena in oc3 cells, revealing cell apoptotic characteristics. in addition, naaso 2 (10-100 µM) and DMA (1-100 mM) significantly decreased OC3 cell survival. In cell cycle regulation detected by flow cytometry, NaAsO 2 and DMA significantly augmented percentage of subG 1 and G 2 /M phases in oc3 cells, respectively. annexin V/Pi double staining assay was further used to confirm NaAsO 2 and dMa did induce oc3 cell apoptosis. in mechanism investigation, western blotting assay was applied and the results showed that naaso 2 and DMA significantly induced phosphorylation of JnK, erK1/2 and p38 and then the cleavages of caspase-8, -9, -3 and poly adP-ribose polymerase (ParP) in oc3 cells, dynamically. in conclusion, naaso 2 and dMa activated MaPK pathways and then apoptotic pathways to induce oc3 oral cancer cell apoptosis.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Sodium arsenite and dimethylarsenic acid induces apoptosis in OC3 oral cavity cancer cells

Lan

Chu

et al. 2022

Mol Med Rep

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“…PVDF membrane with transferred protein was incubated in blocking buffer (5% non-fat milk in 0.1% TBST washing buffer) for 1 h and incubated with primary antibodies for 16–18 h at 4 °C. Membranes were washed 3 times with TBST and incubated with the appropriate dilution of HRP-conjugated secondary antibodies for 1 h. Signaling was visualized through UVP EC3 BioImaging Systems (UVP, Upland, CA, USA) by ECL detection kit [ 38 ]. The quantificational analysis was analyzed with ImageJ program version 1.5 (NIH, Bethesda, MD, USA).…”

Section: Methodsmentioning

confidence: 99%

Cordycepin inhibits ERK pathway to suppress FGF9-induced tumorigenesis with MA-10 mouse Leydig tumor cells

Chen,

Lee

et al. 2023

Journal of Food and Drug Analysis

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Fibroblast growth factor 9 (FGF9) is a member of FGF family, and abnormal expression of FGF9 can promote tumorigenesis. Cordycepin, a major bioactive component in fungus Cordyceps sinensis , could suppress various tumors. We have shown that cordycepin could inhibit FGF9-induced testicular tumor growth in vitro and in vivo with MA-10 mouse Leydig tumor cells. In the present study, the mechanisms related to apoptosis and autophagy were determined. Results show that cordycepin significantly suppressed cell viability and colony formation with correlatedly morphological change related to cell death in FGF9-treated MA-10 cells. Flow cytometry and western blotting results further demonstrate that cordycepin induced apoptosis through the cleavage of caspase-8, -9, -3 and PARP in FGF9-treated MA-10 cells. However, the expressions of LC3-II, beclin-1 and p62 were not stimulated by cordycepin with the presence of FGF9, suggesting cordycepin would activate apoptosis, but not autophagy, in FGF9-treated MA-10 cells. Moreover, inhibition of ERK signal pathway and autophagy would enhance cordycepin-induced cell death effects in FGF9-treated MA-10 cells, referring that ERK signaling was regulated under cordycepin and FGF9 treatments. In NOD-SCID mouse allograft model inoculated with MA-10 cells, cordycepin significantly suppressed tumor growth with the presence of FGF9, and the cleavage of caspase-3 could be observed in tumor tissue, implying cordycepin induced caspase cascade to suppress tumor growth. Moreover, cordycepin plus U0126, ERK inhibitor, further significantly suppressed tumor growth with the presence of FGF9 as compared to the FGF9 only group, confirming the involvement of ERK signaling in this event. In conclusion, cordycepin induced caspase and ERK pathways to promote MA-10 cell apoptosis, but not autophagy, with the presence of FGF9.

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Role of intrinsic apoptosis in environmental exposure health outcomes

Johnson,

Sarosiek

2024

Trends in Molecular Medicine

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Arsenic compounds activate MAPK and inhibit Akt pathways to induce apoptosis in MA‐10 mouse Leydig tumor cells

Cited by 3 publications

References 61 publications

Sodium arsenite and dimethylarsenic acid induces apoptosis in OC3 oral cavity cancer cells

Sodium arsenite and dimethylarsenic acid induces apoptosis in OC3 oral cavity cancer cells

Cordycepin inhibits ERK pathway to suppress FGF9-induced tumorigenesis with MA-10 mouse Leydig tumor cells

Role of intrinsic apoptosis in environmental exposure health outcomes

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