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Dose-dependent expression of extracellular microRNAs in HCT116 colorectal cancer cells exposed to high-dose-rate ionising radiation.

ABSTRACT: Biomarkers of tumour response to radiotherapy may help optimise cancer treatment. The aim of the present study was to identify changes in extracellular microRNAs (miRNAs) as a biomarker of radiation-induced damage to human colorectal cancer cells. HCT116 cells were exposed to increasing doses of X-rays, and extracellular miRNAs were analysed by microarray. The results were correlated with the frequency of micronuclei. A total of 59 miRNAs with a positive correlation and 4 with a negative correlation between dose (up to 6 Gy) and extracellular miRNA expression were identified. In addition, for doses between 0 and 10 Gy, 12 miRNAs among those 59 miRNAs with a positive correlation were identified; for these extracellular miRNAs, a significantly positive correlation was observed between their expression and the frequency of micronuclei for doses up to 10 Gy. These results suggest that specific miRNAs may be considered as cell damage markers and may serve as secreted radiotherapy response biomarkers for colorectal cancer; however, the results must be further validated in serum samples collected from patients undergoing radiotherapy.

SUBMITTER: Monzen S

PROVIDER: S-EPMC8637812 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Dose dependent expression of extracellular microRNAs in HCT116 colorectal cancer cells exposed to high dose rate ionizing radiation

Project description:Biomarkers of tumour response to radiotherapy could help in optimising cancer treatment. In this study, we focus on identifying changes in extracellular miRNA as a biomarker of radiation-induced damage to human colorectal cancer cells. HCT116 cells were exposed to increasing doses of X-rays, and extracellular miRNAs were analysed by microarray. The results were correlated with frequencies of micronuclei. Fifty-nine miRNAs with positive correlation and four with negative correlation between dose (up to 6 Gy) and expression of extracellular miRNA were verified. In addition, for samples between 0 and 10 Gy, 12 miRNAs into those 59 miRNAs with positive correlation were verified. Of these, these miRNAs showed significantly positive correlation up to 10 Gy between micronucleus frequency and expression of extracellular miRNA. These results suggest that specific miRNAs could be cell damage markers and could serve as secreted radiotherapy response biomarkers for colorectal cancer; however, the results must be validated in serum samples collected from patients undergoing radiotherapy.

2021-09-16 | GSE184174 | GEO

Dose dependent expression of extracellular microRNAs in HCT116 colorectal cancer cells exposed to high dose rate ionizing radiation

Project description:Dose dependent expression of extracellular microRNAs in HCT116 colorectal cancer cells exposed to high dose rate ionizing radiation

| PRJNA763507 | ENA

Chronic low-dose-rate ionising radiation affects the hippocampal phosphoproteome in the ApoE-/- Alzheimer's mouse model.

Project description:Accruing data indicate that radiation-induced consequences resemble pathologies of neurodegenerative diseases such as Alzheimer´s. The aim of this study was to elucidate the effect on hippocampus of chronic low-dose-rate radiation exposure (1 mGy/day or 20 mGy/day) given over 300 days with cumulative doses of 0.3 Gy and 6.0 Gy, respectively. ApoE deficient mutant C57Bl/6 mouse was used as an Alzheimer´s model. Using mass spectrometry, a marked alteration in the phosphoproteome was found at both dose rates. The radiation-induced changes in the phosphoproteome were associated with the control of synaptic plasticity, calcium-dependent signalling and brain metabolism. An inhibition of CREB signalling was found at both dose rates whereas Rac1-Cofilin signalling was found activated only at the lower dose rate. Similarly, the reduction in the number of activated microglia in the molecular layer of hippocampus that paralleled with reduced levels of TNF? expression and lipid peroxidation was significant only at the lower dose rate. Adult neurogenesis, investigated by Ki67, GFAP and NeuN staining, and cell death (activated caspase-3) were not influenced at any dose or dose rate. This study shows that several molecular targets induced by chronic low-dose-rate radiation overlap with those of Alzheimer´s pathology. It may suggest that ionising radiation functions as a contributing risk factor to this neurodegenerative disease.

| S-EPMC5342125 | biostudies-literature

The molecular and cellular basis of divergent dose-dependent ionising radiation response

