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Photobiomodulation leads to enhanced radiosensitivity through induction of apoptosis and autophagy in human cervical cancer cells.

ABSTRACT: The radiomodulatory effect of photobiomodulation (PBM) has recently been studied in cancer cells. The aim of this study was to investigate cellular mechanisms involved in the X-ray radiosensitivity of HeLa cells pre-exposed to PBM. HeLa cells were irradiated with 685?nm laser at different energy densities prior to X-ray ionizing radiation. After irradiation, clonogenic cell survival, cell death due to apoptosis and autophagy were determined. Levels of intracellular reactive oxygen species (ROS), DNA damage and, cell cycle distribution after PBM were measured. PBM at different energy densities (5-20?J/cm2 ) was not cytotoxic. However, HeLa cells pre-exposed to 20?J/cm2 showed enhanced inhibition of colony formation following ionizing radiation. Enhanced radiosensitivity was due to increased oxidative stress, DNA damage, and radiation-induced apoptosis and autophagy. These results suggest that 685?nm PBM at a higher energy density could possibly be a promising radiosensitizing agent in cervical cancer, to decrease the radiation dose delivered, and therefore prevent the side-effects that are associated with cancer radiotherapy.

SUBMITTER: Djavid GE

PROVIDER: S-EPMC5668202 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Photobiomodulation leads to enhanced radiosensitivity through induction of apoptosis and autophagy in human cervical cancer cells.

Djavid Gholamreza Esmaeeli GE Bigdeli Bahareh B Goliaei Bahram B Nikoofar Alireza A Hamblin Michael R MR

Journal of biophotonics 20170502 12

The radiomodulatory effect of photobiomodulation (PBM) has recently been studied in cancer cells. The aim of this study was to investigate cellular mechanisms involved in the X-ray radiosensitivity of HeLa cells pre-exposed to PBM. HeLa cells were irradiated with 685 nm laser at different energy densities prior to X-ray ionizing radiation. After irradiation, clonogenic cell survival, cell death due to apoptosis and autophagy were determined. Levels of intracellular reactive oxygen species (ROS), ...[more]

PMID: 28464474

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Project description:PurposeThe study aims to investigate the apoptotic effects of combining LBH589 and AM1241 (a selective CB2 receptor agonist) on cervical cancer cells and elucidating the mechanism of this combined therapy, which may provide innovative strategies for treating this disease.MethodsThe viability of the cervical cancer cells was measured by cell counting kit-8 (CCK-8) assay, and the synergistic effect was analyzed using SynergyFinder. Cell proliferation was tested by cell cloning. The apoptosis and reactive oxygen species (ROS) production in cervical cancer cells were analyzed by flow cytometry. Western blot and quantitative real-time PCR (qRT-PCR) were employed to determine changes in protein and gene levels of pathway-related factors.ResultsBy the results of cytotoxicity assay, SiHa cells were selected and treated with 0.1 μM LBH589 and 4 μM AM1241 for 24 h for subsequent experiments. The combination of both was synergistic as determined by bliss, ZIP, HSA and LOEWE synergy score. Plate cloning results showed that LBH589 combined with AM1241 inhibited the proliferation of cervical cancer cells compared to individual drug. Additionally, compared with LBH589 alone, the combination of LBH589 and AM1241 induced autophagy by increasing LC3II/LC3I and decreasing P62/GAPDH, leading to a significantly higher rate of apoptosis. Pharmacological inhibition of also inhibited apoptosis. Consistently, we found that the endoplasmic reticulum, DNA damage repair pathway were induced after co-administration. Furthermore, cellular ROS increased after co-administration, and apoptosis was inhibited by the addition of ROS scavenger.ConclusionLBH589 combined with AM1241 activated the endoplasmic reticulum emergency pathway, DNA damage repair signaling pathway, oxidative stress and autophagy pathway, ultimately promoting the apoptosis of cervical cancer cells. These findings suggest that the co-administration of LBH589 and AM1241 may be a new treatment plan for the treatment of cervical cancer.

Project description:Radioresistance remains a major clinical challenge in cervical cancer therapy and results in tumor relapse and metastasis. Nevertheless, the detailed mechanisms are still largely enigmatic. This study was conducted to elucidate the prospective impacts of microRNA-29a (miR-29a) on the modulation of radioresistance-associated cervical cancer progression. Herein, we established two pairs of parental wild-type (WT) and radioresistant (RR) cervical cancer cells (CaSki and C33A), and we found that constant suppressed miR-29a, but not miR-29b/c, was exhibited in RR-clones that underwent a dose of 6-Gy radiation treatment. Remarkably, radioresistant clones displayed low radiosensitivity, and the reduced apoptosis rate resulted in augmented surviving fractions, measured by the clonogenic survival curve assay and the Annexin V/Propidium Iodide apoptosis assay, respectively. Overexpression of miR-29a effectively intensified the radiosensitivity and triggered the cell apoptosis in RR-clones. In contrast, suppressed miR-29a modestly abridged the radiosensitivity and abolished the cell apoptosis in WT-clones. Hence, ectopically introduced miR-29a into RR-clones notably attenuated the wound-healing rate and cell migration, whereas reduced miR-29a aggravated cell mobilities of WT-clones estimated via the in vitro wound-healing assay and time-lapse recording assay. Notably, we further established the in vivo short-term lung locomotion metastasis model in BALB/c nude mice, and we found that increased lung localization was shown after tail-vein injection of RR-CaSki cells compared to those of WT-CaSki cells. Amplified miR-29a significantly eliminated the radioresistance-enhanced lung locomotion. Our data provide evidence suggesting that miR-29a is a promising microRNA signature in radioresistance of cervical cancer cells and displays multifaceted innovative roles involved in anti-radioresistance, escalated apoptosis, and anti-cell migration/metastasis. Amalgamation of a nucleoid-based strategy (miR-29a) together with conventional radiotherapy may be an innovative and eminent strategy to intensify the radiosensitivity and further protect against the subsequent radioresistance and the potential metastasis in cervical cancer treatment.

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Photobiomodulation leads to enhanced radiosensitivity through induction of apoptosis and autophagy in human cervical cancer cells.

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Photobiomodulation leads to enhanced radiosensitivity through induction of apoptosis and autophagy in human cervical cancer cells.

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