Ability to undergo apoptosis does not correlate with the intrinsic radiosensitivity (SF2) of human cervix tumor cell lines

Sheridan, Mary T.; West, Catharine M L

doi:10.1016/s0360-3016(01)01496-1

Cited by 18 publications

(4 citation statements)

References 20 publications

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“…Figure 2 illustrates the cell growth of HeLa and CaSki cells, respectively, expressed as a percentage of the cell growth obtained by the control population at various time points. Consistent with previous reports (24), CaSki cells were relatively more radioresistant than HeLa cells. Cell counts of the irradiated CaSki cells were equal to 86% of untreated cell population at 72 hours after irradiation.…”

Section: Resultssupporting

confidence: 92%

Phosphatidylinositol 3-Kinase Inhibition by LY294002 Radiosensitizes Human Cervical Cancer Cell Lines

Lee

Fuhrman

Planelles

et al. 2006

Clinical Cancer Research

110

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Purpose: The phosphatidylinositol 3-kinase (PI3K) catalytic subunit is amplified in cervical cancers, implicating PI3K in cervical carcinogenesis. We evaluated the radiosensitizing effect of PI3K inhibition by LY294002 on clonogenic survival, growth characteristics, and gene expression in cervical cancer cell lines (HeLa and CaSki). Experimental Design: Cervical cancer cells were treated separately and concurrently with the PI3K inhibitor LY294002 (10 Amol/L) and radiation (2 Gy) with serial analysis of cell count, apoptosis, and flow cytometry. PI3K inhibition was assessed by protein analysis of phosphorylated Akt. Clonogenic assays were done with varying doses of radiation and LY294002 and varied time points of administration of LY294002 proximate to the radiation dose. Surviving fractions and dose modification factors (DMF) were calculated. Each experiment was done in triplicate and analyzed using ANOVA regression analysis and Dunnett's t Test. Microarray gene expression analysis was done on the HeLa cell line. Results: PI3K inhibition with LY294002 alone did not decrease cell survival. However, treatment with LY294002 significantly radiosensitized HeLa and CaSki cell lines with DMFs (1log cell kill) of 1.95 and 1.37, respectively. Compared with post-irradiation, pretreatment produced more radiosensitization (P < 0.0001). DMFs were 2.2, 2.0, 2.0, and 1.2 for LY294002 added at 6, 2, and 0.5 hours before irradiation and 6 hours after irradiation, respectively. LY294002 pretreatment in irradiated HeLa cells led to altered gene expression. Conclusions: Although LY294002 alone did not produce cytotoxic effects, PI3K inhibition with LY294002 produced significant radiosensitization, showed significant time-dependent effects, increased apoptosis, and altered gene expression. These findings support future investigation of PI3K inhibitors in combination with radiation therapy for carcinoma of the cervix.

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Section: Resultssupporting

confidence: 92%

Phosphatidylinositol 3-Kinase Inhibition by LY294002 Radiosensitizes Human Cervical Cancer Cell Lines

Lee

Fuhrman

Planelles

et al. 2006

Clinical Cancer Research

110

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“…Such conditions are starvation (22), or low-dose and low-dose-rate irradiation (25,26). Thus, dependent on the conditions, irradiat-ed HeLa S 3 cells die by either of the two processes, like reported for 9 other cervical carcinoma cell lines by Sheridan (27). The observation may be explained with the fact that some HeLa cells express human papilloma virus E6 protein known to cause p53 degradation, which may compromise radiation induced apoptotic response (28).…”

Section: Discussionmentioning

confidence: 96%

Flow cytometry evaluation of HeLa S3 cell death induced by gamma-radiation

Nićiforović¹,

Zarić²,

Dakić

et al. 2004

Jugoslav Med Biohem

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In this study we followed the effects of radiation on human uterin cervix HeLa S3 cells viability, morphology and DNA structure 2-96 hours after treatment with 2-10 Gy from 60Co gamma radiation source. Staining of cells with Annexin V-FITC and propidium iodide showed very low degree of radiation-induced apoptosis. The prevailing form of HeLa S3 cell death according to flow-cytometry, DNA fragmentation and fluorescent microscopy, was necrosis. The gamma-radiation dose necessary to induce 50% of necrosis (termed DD50) was twice higher compared to dose that induced 50% inhibition of cell proliferation (LD50). These in vitro data suggested, that the increase in radiation dose might eradicate tumor cells, rather than just control their proliferation and growth.

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“…Our results are consistent with a study reported by Liu [ 17 ]. However the positive correlation between early phase apoptosis and radiation dose is considered only applicable within a limited dose range [ 18 ]. Recent findings have been reported that large single dose irradiation (8 to 15 Gy) may enhance tumor radiation sensitivity through the induction of tumor blood vessel endothelium apoptosis [ 19 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

In vivo99mTc-HYNIC-annexin V imaging of early tumor apoptosis in mice after single dose irradiation

Guo

Zhao

Tian

et al. 2009

J Exp Clin Cancer Res

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Background: Apoptosis is a major mode of hematological tumor death after radiation. Early detection of apoptosis may be beneficial for cancer adaptive treatment. 99m Tc-HYNIC-annexinV has been reported as a promising agent for in vivo apoptosis imaging. The purpose of this study is to evaluate the feasibility of in vivo 99m Tc-HYNIC-annexinV imaging of radiation-induced apoptosis, and to investigate its correlation with radiosensitivity.

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Ability to undergo apoptosis does not correlate with the intrinsic radiosensitivity (SF2) of human cervix tumor cell lines

Cited by 18 publications

References 20 publications

Phosphatidylinositol 3-Kinase Inhibition by LY294002 Radiosensitizes Human Cervical Cancer Cell Lines

Phosphatidylinositol 3-Kinase Inhibition by LY294002 Radiosensitizes Human Cervical Cancer Cell Lines

Flow cytometry evaluation of HeLa S3 cell death induced by gamma-radiation

In vivo99mTc-HYNIC-annexin V imaging of early tumor apoptosis in mice after single dose irradiation

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