scholarly journals Bioactive peptide of Cicer arietinum L. induces apoptosis in human endometrial cancer via DNA fragmentation and cell cycle arrest

3 Biotech ◽  
2021 ◽  
Vol 11 (2) ◽  
Author(s):  
Neha Gupta ◽  
Sameer Suresh Bhagyawant
2013 ◽  
Author(s):  
Takuhei Yokoyama ◽  
Takayuki Enomoto ◽  
Kousuke Hiramatsu ◽  
Akiko Morimoto ◽  
Yutaka Ueda ◽  
...  

Toxicology ◽  
2003 ◽  
Vol 192 (2-3) ◽  
pp. 237-248 ◽  
Author(s):  
Salwa Abid-Essefi ◽  
Isabelle Baudrimont ◽  
Wafa Hassen ◽  
Zouhour Ouanes ◽  
Théophile A. Mobio ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Iason Psilopatis ◽  
Alexandros Pergaris ◽  
Constantinos Giaginis ◽  
Stamatios Theocharis

Endometrial carcinoma is the most common malignant tumor of the female genital tract in the United States. Epigenetic alterations are implicated in endometrial cancer development and progression. Histone deacetylase inhibitors are a novel class of anticancer drugs that increase the level of histone acetylation in many cell types, thereby inducing cell cycle arrest, differentiation, and apoptotic cell death. This review is aimed at determining the role of histone acetylation and examining the therapeutic potential of histone deacetylase inhibitors in endometrial cancer. In order to identify relevant studies, a literature review was conducted using the MEDLINE and LIVIVO databases. The search terms histone deacetylase, histone deacetylase inhibitor, and endometrial cancer were employed, and we were able to identify fifty-two studies focused on endometrial carcinoma and published between 2001 and 2021. Deregulation of histone acetylation is involved in the tumorigenesis of both endometrial carcinoma histological types and accounts for high-grade, aggressive carcinomas with worse prognosis and decreased overall survival. Histone deacetylase inhibitors inhibit tumor growth, enhance the transcription of silenced physiologic genes, and induce cell cycle arrest and apoptosis in endometrial carcinoma cells both in vitro and in vivo. The combination of histone deacetylase inhibitors with traditional chemotherapeutic agents shows synergistic cytotoxic effects in endometrial carcinoma cells. Histone acetylation plays an important role in endometrial carcinoma development and progression. Histone deacetylase inhibitors show potent antitumor effects in various endometrial cancer cell lines as well as tumor xenograft models. Additional clinical trials are however needed to verify the clinical utility and safety of these promising therapeutic agents in the treatment of patients with endometrial cancer.


2020 ◽  
Vol 45 (2) ◽  
pp. 630-640
Author(s):  
Min Zhang ◽  
Qinsheng Lu ◽  
Huomei Hou ◽  
Dingqian Sun ◽  
Miaojuan Chen ◽  
...  

2020 ◽  
Vol 54 (6) ◽  
pp. 884-893
Author(s):  
D. Sun ◽  
W.-Y. Li ◽  
S.-H. Chen ◽  
Z.-F. Zhi ◽  
H.-S. Lin ◽  
...  

2011 ◽  
Vol 49 (8) ◽  
pp. 1737-1744 ◽  
Author(s):  
Jung-Hoon Cho ◽  
Jong-Gyu Lee ◽  
Yeong-In Yang ◽  
Ji-Hyun Kim ◽  
Ji-Hye Ahn ◽  
...  

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5185
Author(s):  
Mohamed M. Tawfik ◽  
Nourhan Eissa ◽  
Fayez Althobaiti ◽  
Eman Fayad ◽  
Ali H. Abu Almaaty

Jellyfish venom is a rich source of bioactive proteins and peptides with various biological activities including antioxidant, antimicrobial and antitumor effects. However, the anti-proliferative activity of the crude extract of Rhopilema nomadica jellyfish venom has not been examined yet. The present study aimed at the investigation of the in vitro effect of R. nomadica venom on liver cancer cells (HepG2), breast cancer cells (MDA-MB231), human normal fibroblast (HFB4), and human normal lung cells (WI-38) proliferation by using MTT assay. The apoptotic cell death in HepG2 cells was investigated using Annexin V-FITC/PI double staining-based flow cytometry analysis, western blot analysis, and DNA fragmentation assays. R. nomadica venom displayed significant dose-dependent cytotoxicity on HepG2 cells after 48 h of treatment with IC50 value of 50 μg/mL and higher toxicity (3:5-fold change) against MDA-MB231, HFB4, and WI-38 cells. R. nomadica venom showed a prominent increase of apoptosis as revealed by cell cycle arrest at G2/M phase, upregulation of p53, BAX, and caspase-3 proteins, and the down-regulation of anti-apoptotic Bcl-2 protein and DNA fragmentation. These findings suggest that R. nomadica venom induces apoptosis in hepatocellular carcinoma cells. To the best of the authors’ knowledge, this is the first scientific evidence demonstrating the induction of apoptosis and cell cycle arrest of R. nomadica jellyfish venom.


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