Correlation between cell survival and micronuclei-induction in HeLa cells treated with adriamycin after exposure to various doses of γ-radiation

Ellagic acid (EA) is a polyphenol found in grapes, pomegranates, walnuts, etc. exhibits anti-cancer properties. The current study was conducted to understand the radiosensitizing role of EA on HeLa cells. Monotherapy of EA and radiation was initially studied on HeLa cells. The addition of EA before the radiation treatment subsequently made DNA more susceptible to damage thereby developing DNA beaks, which are known to be lethal for cell survival. This was evaluated by performing comet and γ-foci formation assay. Other assays which included cell-cycle distribution, clonogenic cell survival assay, mitochondrial membrane drop, and apoptosis were performed to evaluate the effect of EA with radiation. Our results demonstrate that, when cells were exposed to the combinatorial treatment of EA (10µM) and 2Gy of γ-radiation there was augmented cell death, lesser cell-proliferation, reduction in the colony-forming ability, increased DNA tail length, more number of γ-foci persisting even after 24h, enhanced apoptosis, augmented drop in the mitochondrial membrane potential and a G1 cell-cycle arrest. These results suggest that EA exhibits not only anti-cancer properties in terms of cell-death but also exhibits a radiosensitizing effect when given in combination with γ-radiation. Thus, it can be concluded that EA not only exhibits anticancer effects but also has potential in radiosensitizing HeLa cells.

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Identification of genes and genetic networks associated with BAG3‑dependent cell proliferation and cell survival in human cervical cancer HeLa cells

Molecular Medicine Reports ◽

10.3892/mmr.2018.9383 ◽

2018 ◽

Cited By ~ 1

Author(s):

Yukihiro Furusawa ◽

Tatsuya Yunoki ◽

Tetsushi Hirano ◽

Satsuki Minagawa ◽

Hironori Izumi ◽

...

Keyword(s):

Cervical Cancer ◽

Cell Proliferation ◽

Cell Survival ◽

Hela Cells ◽

Genetic Networks ◽

Dependent Cell ◽

Human Cervical Cancer

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A simple model for calculating relative biological effectiveness of X-rays and gamma radiation in cell survival

British Journal of Radiology ◽

10.1259/bjr.20190949 ◽

2020 ◽

Vol 93 (1112) ◽

pp. 20190949 ◽

Cited By ~ 1

Author(s):

Oleg N. Vassiliev ◽

Christine B. Peterson ◽

David R. Grosshans ◽

Radhe Mohan

Keyword(s):

Experimental Data ◽

Cell Survival ◽

Relative Biological Effectiveness ◽

Survival Curve ◽

Linear Functions ◽

Model Parameters ◽

High Dose ◽

X Rays ◽

Γ Radiation ◽

Biological Effectiveness

Objectives: The relative biological effectiveness (RBE) of X-rays and γ radiation increases substantially with decreasing beam energy. This trend affects the efficacy of medical applications of this type of radiation. This study was designed to develop a model based on a survey of experimental data that can reliably predict this trend. Methods: In our model, parameters α and β of a cell survival curve are simple functions of the frequency-average linear energy transfer (LF) of delta electrons. The choice of these functions was guided by a microdosimetry-based model. We calculated LF by using an innovative algorithm in which LF is associated with only those electrons that reach a sensitive-to-radiation volume (SV) within the cell. We determined model parameters by fitting the model to 139 measured (α,β) pairs. Results: We tested nine versions of the model. The best agreement was achieved with [Formula: see text] and β being linear functions of [Formula: see text] .The estimated SV diameter was 0.1–1 µm. We also found that α, β, and the α/β ratio increased with increasing [Formula: see text] . Conclusions: By combining an innovative method for calculating [Formula: see text] with a microdosimetric model, we developed a model that is consistent with extensive experimental data involving photon energies from 0.27 keV to 1.25 MeV. Advances in knowledge: We have developed a photon RBE model applicable to an energy range from ultra-soft X-rays to megaelectron volt γ radiation, including high-dose levels where the RBE cannot be calculated as the ratio of α values. In this model, the ionization density represented by [Formula: see text] determines the RBE for a given photon spectrum.

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Dual Role of Pim-2 Depends on the Associated Proteome.

Blood ◽

10.1182/blood.v108.11.4334.4334 ◽

2006 ◽

Vol 108 (11) ◽

pp. 4334-4334

Author(s):

Daphna Levy ◽

Amos M. Cohen ◽

Jeremy Don

Keyword(s):

Cell Survival ◽

Hela Cells ◽

Cell Types ◽

Dual Role ◽

Lymphocytic Leukemia ◽

Dominant Negative ◽

G1 Arrest ◽

Apoptotic Pathway ◽

Hodgkin's Lymphomas ◽

Apoptotic Effects

Abstract Pim-2, a Ser/Thr kinase, is a proto-oncogene originally identified as common proviral insertion sites in T and B cell lymphomas in mice. Deregulation of Pim-2 expression has been documented in several human malignancies, including leukemia, lymphoma, multiple myeloma and prostate cancer. In human non-Hodgkin’s lymphomas and in chronic lymphocytic leukemia Pim-2 is up-regulated and its expression correlates with disease activity. Pim-2 promotes cell survival in response to a wide variety of proliferative signals. Pim-2 promotes cell survival by phosphorylation of Bad and Cot. The goal of this study was to clarify the significance of our new unanticipated aspect of Pim-2′s function, namely, that over-expression of Pim-2 in HeLa cells led to cell cycle arrest at G1 and to increased apoptosis. We found that the G1 arrest was associated with increased (T14/Y15) phosphorylation of CDK2, increased proteosomic degradation of CDC25A, and increased levels of the CDK inhibitor p57. In addition, we found increased E2F-1 levels, which suggested the usage of the E2F-1 dependent apoptotic pathway. Using dominant negative forms of either E2F-1 or p73, which were co-expressed with Pim-2 in HeLa cells, revealed significant rescue of the G1 arrest and apoptotic phenomena. Silencing of Pim-2 in these cells, via siRNA, reversed the G1 arrest and pro-apoptotic effects, and verified the Pim-2 dependent specificity. We conclude that Pim-2 might play a dual role. Our data suggest that under certain environmental circumstances and in various cell types, Pim-2 appears to increase cell survival by abrogating some pro-apoptotic substrates, but under different proteomic associations Pim-2 might favor G1 arrest and apoptosis.

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