The influence of arsenic trioxide on the cell cycle, apoptosis and expression of cyclin D1 in the Jurkat cell line

Żuryń, Agnieszka; Litwiniec, Anna; Gagat, Maciej; Drzewucka, Joanna; Gackowska, Lidia; Grzanka, Alina

doi:10.1016/j.acthis.2014.08.008

Cited by 10 publications

(4 citation statements)

References 30 publications

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“…Notably, MIC, at 25 and 50 µM, stimulated p53 expression in the TSGH-8301 (wild-type) cells, but not in the T24 (p53 mutant) cells as compared to the untreated cells. However, 25 or 50 µM MIC inhibited expression of cyclin D1, which is required for G1/S transition (20), in the TSGH-8301 cells, resulting in growth arrest. However, MIC at these concentrations stimulated cyclin D1 expression in the T24 cells.…”

Section: Mic Increases P21 and P27 Levels And Inhibits Cyclin E1 CDmentioning

confidence: 99%

Miconazole induces apoptosis via the death receptor 5-dependent and mitochondrial-mediated pathways in human bladder cancer cells

Yuan

Shiau

et al. 2017

Oncology Reports

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Abstract. Miconazole (MIC), an antifungal agent, diplays anti-tumorigenic activity in various types of human cancers, including bladder cancer, yet its mechanism of antitumor action is not well understood. In the present study, we demonstrated that, in a cell viability assay, MIC had a cytotoxic effect on human T24, J82 and TSGH-8301 bladder cancer cells in a dose-and time-dependent manner, but did not exhibit significant toxicity toward human peripheral blood mononuclear cells. Cell cycle analysis revealed that MIC at concentrations of 25 and 50 µM significantly caused G0/G1 arrest in the TSGH-8301 and T24 cells, respectively. DNA fragmentation, mitochondrial membrane potential and western blot analyses showed that MIC inhibited the growth of these cells by both mitochondrial-mediated and death receptor (DR5)-mediated apoptosis pathways. Specifically, MIC increased the protein levels of p21 and p27, but decreased the expression of cyclin E1, CDK2 and CDK4. MIC augmented the expression of DR5, cleaved forms of caspase-3 -8 and -9, poly(ADP-ribose) polymerase and Bax, decreased the expression of Bcl-2 but increased cytosol levels of cytochrome c. Our results suggest that MIC inhibits the growth of bladder cancer cells through induction of G0/G1 arrest and apoptosis via activation of both the extrinsic and intrinsic apoptotic pathways. MIC is a potential chemotherapeutic agent for treating bladder cancer in humans.

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Section: Mic Increases P21 and P27 Levels And Inhibits Cyclin E1 CDmentioning

confidence: 99%

Miconazole induces apoptosis via the death receptor 5-dependent and mitochondrial-mediated pathways in human bladder cancer cells

Yuan

Shiau

et al. 2017

Oncology Reports

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“…The results from the present study indicated that AKT/GSK-3β pathway was activated, resulting in the change of p-AKT, p-GSK-3β, p-Rb and cyclin D1 protein expression. These proteins are strongly associated with cell cycle progression and apoptosis ( 32 – 34 ). Furthermore, the A549 cell cycle transitioned from G 1 to S phase, which stimulates proliferation and inhibits apoptosis ( 35 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑421 promotes the viability of A549 lung cancer cells by targeting forkhead box O1

