scholarly journals Parthenolide Induces Apoptosis and Cell Cycle Arrest by the Suppression of miR-375 Through Nucleolin in Prostate Cancer

2021 ◽  
pp. 215-227
Author(s):  
Rajesh Kannan Moorthy ◽  
Sridharan Jayamohan ◽  
Mahesh Kumar Kannan ◽  
Antony Joseph Velanganni Arockiam
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Cycle Arrest ◽  
Morphological Changes ◽  
Microscopic Analysis ◽  
Cycle Arrest ◽  
G0 Phase ◽  
Bax Gene ◽  
Microscopic Techniques

Aims: To investigate the effect of parthenolide on nucleolin in controlling the expression of miR-375 that induces apoptosis and cell cycle arrest in prostate cancer. Study Design: This study is an experimental study. Methodology: The cytotoxicity effect of parthenolide was tested by MTT assay for 48 h. Microscopic techniques were used to identify the morphological changes of the cell line. The expression of apoptotic and cell cycle regulatory genes was analyzed by the Real-Time PCR. The phase of cell cycle arrest was identified by Flow cytometry. Results: The obtained results indicated that parthenolide induced cytotoxicity and suppressed the proliferation by reducing the growth of LNCaP cells in 48 h. The microscopic analysis showed the alteration of cell morphology and increase of cytoplasmic reactive oxygen species.  Parthenolide promotes apoptosis by the downregulation of nucleolin, Bcl-2, and up-regulation of Bax gene. Moreover, the flow cytometry assay showed the G1/G0 phase of cell cycle arrest. Conclusion: Parthenolide induces apoptosis and cell cycle arrest through nucleolin by the suppression of miR-375 in prostate cancer cells.

scholarly journals Peiminine Inhibits Glioblastoma in Vitro and in Vivo Through Cell Cycle Arrest and Autophagic Flux Blocking

2018 ◽  
Vol 51 (4) ◽  
pp. 1566-1583 ◽  
Author(s):  
Boxian Zhao ◽  
Chen Shen ◽  
Zhixing Zheng ◽  
Xiaoxiong Wang ◽  
Wenyang Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Cycle Arrest ◽  
Colony Formation ◽  
Morphological Changes ◽  
Autophagic Flux ◽  
Anticancer Activities ◽  
Cycle Arrest

Background/Aims: Glioblastoma multiforme (GBM) is the most devastating and widespread primary central nervous system tumour in adults, with poor survival rate and high mortality rates. Existing treatments do not provide substantial benefits to patients; therefore, novel treatment strategies are required. Peiminine, a natural bioactive compound extracted from the traditional Chinese medicine Fritillaria thunbergii, has many pharmacological effects, especially anticancer activities. However, its anticancer effects on GBM and the underlying mechanism have not been demonstrated. This study was conducted to investigate the potential antitumour effects of peiminine in human GBM cells and to explore the related molecular signalling mechanisms in vitro and in vivo Methods: Cell viability and proliferation were detected with MTT and colony formation assays. Morphological changes associated with autophagy were assessed by transmission electron microscopy (TEM). The cell cycle rate was measured by flow cytometry. To detect changes in related genes and signalling pathways in vitro and in vivo, RNA-seq, Western blotting and immunohistochemical analyses were employed. Results: Peiminine significantly inhibited the proliferation and colony formation of GBM cells and resulted in changes in many tumour-related genes and transcriptional products. The potential anti-GBM role of peiminine might involve cell cycle arrest and autophagic flux blocking via changes in expression of the cyclin D1/CDK network, p62 and LC3. Changes in Changes in flow cytometry results and TEM findings were also observed. Molecular alterations included downregulation of the expression of not only phospho-Akt and phospho-GSK3β but also phospho-AMPK and phospho-ULK1. Furthermore, overexpression of AKT and inhibition of AKT reversed and augmented peiminine-induced cell cycle arrest in GBM cells, respectively. The cellular activation of AMPK reversed the changes in the levels of protein markers of autophagic flux. These results demonstrated that peiminine mediates cell cycle arrest by suppressing AktGSk3β signalling and blocks autophagic flux by depressing AMPK-ULK1 signalling in GBM cells. Finally, peiminine inhibited the growth of U251 gliomas in vivo. Conclusion: Peiminine inhibits glioblastoma in vitro and in vivo via arresting the cell cycle and blocking autophagic flux, suggesting new avenues for GBM therapy.

scholarly journals Alantolactone pyrazoline analogue inhibits cancer cell proliferation and induces apoptosis in non-small cell lung carcinoma cells

2015 ◽  
Vol 10 (2) ◽  
pp. 409 ◽  
Author(s):  
Jing Lv ◽  
Ming-Qin Cao ◽  
Jian-Chun Yu
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Cell Cycle Arrest ◽  
Chromatin Condensation ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Cycle Arrest ◽  
H460 Cells ◽  
Dose Dependent

<p>The aim of the current study was to evaluate the anticancer and apoptotic effects of alantolactone pyrazoline analogue in human non-small cell lung cancer (NCI-H460) cells. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetra-zolium bromide) assay was used to evaluate the cell viability while as fluorescence microscopy was used to assess the effect on apoptosis, cellular and nuclear morphology. Flow cytometry evaluated the effect of APA on cell cycle arrest in these cells. The results revealed that APA induced potent, time and dose-dependent cytotoxic effects on the growth of NCI-H460 cells. It also inhibited colony forming tendency as well as cell invasion capability of these cancer cells. APA induced dose-dependent nuclear and cellular morphological effects including chromatin condensation and DNA fragmentation. Flow cytometry revealed that the anticancer effects of APA might be due to its cell cycle arrest inducing tendency in G0/G1 phase of the cell cycle.</p>

scholarly journals  -Mangostin, a xanthone from mangosteen fruit, promotes cell cycle arrest in prostate cancer and decreases xenograft tumor growth

