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Results for “Radioresistance”

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At least 19 recordsLinked to original sources
PubMed2026

A three-gene radioresistance signature predicts tumor progression in cervical cancer.

BACKGROUND: As a primary curative treatment for locally advanced cervical cancer, radiotherapy is frequently undermined by radioresistant tumor cells that evade cell death and subsequently drive post-treatment tumor progression. This study aimed to identify candidate genes associated with radioresistance in cervical cancer and to explore their potential in predicting unfavorable outcomes among radioresistant patients, thereby providing a reference for future research. METHODS: We screened for co-expressed genes using transcriptomic data from radiation non-complete response (NCR) cervical cancer patients in Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. Cox regression analyses were conducted to identify the most significant radioresistance-associated genes for constructing a prognostic model. The predictive performance of this model was further validated through logistic regression, weighted gene co-expression network analysis (WGCNA), and pan-cancer analyses. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was performed to quantify the expression levels of key genes in cervical cancer tissue samples from radiosensitive and radioresistant patients. RESULTS: The resulting prognostic model comprised three genes: MTMR11, VANGL1, and CD46. This gene panel was significantly associated with the prognosis of cervical cancer patients receiving radiotherapy and showed acceptable predictive performance across multiple cancer types. qRT-PCR analysis revealed that the expression patterns of MTMR11 and VANGL1 were generally consistent with radioresistance of cervical cancer, whereas CD46 exhibited an unexpected expression trend. CONCLUSIONS: Our findings indicate that MTMR11, VANGL1, and CD46 are associated with radioresistance and prognosis in cervical cancer. Their potential clinical utility, especially in predicting radiotherapy response at the individual patient level, requires further validation in larger, independent, and prospective cohorts.

Cervical cancer↗
PubMed2026

lncRNA JPX promotes radioresistance in nasopharyngeal carcinoma via the miR-1301-3p/PIK3R2-mediated autophagy pathway.

BACKGROUND: Nasopharyngeal carcinoma (NPC) represents an aggressive head and neck malignancy with high metastatic potential. Radioresistance remains a major therapeutic obstacle associated with poor prognosis. Although the long non-coding RNA (lncRNA) JPX has been implicated in various cancers, its specific role in NPC radioresistance requires further elucidation. This study aimed to investigate whether JPX modulates radiosensitivity through autophagy regulation and to delineate the underlying molecular mechanisms. METHODS: JPX expression was analyzed in NPC cell lines and The Cancer Genome Atlas (TCGA) datasets, with subcellular localization determined through cellular fractionation. Functional characterization was performed using short hairpin RNA (shRNA)-mediated knockdown in CNE-2 and HONE-1 cell lines. Radiosensitivity was evaluated by clonogenic survival assays at a clinically relevant radiation dose, with cell viability assessed by MTT as a screening measure. while autophagy activity was assessed through Western blot analysis of LC3-II and p62. Molecular interactions were validated using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. RESULTS: JPX was significantly upregulated in head and neck squamous cell carcinoma (HNSCC) tissues and NPC cell lines, showing predominant cytoplasmic localization. Clinical association analysis in the TCGA-HNSCC cohort revealed that elevated JPX expression correlated with advanced tumor stage and poor overall survival, although NPC-specific clinical validation remains to be established. Genetic silencing of JPX attenuated autophagic flux and enhanced radiosensitivity. Mechanistic investigations revealed that JPX functions as a competitive endogenous RNA (ceRNA) functionally associating with miR-1301-3p, thereby alleviating miR-1301-3p-mediated repression of PIK3R2 and subsequently activating pro-survival autophagy pathways. CONCLUSIONS: The findings demonstrate that JPX promotes radioresistance in NPC through a ceRNA mechanism involving the miR-1301-3p/PIK3R2/autophagy regulatory axis. The JPX/miR-1301-3p/PIK3R2 axis thus emerges as a potential mechanistic candidate for radiosensitization; however, this notion remains strictly provisional and requires rigorous validation in authenticated NPC models, in vivo systems, and patient-derived samples before any translational consideration can be justified. Despite the cell line limitations acknowledged herein, our findings provide a mechanistic framework for understanding JPX-mediated radioresistance that warrants further investigation in more physiologically relevant models.

JPX↗
PubMed1975

Lambda bacteriophage gene produces and X-ray sensitivity of Escherichia coli: comparison of red-dependent and gam-dependent radioresistance.

