title: In Vitro Apoptosis Triggering in the BT-474 Human Breast Cancer Cell Line by Lyophilised Camel's Milk.
abstract: Breast cancer is a global health concern and is a major cause of death among women. In Oman, it is the most common cancer in women, with an incidence rate of 15.6 per 100,000 Omani females. Various anticancer remedies have been discovered from natural products in the past and the search is continuing for additional examples. Cytotoxic natural compounds may have a major role in cancer therapy either in potentiating the effect of chemotherapy or reducing its harmful effects. Recently, a few studies have reported advantages of using crude camel milk in treating some forms of cancer. However, no adequate data are available on the lyophilised camel's milk responsibility for triggering apoptosis and oxidative stress associated with human breast cancer. The present study aimed to address the role of the lyophilised camel's milk in inducing proliferation repression of BT-474 and HEp-2 cells compared with the non-cancer HCC1937 BL cell line. Lyophilized camel's milk fundamentally repressed BT-474 cells growth and proliferation through the initiation of either the intrinsic and extrinsic apoptotic pathways as indicated by both caspase-3 mRNA and its action level, and induction of death receptors in BT-474 but not the HEp-2 cell line. In addition, lyophilised camel's milk enhanced the expression of oxidative stress markers, heme-oxygenase-1 and reactive oxygen species production in BT-474 cells. Increase in caspase-3 mRNA levels by the lyophilised camel's milk was completely prevented by the actinomycin D, a transcriptional inhibitor. This suggests that lyophilized camel's milk increased newly synthesized RNA. Interestingly,it significantly (p<0.003) repressed the growth of HEp-2 cells and BT-474 cells after treatment for 72 hours while 24 hours treatment repressed BT-474 cells alone. This finding suggests that the lyophilised camel's milk might instigate apoptosis through initiation of an alternative apoptotic pathway.
authors.affiliation: Department of Microbiology and Immunology, College of Medicine and Health Sciences, Sultan Qaboos University, Al-Khod, Oman E-mail : shyahasson@squ.edu.om.
authors.forename: Sidgi S A A
authors.initials: SS
authors.lastname: Hasson
authors.forename: Juma Zaid
authors.initials: JZ
authors.lastname: Al-Busaidi
authors.forename: Zahra A M
authors.initials: ZA
authors.lastname: Al-Qarni
authors.forename: S
authors.initials: S
authors.lastname: Rajapakse
authors.forename: Shadia
authors.initials: S
authors.lastname: Al-Bahlani
authors.forename: Mohamed Ahmed
authors.initials: MA
authors.lastname: Idris
authors.forename: Talal A
authors.initials: TA
authors.lastname: Sallam
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001943:Breast Neoplasms / Q000188:drug therapy*; D002162:Camelus; D053148:Caspase 3 / Q000235:genetics; D049108:Cell Enlargement / Q000187:drug effects; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D005612:Freeze Drying; D006801:Humans; D007822:Laryngeal Neoplasms / Q000188:drug therapy*; D008892:Milk; D018384:Oxidative Stress / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D053218:Receptors, Death Domain / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D014158:Transcription, Genetic / Q000187:drug effects
chemical_list: D012333:RNA, Messenger; D017382:Reactive Oxygen Species; D053218:Receptors, Death Domain; D053148:Caspase 3