scholarly journals Aloperine executes antitumor effects through the induction of apoptosis and cell cycle arrest in prostate cancer in vitro and in vivo

2018 ◽  
Vol Volume 11 ◽  
pp. 2735-2743 ◽  
Author(s):  
Zhixin Ling ◽  
Han Guan ◽  
Zonghao You ◽  
Can Wang ◽  
Ling Hu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Antitumor Effects ◽  
Cycle Arrest ◽  
Induction Of Apoptosis

scholarly journals Solasonine Suppresses the Proliferation of Acute Monocytic Leukemia Through the Activation of the AMPK/FOXO3A Axis

2021 ◽  
Vol 10 ◽  
Author(s):  
Hong Zhang ◽  
Fang Tian ◽  
Pengjun Jiang ◽  
Shushu Qian ◽  
Xingbin Dai ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Acute Monocytic Leukemia ◽  
Monocytic Leukemia ◽  
Antitumor Effects ◽  
Cycle Arrest ◽  
Compound C ◽  
M Phase

Solasonine, the main active ingredient of Solanum nigrum L., has been reported to exert extensive antitumor activity. However, the antitumor effects in acute monocytic leukemia and the exact mechanisms involved are unknown. In this study, we investigated the role of solasonine on inhibiting the progression of acute monocytic leukemia. Our findings showed that solasonine inhibited the proliferation of acute monocytic leukemic cell lines (THP-1 and MV4-11) in vitro. Solasonine promoted apoptosis and induced cell cycle arrest in the G2/M phase. Analysis of RNA-seq data suggested that solasonine correlated with increased expression of genes in the AMPK/FOXO3A pathway. Inhibition of AMPK with compound C followed by treatment with solasonine showed that solasonine reduced apoptosis, caused less cell cycle arrest, and inactivated the AMPK/FOXO3A axis in THP-1 and MV4-11 cells. Solasonine also inhibited tumor growth by the activation of the AMPK/FOXO3A axis. In conclusion, solasonine inhibited the progress of acute monocytic leukemia in vitro and in vivo and triggered the apoptosis and cell cycle arrest in the G2/M phase by upregulating the AMPK/FOXO3A pathway.

scholarly journals Mechanism of Growth Inhibition of Prostate Cancer Xenografts by Valproic Acid

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Abhinav Sidana ◽  
Muwen Wang ◽  
Shabana Shabbeer ◽  
Wasim H. Chowdhury ◽  
George Netto ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Valproic Acid ◽  
Tumor Growth ◽  
Growth Inhibition ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
Angiogenic Effect

Valproic Acid (VPA), a histone deacetylase inhibitor, has been demonstrated to cause a marked decrease in proliferation of prostate cancer (PCa) cellsin vitroand a significant reduction in tumor volumein vivo. The goal of this study is to better understand the VPA-induced growth inhibitionin vivo, by studying expression of various markers in PCa xenografts.Methods. Forin vitroexperiments, PCa cells were treated with 0, 0.6, and 1.2 mM VPA for 14 days. Forin vivomodels, experimental animals received 0.4% VPA in drinking water for 35 days. Tissue microarray was generated using cell pellets and excised xenografts.Results. VPA treatment causes cell cycle arrest in PCa cellsin vivo, as determined by increase in p21 and p27 and decrease in cyclin D1 expression. Increased expression of cytokeratin18 was also seen in xenografts. LNCaP xenografts in treated animals had reduced androgen receptor (AR) expression. While decreased proliferation was foundin vitro, increase in apoptosis was found to be the reason for decreased tumor growthin vivo. Also, an anti-angiogenic effect was observed after VPA treatment.Conclusion. VPA inhibits tumor growth by multiple mechanisms including cell cycle arrest, induction of differentiation, and inhibition of growth of tumor vasculature.

scholarly journals Crocin Exhibits Antitumor Effects on Human Leukemia HL-60 Cells In Vitro and In Vivo