Qin

Wang

et al. 2020

Oncol Lett

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MicroRNA (miR)-421 has been reported to serve various important roles in numerous types of cancer, including neuroblastoma and gastric cancer. However, to the best of our knowledge, few reports have determined the role of miR-421 in lung cancer. The aim of the current study was to analyze the expression levels of miR-421 in A549 lung cancer cells, to determine the target gene of miR-421, and to investigate the function and mechanism of miR-421 in cellular cytotoxicity. miR-421 expression levels were analyzed in A549 lung cancer cells using reverse transcription-quantitative PCR, a MTT assay was performed to determine the effect of miR-421 on A549 cell cytotoxicity and the protein expression levels of forkhead box O1 (FOXO1) were determined via western blotting. The target gene of miR-421 was predicted and verified using TargetScan and a dual-luciferase reporter assay, respectively. The results revealed that miR-421 expression levels were significantly upregulated in A549 lung cancer cell lines compared with the normal cells (P<0.01). Additionally, it was discovered that miR-421 promoted A549 cell viability (P<0.01) compared with A549 transfected with negative control. miR-421 was also identified to bind to the 3'-untranslated region of FOXO1. In A549 cells transfected with miR-421-mimics, the expression levels of phosphorylated (p)-AKT, p-glycogen synthase kinase-3β, p-retinoblastoma and cyclin D1 were significantly upregulated (P<0.01), whereas the expression levels of FOXO1 and p21 were significantly downregulated (P<0.01) compared with the control group. In conclusion, the results of the present study suggested that miR-421 may promote the viability of A549 lung cancer cells by targeting FOXO1 and modulating cell cycle, indicating that targeting miR-421 and FOXO1 may represent future therapeutic strategies for the treatment of patients with lung cancer.

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“…Treatment of HT-29 cells with the combination of 5-FU and CFL reduced FAK expression and [iCa2+] levels and showed antitumor ability through activation of p21 protein. Previously, some proteins and peptides with antitumor activities have been found in CFL [20–22].…”

Section: Discussionmentioning

confidence: 99%

Coelomic Fluid of Lumbricus rubellus Synergistically Enhances Cytotoxic Effect of 5-Fluorouracil through Modulation of Focal Adhesion Kinase and p21 in HT-29 Cancer Cell Line

Endharti

Purnamasari

Primasari

et al. 2019

The Scientific World Journal

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Coelomic fluid of Lumbricus rubellus (CFL) has attracted interest due to its pharmacological properties, including antitumor effect. Furthermore, it is necessary to evaluate the response to treatment with new cancer therapeutic agents. This study aims to investigate whether the combination of CFL and 5-fluorouracil could reduce FAK protein level and iCa2+ and enhance p21 level. Furthermore, it is necessary to evaluate the response to treatment with new cancer therapeutic agents. After 24 hours of treatment, it was necessary to assess the percentage of apoptosis, FAK, and p21 protein expression by flow cytometry. iCa2+ concentration was measured using immunofluorescence. The combination therapy of CFL with 5-fluorouracil potently suppressed six treatment groups were included in this study. HT-29 cell lines were cultured and divided into six groups: group 1 was treated with vehicle (negative control), groups 2-5 were treated with 5-fluorouracil, groups 3-5 were treated with either CFL 5, 10, or 20 µg/ml immediately after 5-fluorouracil, and group 6 was treated with CFL 20 µg/ml, the progression of colorectal cancer. Combination of CFL and 5-fluorouracil significantly decreased FAK expression (p<0.05), iCa2+ (p<0.05), and increased p21 expression (p<0.05) in HT-29 cells. Our results suggest that CFL has an anticancer potential in colorectal cancer when combined with 5-fluorouracil.

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The influence of arsenic trioxide on the cell cycle, apoptosis and expression of cyclin D1 in the Jurkat cell line

Cited by 10 publications

References 30 publications

Miconazole induces apoptosis via the death receptor 5-dependent and mitochondrial-mediated pathways in human bladder cancer cells

Miconazole induces apoptosis via the death receptor 5-dependent and mitochondrial-mediated pathways in human bladder cancer cells

miR‑421 promotes the viability of A549 lung cancer cells by targeting forkhead box O1

Coelomic Fluid of Lumbricus rubellus Synergistically Enhances Cytotoxic Effect of 5-Fluorouracil through Modulation of Focal Adhesion Kinase and p21 in HT-29 Cancer Cell Line

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