When gene products of lambda bacteriophage are introduced into a cell by transient induction of a lysogen, increased resistance of the cells to X rays results. This phenomenon has been called phage-induced radioresistance. Genetic studies show at least two classes of induced radioresistance. The first type depends on the products of the lambda red genes and is observed in bacteria that are mutated in the recB gene. It is thought that the lambda red products compensate for the missing RecBC nuclease in the repair of X-ray damage. An optimal effect is obtained even when the lambda red products are supplied 1 h after irradiation. The lesions that are affected by the red-dependent process are probably not deoxyribonucleic acid strand breaks because the extent of deoxyribonucleic acid strand rejoining is not altered by the red products. The second type of phage-induced radioresistance requires the gam product of lambda and is observed in wild-type and polA strains. The lambda gam+ gene produce must be present immediately after irradiation to exert its full effect. In its presence, DNA breakdown is decreased, and a greater fraction of DNA is converted back to high molecular weight. Strains carrying lex, recA, or certain other combinations of mutations do not show any detectable phage-induced radioresistance.

Coliphages↗
PubMed2025

Adaptive laboratory evolution of Micrococcus luteus and identification of genes associated with radioresistance through genome-wide association study.

Micrococcus luteus (V017) is a Gram-positive bacterium that was isolated from a sterilization area exposed to 60Co radiation. In this study, we performed an adaptive laboratory evolution experiment with M. luteus, exposing it to 24 continuous cycles of gamma irradiation at four different doses (1.5 kGy, 3.5 kGy, 5.5 kGy, and 7.5 kGy). This led to the creation of four evolved populations with different levels of radioresistance, which were positively correlated with the radiation dose applied. The survival rate of the evolved population that underwent adaptive treatment at the highest dose (7.5 kGy) was 0.69% after exposure to 5.5 kGy, which is about five orders of magnitude higher than that of the original strain V017. Furthermore, 76 evolved strains were selected from these populations, and their genomes were re-sequenced, uncovering a total of 3072 mutations. A genome-wide association study identified 56 single nucleotide polymorphisms (SNPs) significantly associated with radioresistance, linked to 62 candidate genes. Ultimately, 9 genes were selected for functional validation. Inactivating 6 of these genes, including H0H31_RS03855 (SMC family ATPase, SbcC), H0H31_RS04250 (ribonuclease HII), H0H31_RS04570 (endonuclease VIII), H0H31_RS07595 (bifunctional 3'-5' exonuclease/DNA polymerase I), H0H31_RS00170 (serine/threonine phosphatase PPP), and H0H31_RS05860 (CBS-domain-containing protein), significantly increased sensitivity to gamma radiation, underscoring their importance in radioresistance.

Micrococcus luteus↗
PubMed1978

Induced radioresistance in four strains of Escherichia coli, two with lambda lysogens.

Cells of E. coli that are recA+ and lex+ show a phenomenon of induced radioresistance. A preexposure to ultraviolet light, or ionizing radiation followed by incubation to allow protein synthesis, followed by treatment with rifampin to prevent further induction, renders the cells resistant to further doses of radiation. When this is attempted with lambda lysogens of the same strains, no radioresistance is seen, even though the preexposure is too small to induce lambda itself. If the lysogens are ind-, namely lambda C1857, about the normal radioresistance can be developed by pretreatment. These findings suggest that the lambda repressors can bind to single-strand breaks caused by the inducing agent and can modify the course of induction.

Coliphages↗
PubMedDate not supplied

[Deamination reactions involving several nitrogen compounds and mammalian radioresistance].

Inhibition of monoamine oxidase (substrates tyramine or serotonin) with simultaneous appearance of diamine oxidase (substrates histamine or putrescine) and distinct increase in AMP-deaminating activities were found after total body X-ray irradiation (700 r) of white mice or rats in mitochondrial fractions isolated from their liver and intestines. These impairments in deamination of nitrogenous compounds in liver mitochondria of guinea pigs, which are must less radioresistant as compared with mice or rats, were noted after the irradiation at a dose 300 r, but in the liver mitochondria of mongolian gerbyls (Mariones unguiculatus), which are highly radioresistant, the irradiation even at a dose 1500 r did not cause appearance either of histamine or of AMP-deaminating activities while the decrease in the monoamine oxidase activity was not statistically significant. Feeding to the mice the grasses, which comprize the fodder of mongolian gerbyls under natural conditions, increased radioresistance of the animals and prevented at the same time appearance in the mitochondrial fractions of liver and intestines of those impairments in deamination of nitrogenous compounds which accompanied development of irradiation injuries.

Adenosine Monophosphate↗
PubMed1976

[Influence of a preliminary irradiation once or twice on radioresistance of mice*].