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Yan Sun ◽  
Hui-Juan Xu ◽  
Yan-Xia Zhao ◽  
Ling-Zhen Wang ◽  
Li-Rong Sun ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Nude Mice ◽  
Dependent Manner ◽  
Antitumor Effects ◽  
Tumor Weight ◽  
Cycle Arrest

Crocin is a carotenoid of the saffron extract that exhibits antitumor activity against many human tumors. However, the effects of crocin on HL-60 cells in vivo have not been evaluated. This study aimed to examine the effects of crocin on HL-60 cells in vitro and in vivo and investigate the underlying mechanisms. HL-60 cells were treated by crocin, and cell proliferation, apoptosis, and cell cycle profiles were examined by MTT assay, AO/EB staining, and flow cytometry, respectively. Furthermore, HL-60 cells were xenografted into nude mice and treated by crocin, the tumor weight and size were calculated, and the expression of Bcl-2 and Bax in xenografts was detected by immunohistochemical staining. The results showed that crocin (0.625–5 mg/mL) inhibited HL-60 cell proliferation and induced apoptosis and cell cycle arrest at G0/G1 phase, in a concentration and time-dependent manner. In addition, crocin (6.25, 25 mg/kg) inhibited the tumor weight and size of HL-60 xenografts in nude mice, inhibited Bcl-2 expression, and increased Bax expression in xenografts. In summary, crocin inhibits the proliferation and tumorigenicity of HL-60 cells, which may be mediated by the induction of apoptosis and cell cycle arrest and the regulation of Bcl-2 and Bax expression.

scholarly journals All-Purpose Nanostrategy Based on Dose Deposition Enhancement, Cell Cycle Arrest, DNA Damage and ROS Production as Prostate Cancer Radiosensitizer for Potential Clinical Translation

2021 ◽  
Author(s):  
Xiao-xiao Guo ◽  
Zhen-hu Guo ◽  
Meng Wu ◽  
Jing-song Lu ◽  
Wen-sheng Xie ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Clinical Translation ◽  
Ros Production ◽  
Cycle Arrest ◽  
Dose Deposition

Abstract Background Radiotherapy (RT) is one of the main treatments for men with prostate cancer (PCa). Yet, to date, with numerous sophisticated nano-formulations as radiosensitizers have been synthesized with inspiring therapeutic effect both in vitro and in vivo, there still lacks the successful clinical translation of such nanosystems. Meanwhile, almost all the attention has been paid on the enhanced dose deposition effect by secondary electrons of nanomaterials with high atomic numbers (Z), despite that cell-cycle arrest, DNA damage and also reactive oxygen species (ROS) production are critical working mechanisms accounting for radiosensitization. Methods Herein, an ‘all-purpose’ nanostrategy based on dose deposition enhancement, cell cycle arrest and ROS production as prostate cancer radiosensitizer for potential clinical translation was proposed. The rather simple structure of docetaxel loaded Au nanoparticles (NPs) with prostate specific membrane antigen (PSMA) ligand conjugation have been successfully synthesized by a rather facile protocol. Results Enhanced cellular uptake achieved via selective internalization of the NPs by PCa cells with positive PSMA expression could guarantee the enhanced dose deposition. Moreover, the as-synthesized nanosystem could arrest cell cycle at G2/M phases, which would reduce the ability of DNA damage repair for more irradiation sensitive of the PCa cells. Meanwhile, G2/M phases arrest would further promote cascade retention and enrichment of the NPs within the cells. Furthermore, ROS generation and double strand breaks greatly promoted by the NPs under irradiation (IR) could also provide an underlying basis for effective radiosensitizers. Conclusions Investigations from in vitro and in vivo confirmed the as-synthesized NPs as an effective nano-radiosensitizer with ideal safety. More importantly, all the moieties within the present nanosystem have been approved by FDA for the purpose of PCa treatment, thus making the it highly attractive for clinical translation.

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