2011 ◽  
Vol 33 (2) ◽  
pp. 413-419 ◽  
Author(s):  
J. J. Johnson ◽  
S. M. Petiwala ◽  
D. N. Syed ◽  
J. T. Rasmussen ◽  
V. M. Adhami ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Tumor Growth ◽  
Cell Cycle Arrest ◽  
Xenograft Tumor ◽  
Cycle Arrest ◽  
Xenograft Tumor Growth

scholarly journals APE1/Ref-1 redox-specific inhibition decreases survivin protein levels and induces cell cycle arrest in prostate cancer cells

Oncotarget ◽  
2017 ◽  
Vol 9 (13) ◽  
pp. 10962-10977 ◽  
Author(s):  
David W. McIlwain ◽  
Melissa L. Fishel ◽  
Alexander Boos ◽  
Mark R. Kelley ◽  
Travis J. Jerde
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Specific Inhibition ◽  
Prostate Cancer Cells ◽  
Protein Levels ◽  
Survivin Protein ◽  
Cycle Arrest

scholarly journals Effect of Piceatannol on Cell Cycle Progression in Prostate Cancer Cells (P05-005-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Larissa Kido ◽  
Eun-Ryeong Hahm ◽  
Valeria Cagnon ◽  
Mário Maróstica ◽  
Shivendra Singh
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Cell Cycle Progression ◽  
Cell Cycle Distribution ◽  
Mutant P53 ◽  
Wild Type ◽  
Cycle Progression ◽  
Cycle Arrest

Abstract Objectives Piceatannol (PIC) is a polyphenolic and resveratrol analog that is found in many vegetables consumed by humans. Like resveratrol, PIC has beneficial effects on health due to its anti-inflammatory, anti-oxidative and anti-proliferative features. However, the molecular targets of PIC in prostate cancer (PCa), which is the second most common cancer in men worldwide, are still poorly understood. Preventing cancer through dietary sources is a promising strategy to control diseases. Therefore, the aim of present study was to investigate the molecular mechanistic of actions of PIC in PCa cell lines with different genetic background common to human prostate cancer. Methods Human PCa cell lines (PC-3, 22Rv1, LNCaP, and VCaP) were treated with different doses of PIC (5–40 µM) and used for cell viability assay, measurement of total free fatty acids (FFA) and lactate, and cell cycle distribution. Results PIC treatment dose- and time-dependently reduced viability in PC-3 (androgen-independent, PTEN null, p53 null) and VCaP cells (androgen-responsive, wild-type PTEN, mutant p53). Because metabolic alterations, such as increased glucose and lipid metabolism are implicated in pathogenesis of in PCa, we tested if PIC could affect these pathways. Results from lactate and total free fatty acid assays in VCaP, 22Rv1 (castration-resistant, wild-type PTEN, mutant p53), and LNCaP (androgen-responsive, PTEN null, wild-type p53) revealed no effect of PIC on these metabolisms. However, PIC treatment delayed cell cycle progression in G0/G1 phase concomitant with the induction of apoptosis in both LNCaP and 22Rv1 cells, suggesting that growth inhibitory effect of PIC in PCa is associated with cell cycle arrest and apoptotic cell death at least LNCaP and 22Rv1 cells. Conclusions While PIC treatment does not alter lipid or glucose metabolism, cell cycle arrest and apoptosis induction are likely important in anti-cancer effects of PIC. Funding Sources São Paulo Research Foundation (2018/09793-7).

scholarly journals Lipophilized Epigallocatechin Gallate Derivative Exerts Anti-Proliferation Efficacy through Induction of Cell Cycle Arrest and Apoptosis on DU145 Human Prostate Cancer Cells

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 92 ◽  
Author(s):  
Jun Chen ◽  
Linli Zhang ◽  
Changhong Li ◽  
Ruochen Chen ◽  
Chengmei Liu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Epigallocatechin Gallate ◽  
Human Prostate ◽  
Enzymatic Esterification ◽  
Cytochrome C Release ◽  
Cycle Arrest ◽  
13C Nuclear Magnetic Resonance ◽  
Du145 Cells

Epigallocatechin gallate (EGCG) is the predominant tea polyphenol and it exhibits a hydrophilic character. The lipophilized EGCG derivative (LEGCG) was synthesized by enzymatic esterification of EGCG with lauric acid to enhance its bioactivity. The tetralauroyl EGCG was confirmed by high-performance liquid chromatography-tandem mass spectrometry and further identified as 3′, 5′, 3″, 5″-4-O-lauroyl EGCG by 1H and 13C nuclear magnetic resonance. The anti-proliferation effect of LEGCG on DU145 human prostate carcinoma cells was evaluated by MTT assay. In addition, the underlying molecular mechanism by which LEGCG exerts anti-proliferation efficacy was elucidated by flow cytometry and immunoblot analysis. Results suggested that LEGCG exhibited a dose-dependent anti-proliferation effect on DU145 cells by G0/G1 phase arrest and induction of apoptosis. LEGCG induced cell cycle arrest via p53/p21 activation, which down-regulated the cyclin D1 and CDK4 expression. In addition, LEGCG induced apoptosis by increasing the Bax/Bcl-2 ratio, the cytochrome c release, and the caspases cleavage on DU145 cells. The results provide theoretical support to prevent prostate cancer with LEGCG.

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