Death receptor pathway genes (Caspase and BID) expression analysis in cancerous cells in response to extracts of amla and turmeric

被引:0
作者
Younas, Hooria [1 ]
Ajmal, Sidra [1 ]
Mahmood, Nasir [2 ,3 ,4 ]
Shahid, Saman [5 ]
Zafar, Maryam [1 ]
机构
[1] Kinnaird Coll Women, Dept Biochem, Lahore, Pakistan
[2] Univ Hlth Sci UHS, Dept Biochem, Lahore, Pakistan
[3] Univ Hlth Sci UHS, Human Genet & Mol Biol, Lahore, Pakistan
[4] Univ Toronto, Dept Cell & Syst Biol, Toronto, ON, Canada
[5] Natl Univ Comp & Emerging Sci NUCES, Fdn Advancement Sci & Technol FAST, Dept Sci & Humanities, Lahore, Pakistan
关键词
Cell-death; death receptor pathway; BID; caspases; 3; 8; Curcuma longa; Emblica officinalis; CLINICAL-TRIAL; IN-VITRO; CURCUMIN; APOPTOSIS; INHIBITION; INDUCTION; AGENT; VIVO;
D O I
10.36721/PJPS.2023.36.2.REG.437-445.1
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Plant extracts antiproliferative effects were determined by using mammalian cells along the expression profile of Caspases 3, 8, and the BID gene of the death receptor-induced pathway. Two medicinal plants viz., Turmeric (Curcuma longa) and Amla (Emblica officinalis) extracts were examined for antiproliferative effect through Neutral Red-Dye uptake assay on Vero and MDA-MB 231 cell lines. A reverse transcriptase polymerase chain reaction was used to determine the expression of genes while GAPDH expression was used as an internal control. Expression of BID was up-regulated in methanolic turmeric extract-induced MDA-MB 231 cells while Caspases 3,8 expressions were the same in induced and uninduced MDA-MB 231 cells. Activated BID cleaved into tBID and activated the intrinsic pathway which caused death in methanolic turmeric extract-induced cancerous cells. Ethanolic extracts of turmeric exerted the strongest antiproliferative effects on Vero and methanolic extracts on MDA-MB 231 cells. The morphological studies of cell lines and gene expression analysis of turmeric methanolic extract-treated cells showed activation of apoptosis via converting BID into t-BID (intrinsic pathway) and activating Caspase-3 and Caspase-8 (extrinsic pathway). With the differential cytotoxicity and induction of apoptosis in induced cancer cells in comparison to uninduced cancerous cells, hence turmeric is a natural source of new anti-cancerous compounds.
引用
收藏
页码:437 / 445
页数:9
相关论文
共 35 条
[1]  
Abdel-Hameed E. S. S., 2012, European Journal of Medicinal Plants, V2, P93
[2]   Evidence that curcumin suppresses the growth of malignant gliomas in vitro and in vivo through induction of autophagy: Role of Akt and extracellular signal-regulated kinase signaling pathways [J].
Aoki, Hiroshi ;
Takada, Yasunari ;
Kondo, Seiji ;
Sawaya, Raymond ;
Aggarwal, Bharat B. ;
Kondo, Yasuko .
MOLECULAR PHARMACOLOGY, 2007, 72 (01) :29-39
[3]   Apoptosis control by death and decoy receptors [J].
Ashkenazi, A ;
Dixit, VM .
CURRENT OPINION IN CELL BIOLOGY, 1999, 11 (02) :255-260
[4]   Curcumin as an Anti-Cancer Agent: Review of the Gap Between Basic and Clinical Applications [J].
Bar-Sela, G. ;
Epelbaum, R. ;
Schaffer, M. .
CURRENT MEDICINAL CHEMISTRY, 2010, 17 (03) :190-197
[5]   Phase I dose escalation trial of docetaxel plus curcumin in patients with advanced and metastatic breast cancer [J].
Bayet-Robert, Mathilde ;
Kwiatkowski, Fabrice ;
Leheurteur, Marianne ;
Gachon, Francoise ;
Planchat, Eloise ;
Abrial, Catherine ;
Mouret-Reynier, Marie-Ange ;
Durando, Xavier ;
Barthomeuf, Chantal ;
Chollet, Philippe .
CANCER BIOLOGY & THERAPY, 2010, 9 (01) :8-14
[6]   Bid: a Bax-like BH3 protein [J].
Billen, L. P. ;
Shamas-Din, A. ;
Andrews, D. W. .
ONCOGENE, 2008, 27 (Suppl 1) :S93-S104
[7]  
Butt MS, 2013, EXCLI J, V12, P1043
[8]  
Cheng AL, 2001, ANTICANCER RES, V21, P2895
[9]   Emblica officinalis Extract Induces Autophagy and Inhibits Human Ovarian Cancer Cell Proliferation, Angiogenesis, Growth of Mouse Xenograft Tumors [J].
De, Alok ;
De, Archana ;
Papasian, Chris ;
Hentges, Shane ;
Banerjee, Snigdha ;
Haque, Inamul ;
Banerjee, Sushanta K. .
PLOS ONE, 2013, 8 (08)
[10]   Death receptors in chemotherapy and cancer [J].
Debatin, KM ;
Krammer, PH .
ONCOGENE, 2004, 23 (16) :2950-2966