Project description:Cancer risk from medical exposure to low dose (LD) ionizing radiation (IR) is linearly extrapolated from high dose (HD) IR without sufficient mechanistic understanding and definitive evidence. The long-term health effects of radiotherapy for cancer are unclear as secondary tumours possibly arise from the ‘low-dose bath’ of normal tissue,. By the age of ~45 years, most (>90%) of the survivors of paediatric cancers develop secondary tumours from cancer therapy (including radiotherapy). Here, we show that LD and HD drive molecular and cellular responses to reactive oxygen species (ROS) production and DNA damage, respectively. We found dose-proportionality only for the phosphorylation events in the DNA damage response (DDR); signalling via PPP1R7 and global (de)phosphorylation events govern the G2/M checkpoint, whereas impaired DSB repair affected the DDR signalling duration rather than amplitudes. Contrastingly, LD specifically activated NRF2-regulated antioxidant defence, redox-sensitive ERK1/2/MAPK signalling, kinome/phosphatome, mitochondrial metabolic and glycolytic pathways, whereas HD induced replication stress signalling, p53 transcription and proliferation inhibition. Dose-proportional (10-200 mGy) chromosomal damage induction suggests non(slowly) repairable DNA breaks generation without a threshold, whereas LD-specific enhanced ROS-related responses induction implies survival of cells with residual DNA damage.

2022-07-01 | GSE130066 | GEO

Expression data in mouse liver exposed to low dose-rate radiation

2011-01-01 | GSE20562 | GEO

Expression data in mouse liver exposed to low dose-rate radiation

Project description:Expression profiles in mouse liver exposed to long-term gamma-irradiation were examined to assess in vivo effects of low dose-rate radiation. Three groups of male C57BL/6J mice were exposed to whole body irradiation at dose-rates of 17-20 mGy/day, 0.86-1.0 mGy/day or 0.042-0.050 mGy/day for 401-485 days (cumulative doses were approximately 8 Gy, 0.4 Gy or 0.02 Gy, respectively). Expression profiles were produced for RNA isolated from irradiated individual animals and for pooled RNA from sham-irradiated 3 animals for control. The expression levels of 6 irradiated animals for each dose were compared individually with those of 2 pooled controls (3 irradiated samples to one pooled control in first and second experiments). The experiments were conducted twice at similar dose-rates. In the first experiment, three groups of 8 weeks old male C57BL/6J mice were exposed to whole body irradiation at dose-rates of either 16.6 mGy/day (H1), 0.858 mGy/day (M1) or 0.042 mGy/day (L1) for 485 days (cumulative doses were 8030 mGy, 416 mGy or 20.6 mGy, respectively). In the second experiment, the doe-rates were slightly elevated as 20.0 mGy/day (H2), 1.000 mGy/day (M2) or 0.050 mGy/day (L2) for 401 days (doses were 8015 mGy, 401 mGy or 20 mGy, respectively). A group of control unirradiated mice were set for each experiment (C1, C2).

2011-01-01 | E-GEOD-20562 | biostudies-arrayexpress

Non-targeted effects of ionising radiation--implications for low dose risk.

Project description:Non-DNA targeted effects of ionising radiation, which include genomic instability, and a variety of bystander effects including abscopal effects and bystander mediated adaptive response, have raised concerns about the magnitude of low-dose radiation risk. Genomic instability, bystander effects and adaptive responses are powered by fundamental, but not clearly understood systems that maintain tissue homeostasis. Despite excellent research in this field by various groups, there are still gaps in our understanding of the likely mechanisms associated with non-DNA targeted effects, particularly with respect to systemic (human health) consequences at low and intermediate doses of ionising radiation. Other outstanding questions include links between the different non-targeted responses and the variations in response observed between individuals and cell lines, possibly a function of genetic background. Furthermore, it is still not known what the initial target and early interactions in cells are that give rise to non-targeted responses in neighbouring or descendant cells. This paper provides a commentary on the current state of the field as a result of the non-targeted effects of ionising radiation (NOTE) Integrated Project funded by the European Union. Here we critically examine the evidence for non-targeted effects, discuss apparently contradictory results and consider implications for low-dose radiation health effects.

| S-EPMC4091999 | biostudies-literature

Differences in sustained alterations in protein expression between livers of mice exposed to high-dose-rate and low-dose-rate radiation.

