Page 129 - 2014 Printable Abstract Book
P. 129
regulating the repair mechanism through ligation. However, more experiments are in process to confirm
if there is some other mechanism participating.
(PS1-49) The generality of the intercellular induction of apoptosis signaling system. Abdelrazek Bedir
2
1
1
2
Abdelrazzak. Ahmed, D. Phil ; Mark Hill ; and Peter O'Neill, National Research Centre, Giza, Egypt and
Oxford University, Oxford, United Kingdom
2
Intercellular induction of apoptosis (IIA) has been identified as a signaling system by which normal
208F fibroblast cells can selectively induce apoptosis in pre-cancerous 208Fsrc3 cells through ROS/RNS
and cytokine signaling. An important question related to the intercellular induction of apoptosis (IIA)
system is its generality and whether or not it applies to other cell lines and is more general rather than
just being applicable to the 208F and 208Fsrc3 cells. The generality of the IIA system is addressed here in
three ways; first, whether apoptosis can be induced in transformed 208Fsrc3 cells by non-transformed
cells other than 208F cells; secondly, whether apoptosis can be induced by non-transformed 208F cells in
transformed cells other than 208Fsrc3 cells; and thirdly, can the epithelial non-transformed cells induce
apoptosis in the epithelial transformed cells. The IIA system is dependent on the production of superoxide
anions O2-• around the transformed cell and as a consequence selectively targets the cells to undergo
apoptosis involving the apoptotic signaling pathways (Bauer 2000; Bauer 2002). The non-transformed rat
ovarian surface epithelial cell line (ROSE199) and K-RAS transformed rat ovarian surface epithelial cell line
(ROSE A2/5) were chosen for this study as these also lead to the production of O2-• around the cell. The
results show that epithelial ROSE199 cells can induce apoptosis in fibroblast 208Fsrc3 cells and are even
more efficient in inducing apoptosis in than 208F cells with the induction of apoptosis in 208Fsrc3 cells by
ROSE 199 cells is TGF-β dependent. Moreover, the IIA signaling was found to be through the PO/HOCl and
NO•/ONOO- pathways. Although the ROSE A2/5 cells show an ability to undergo autocrine destruction
(AD), they show high resistance to the induction of apoptosis by either 208F cells or ROSE199 cells.
(PS1-50) Roles of p53 and related signals in the bystander effects induced by gamma-ray and high LET
1
2
2
1
1
heavy ion radiation. Mingyuan He ; Chen Dong ; Teruaki Konishi ; Wenzhi Tu ; Naoko Shiomi ; Alisa
4
2
2
3
1
4
2
Kobayashi ; Yukio Uchihori ; Yoshiya Furusawa ; Tom K. Hei ; Bingrong Dang ; Wenjian Li ; Chunlin Shao
Institute of Radiation Medicine, Shanghai, China ; National Institute of Radiological Sciences, Inage, Chiba,
1
2
3
Japan ; Columbia University Medical Center, New York, NY ; and Institute of Modern Physics, Chinese
Academy of Sciences, Lanzhou, China
4
Irradiated cells can induce biological effects on vicinal non-irradiated bystander cells (RIBE),
meanwhile the bystander cells may rescue the irradiated cells through a feedback signaling stress. With a
cell co-culture system containing α-irradiated human macrophage cells U937 and its bystander HL-7702
hepatocyte cells, we found that apoptosis was induced in the HL-7702 cells but the formation of
micronuclei (MN) in the irradiated U937 cells was markedly decreased since the cell co-culture treatment.
Further studies disclosed that cAMP could be released from bystander HL-7702 cells and compensated to
α-irradiated U937 cells through a membrane signaling pathway and this cAMP communication played a
profound role in regulating the reciprocal bystander effects of mitigating radiation damage in U739 cells
and enhancing bystander apoptosis that was dependent on the p53 status of recipient cells. The role of
p53 of targeted cells in RIBE was further investigated by exposing lymphocyte cells of TK6 (wtp53) and
127 | P a g e
if there is some other mechanism participating.
