Bcl-2 inhibitors potentiate the cytotoxic effects of radiation in Bcl-2 overexpressing radioresistant tumor cells

Hara, Takamitsu; Omura-Minamisawa, Motoko; Chen, Cheng; Nakagami, Yoshihiro; Ito, Megumi; Inoue, Tomio

doi:10.1016/j.ijrobp.2004.10.008

Cited by 39 publications

(28 citation statements)

References 35 publications

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“…However, we did observe an increase in early apoptosis, mainly by caspases 3+7 activity, in LNCaP-BST and PC3-BST cells, which did not ultimately translate into a significant reduction in clonogenic survival. The differences between Hara et al (34) and our results may be related to downstream factors in the cell lines used.…”

Section: Discussioncontrasting

confidence: 97%

“…They observed essentially no effect on clonogenic survival by Tetracarcin A or antisense Bcl-2 on wild-type HeLa cells, while we found significant radiosensitivity of both wild-type LNCaP and PC3 cells. Hara et al (34) found significant radiosensitization by clonogenic assay only in bcl-2 overexpressing HeLa cells, while we found reduced clonogenic responses in bcl-2 overexpressing LNCaP-BST and PC3-BST cells. However, we did observe an increase in early apoptosis, mainly by caspases 3+7 activity, in LNCaP-BST and PC3-BST cells, which did not ultimately translate into a significant reduction in clonogenic survival.…”

Section: Discussioncontrasting

confidence: 63%

“…In one example, Coffey et al (33) found that diethyl-maleate (DEM) restored sensitivity to radiation induced apoptosis in bcl-2 overexpressing LNCaP cells by inhibiting Bcl-2 protein expression. Although prior studies have indicated that bcl-2 expression affects response to RT, in only one prior study has the interaction of AS and RT been investigated (34).…”

Section: Discussionmentioning

confidence: 99%

“…More recently, Hara et al (34) found that the inhibition of Bcl-2 function and transcription by Tetracarcin A (TC-A) and antisense-Bcl-2 in bcl-2 overexpressing HeLa cells enhanced the response to radiation. Their results are notably different from ours.…”

Section: Discussionmentioning

confidence: 99%

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Antisense Bcl-2 sensitizes prostate cancer cells to radiation

Hachem

Pollack

2005

Prostate

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BACKGROUND-Bcl-2 is anti-apoptotic and overexpression is associated with prostate tumor aggressiveness. We hypothesized that Bcl-2 has a role in prostate cancer radiation (RT) response. The relationship of Bcl-2 expression in four prostate cancer cell lines, and the effect of modulating expression with a Bcl-2 antisense oligonucleotide (G3139, Genasense ® , oblimersen sodium, Genta Incorporated), to RT was examined.

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Section: Discussioncontrasting

confidence: 97%

Section: Discussioncontrasting

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Antisense Bcl-2 sensitizes prostate cancer cells to radiation

Hachem

Pollack

2005

Prostate

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“…We previously showed that Bcl-2 cells express ninefold higher levels of Bcl-2 proteins and are more resistant to γ-rays than Neo cells (Hara et al, 2005;Hamada et al, 2008e), and that there is no statistically significant difference in population doubling time and plating efficiency between sham-irradiated Neo and Bcl-2 cells . To assess the impact of Bcl-2 overexpression on the bystander effect for the survival, 10 particles was delivered to each of 1, 5 and 25 sites in situations whereby particle(s) traversed only 0.0002, 0.0009 and 0.005% of the cells, respectively.…”

Section: Impact Of Bcl-2 Overexpression On the Bystander Responsementioning

confidence: 99%

Heavy-Ion Microbeam Irradiation Induces Bystander Killing of Human Cells

et al. 2008

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Significant evidence indicates that ionizing radiation causes biological effects in nonirradiated bystander cells having received signals from directly irradiated cells. There is little information available hitherto as to the bystander effect of energetic heavy ions; however, our previous work has shown that in confluent cultures of normal human fibroblast AG01522 cells, targeted exposure of 0.0003% of cells to microbeams of 18.3 MeV/u 12 C (103 keV/µm) and 13.0 MeV/u 20 Ne (375 keV/µm) ions can similarly cause almost 10% decreases in the clonogenic survival, and twofold increments in the incidence of apoptosis whose temporal kinetics varies between irradiated and bystander cells. Using this experimental system, here we further report that bystander responses of AG01522 cells to 17.5 MeV/u 20 Ne ions (294 keV/µm) are consistent with those to 18.3 MeV/u 12 C and 13.0 MeV/u 20 Ne ions. We also demonstrate that such bystander-induced reductions in the survival are less pronounced and occur independently of Bcl-2 overexpression in human cervical cancer HeLa cells.

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