Project description:Molecular mechanisms of radiation dose-rate effects are not well understood. Among many possibilities, long-lasting sustained alterations in protein levels would provide critical information. To evaluate sustained effects after acute and chronic radiation exposure, we analyzed alterations in protein expression in the livers of mice. Acute exposure consisted of a lethal dose of 8 Gy and a sublethal dose of 4 Gy, with analysis conducted 6 days and 3 months after irradiation, respectively. Chronic irradiation consisted of a total dose of 8 Gy delivered over 400 days (20 mGy/day). Analyses following chronic irradiation were done immediately and at 3 months after the end of the exposure. Based on antibody arrays of protein expression following both acute lethal and sublethal dose exposures, common alterations in the expression of two proteins were detected. In the sublethal dose exposure, the expression of additional proteins was altered 3 months after irradiation. Immunohistochemical analysis showed that the increase in one of the two commonly altered proteins, MyD88, was observed around blood vessels in the liver. The alterations in protein expression after chronic radiation exposure were different from those caused by acute radiation exposures. Alterations in the expression of proteins related to inflammation and apoptosis, such as caspase 12, were observed even at 3 months after the end of the chronic radiation exposure. The alterations in protein expression depended on the dose, the dose rate, and the passage of time after irradiation. These changes could be involved in long-term effects of radiation in the liver.

| S-EPMC5570048 | biostudies-literature

Lymphoma and multiple myeloma in cohorts of persons exposed to ionising radiation at a young age.

Project description:There is limited evidence that non-leukaemic lymphoid malignancies are radiogenic. As radiation-related cancer risks are generally higher after childhood exposure, we analysed pooled lymphoid neoplasm data in nine cohorts first exposed to external radiation aged <21 years using active bone marrow (ABM) and, where available, lymphoid system doses, and harmonised outcome classification. Relative and absolute risk models were fitted. Years of entry spanned 1916-1981. At the end of follow-up (mean 42.1 years) there were 593 lymphoma (422 non-Hodgkin (NHL), 107 Hodgkin (HL), 64 uncertain subtype), 66 chronic lymphocytic leukaemia (CLL) and 122 multiple myeloma (MM) deaths and incident cases among 143,136 persons, with mean ABM dose 0.14 Gy (range 0-5.95 Gy) and mean age at first exposure 6.93 years. Excess relative risk (ERR) was not significantly increased for lymphoma (ERR/Gy = -0.001; 95% CI: -0.255, 0.279), HL (ERR/Gy = -0.113; 95% CI: -0.669, 0.709), NHL + CLL (ERR/Gy = 0.099; 95% CI: -0.149, 0.433), NHL (ERR/Gy = 0.068; 95% CI: -0.253, 0.421), CLL (ERR/Gy = 0.320; 95% CI: -0.678, 1.712), or MM (ERR/Gy = 0.149; 95% CI: -0.513, 1.063) (all p-trend > 0.4). In six cohorts with estimates of lymphatic tissue dose, borderline significant increased risks (p-trend = 0.02-0.07) were observed for NHL + CLL, NHL, and CLL. Further pooled epidemiological studies are needed with longer follow-up, central outcome review by expert hematopathologists, and assessment of radiation doses to lymphoid tissues.

| S-EPMC8484030 | biostudies-literature

Extracellular miRNAs in serum and feces of mice exposed to high-dose radiation

Project description:Exposure to high-dose radiation causes life-threatening serious intestinal damage. Histological analysis is the most accurate method for judging the extent of intestinal damage after death. However, it is difficult to predict the extent of intestinal damage to body samples. Here we focused on extracellular microRNAs (miRNAs) released from cells and investigated miRNA species that increased or decreased in serum and feces using a radiation-induced intestinal injury mouse model. A peak of small RNA of 25–200 nucleotides was detected in mouse serum and feces 72 h after radiation exposure, and miRNA presence in serum and feces was inferred. MiRNAs expressed in the small intestine and were increased by more than 2.0-fold in serum or feces following a 10 Gy radiation exposure were detected by microarray analysis and were 4 in serum and 19 in feces. In this study, miR-375-3p, detected in serum and feces, was identified as the strongest candidate for a high-dose radiation biomarker in serum and/or feces using a radiation-induced intestinal injury model.

2023-12-15 | GSE247876 | GEO

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