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RISS 인기검색어
- 검색키워드
- 저자 : Al-Bahlani, Shadia (검색결과 2 건)
- 무료
- 기관 내 무료
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Al-Bahlani, S,Fraser, M,Wong, A Y C,Sayan, B S,Bergeron, R,Melino, G,Tsang, B K Nature Publishing Group 2011 Oncogene Vol.30 No.41
<P>P73 is important in drug-induced apoptosis in some cancer cells, yet its role in the regulation of chemosensitivity in ovarian cancer (OVCA) is poorly understood. Furthermore, if and how the deregulation of p73-mediated apoptosis confers resistance to cisplatin (CDDP) treatment is unclear. Here we demonstrate that TAp73α over-expression enhanced CDDP-induced PARP cleavage and apoptosis in both chemosensitive (OV2008 and A2780s) and their resistant counterparts (C13* and A2780cp) and another chemoresistant OVCA cells (Hey); in contrast, the effect of ΔNp73α over-expression was variable. P73α downregulation attenuated CDDP-induced PUMA and NOXA upregulation and apoptosis in OV2008 cells. CDDP decreased p73α steady-state protein levels in OV2008, but not in C13*, although the mRNA expression was identical. CDDP-induced p73α downregulation was mediated by a calpain-dependent pathway. CDDP induced calpain activation and enhanced its cytoplasmic interaction and co-localization with p73α in OV2008, but not C13* cells. CDDP increased the intracellular calcium concentration ([Ca<SUP>2+</SUP>]<SUB>i</SUB>) in OV2008 but not C13* whereas cyclopiazonic acid (CPA), a Ca<SUP>2+</SUP>-ATPase inhibitor, caused this response and calpain activation, p73α processing and apoptosis in both cell types. CDDP-induced [Ca<SUP>2+</SUP>]<SUB>i</SUB> increase in OV2008 cells was not effected by the elimination of extracellular Ca<SUP>2+</SUP>, but this was attenuated by the depletion of internal Ca<SUP>2+</SUP> store, indicating that mobilization of intracellular Ca<SUP>2+]</SUP> stores was potentially involved. These findings demonstrate that p73α and its regulation by the Ca<SUP>2+</SUP>-mediated calpain pathway are involved in CDDP-induced apoptosis in OVCA cells and that dysregulation of Ca<SUP>2+</SUP>/calpain/p73 signaling may in part be the pathophysiology of CDDP resistance. Understanding the cellular and molecular mechanisms of chemoresistance will direct the development of effective strategies for the treatment of chemoresistant OVCA.</P>
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Hasson, Sidgi S.A.A,Al-Busaidi, Juma Zaid,Al-Qarni, Zahra A.M.,Rajapakse, S.,Al-Bahlani, Shadia,Idris, Mohamed Ahmed,Sallam, Talal A. Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.15
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.
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