(PS1-49) The generality of the intercellular induction of apoptosis signaling system. Abdelrazek Bedir
2
1
1
2
Abdelrazzak. Ahmed, D. Phil ; Mark Hill ; and Peter O'Neill, National Research Centre, Giza, Egypt and
Oxford University, Oxford, United Kingdom
2
Intercellular induction of apoptosis (IIA) has been identified as a signaling system by which normal
208F fibroblast cells can selectively induce apoptosis in pre-cancerous 208Fsrc3 cells through ROS/RNS
and cytokine signaling. An important question related to the intercellular induction of apoptosis (IIA)
system is its generality and whether or not it applies to other cell lines and is more general rather than
just being applicable to the 208F and 208Fsrc3 cells. The generality of the IIA system is addressed here in
three ways; first, whether apoptosis can be induced in transformed 208Fsrc3 cells by non-transformed
cells other than 208F cells; secondly, whether apoptosis can be induced by non-transformed 208F cells in
transformed cells other than 208Fsrc3 cells; and thirdly, can the epithelial non-transformed cells induce
apoptosis in the epithelial transformed cells. The IIA system is dependent on the production of superoxide
anions O2-• around the transformed cell and as a consequence selectively targets the cells to undergo
apoptosis involving the apoptotic signaling pathways (Bauer 2000; Bauer 2002). The non-transformed rat
ovarian surface epithelial cell line (ROSE199) and K-RAS transformed rat ovarian surface epithelial cell line
(ROSE A2/5) were chosen for this study as these also lead to the production of O2-• around the cell. The
results show that epithelial ROSE199 cells can induce apoptosis in fibroblast 208Fsrc3 cells and are even
more efficient in inducing apoptosis in than 208F cells with the induction of apoptosis in 208Fsrc3 cells by
ROSE 199 cells is TGF-β dependent. Moreover, the IIA signaling was found to be through the PO/HOCl and
NO•/ONOO- pathways. Although the ROSE A2/5 cells show an ability to undergo autocrine destruction
(AD), they show high resistance to the induction of apoptosis by either 208F cells or ROSE199 cells.
(PS1-50) Roles of p53 and related signals in the bystander effects induced by gamma-ray and high LET
1
2
2
1
1
heavy ion radiation. Mingyuan He ; Chen Dong ; Teruaki Konishi ; Wenzhi Tu ; Naoko Shiomi ; Alisa
4
2
2
3
1
4
2
Kobayashi ; Yukio Uchihori ; Yoshiya Furusawa ; Tom K. Hei ; Bingrong Dang ; Wenjian Li ; Chunlin Shao
Institute of Radiation Medicine, Shanghai, China ; National Institute of Radiological Sciences, Inage, Chiba,
1
2
3
Japan ; Columbia University Medical Center, New York, NY ; and Institute of Modern Physics, Chinese
Academy of Sciences, Lanzhou, China
4
Irradiated cells can induce biological effects on vicinal non-irradiated bystander cells (RIBE),
meanwhile the bystander cells may rescue the irradiated cells through a feedback signaling stress. With a
cell co-culture system containing α-irradiated human macrophage cells U937 and its bystander HL-7702
hepatocyte cells, we found that apoptosis was induced in the HL-7702 cells but the formation of
micronuclei (MN) in the irradiated U937 cells was markedly decreased since the cell co-culture treatment.
Further studies disclosed that cAMP could be released from bystander HL-7702 cells and compensated to
α-irradiated U937 cells through a membrane signaling pathway and this cAMP communication played a
profound role in regulating the reciprocal bystander effects of mitigating radiation damage in U739 cells
and enhancing bystander apoptosis that was dependent on the p53 status of recipient cells. The role of
p53 of targeted cells in RIBE was further investigated by exposing lymphocyte cells of TK6 (wtp53) and
127 | P a g e