The radioresistance of mice was tested in order to find out in which way it was influence by one or two preliminary irradiations. The thirty-day survival rate after a single total irradiation was taken as a criterion of the radioresistance. Only one test group showed a significant increase of radioresistance after two preliminary irradiations, whereas the resistance of three other groups was reduced remarkably after irradiation doses of 300 resp. 400 R. From these facts we draw the following conclusion: either radiotoxins and the remote effects produced by them are only playing a minor role in NMRI/Han mice or these mice are particular "low-responders" as far as the produciton of antibodies against radiotoxins is concerned.

Animals↗
PubMed2026

The KEAP1-NFE2L2/NRF2 Axis in Non-Small Cell Lung Cancer Radioresistance: Redox Homeostasis and Emerging DNA Damage Response Mechanisms.

Radioresistance and local recurrence remain major barriers to effective radiotherapy in non-small cell lung cancer (NSCLC). Loss-of-function KEAP1 alterations or activating NFE2L2 alterations can stabilize NRF2, but do not alone establish sustained transcriptional activity or functional dependency. This focused narrative review evaluates clinical radiotherapy studies and mechanistically informative preclinical studies linking the KEAP1-NFE2L2/NRF2 axis to NSCLC radioresistance. We prioritized clinical studies reporting radiotherapy-specific outcomes and preclinical studies coupling NRF2-related molecular status or perturbation with radiation-response endpoints; contextual studies informed metabolic, DNA damage response (DDR), immune and normal-lung effects. Evidence most consistently supports NRF2-mediated redox protection through glutathione-dependent defense, cellular reducing capacity and antioxidant enzymes, limiting radiation-induced reactive oxygen species (ROS) accumulation and oxidative injury. Limited studies further suggest that NRF2 may affect DNA-damage signaling, checkpoint control and repair. The detailed RPA32-TOPBP1-ATR-CHK1 model is therefore considered proposed rather than established in NRF2-active NSCLC. Retrospective clinical studies associate pathogenic KEAP1/NFE2L2 alterations with impaired local control in some radiotherapy-treated cohorts, but do not justify treating genomic status, protein abundance, transcriptional activity and functional dependency as equivalent measures or demonstrate treatment-predictive value. NRF2-mediated normal-lung protection also constrains systemic inhibition. Prospective studies integrating molecular classification, radiation-response endpoints, local control and normal-tissue toxicity are required before biomarker-guided radiosensitization can be considered.

DNA damage response↗
PubMed1979

Relationships among differentiated T-cell subpopulations. V. T-cell dependent mechanism of xenograft rejection and its radioresistant nature.

Rat tumours grew progressively in nu/nu mice but not in nu/+ mice, normal AKR mice or sublethally irradiated AKR mice after subcutaneous inoculation. Suppression of tumour growth appeared to depend on radioresistant cytotoxic T cells which were detected in in vivo neutralization tests (Winn's test) with spleen cells of mice immunized with rat lymphocytes or tumour cells 5 days previously. Radioresistant cytotoxic activity was detected by 51Cr-release test in glass-non-adherent peritoneal exudate cells 5 days after intraperitoneal immunization with rat lymphocytes. These results suggested that immune lymphocytes might differentiate to mature cytotoxic cells at the site of direct graft rejection.

Animals↗
PubMed1975

Radioresistance in natural populations of Drosophila nebulosa from a Brazilian area of high background radiation.

D. nebulosa, collected in two woods of a high background radiation area (both in Iron Hills, State of Minas Gerais, Brazil), were compared to and found to be more resistant than flies collected as controls in two other woods of an adjacent area. This was the second time that average differences in radioresistance between natural populations were established. Previous experiments were carried out with D. willistoni, in the same area and in comparable fashion. In spite of their higher radiation resistance the flies from the radiation area carried a higher expressed load than the controls. The following tests were performed to estimate the differences: (a) survival, after whole body exposure to 90 000 R of 60Co-gamma-rays on 120 strains set up from single inseminated females and (b) reproductive performance, in 240 duplicate croses, measured in terms of the difference between irradiated series (males received 3000 R of 60Co-gamma-rays) and their unirradiated counterparts. The data are based on an offspring of 293784 individuals. Futhermore, two diallel crosses between sensitive and resistant strains have shown that the differences probably are due mainly to additive genes.

Animals↗
PubMed1975

Induction of radioresistance in Escherichia coli.

The effect of prior treatment by inducing agents on the radioresistance of cells of Escherichia coli has been studied. In order to separate the induction process from the radiation-damage process, cells were first treated with inducing agents such as ultraviolet light, ionizing radiation, or nalidixic acid, allowed to become induced by incubation for 50 min and then given rifampin to prevent further induction. They were then tested for radiation sensitivity. It was found that all strains tested except recA-, lex-, and recB showed very apparent protection. Induction by UV had the most effect and by nalidixic acid the least. The time course of development of protection was observed in one case: it is 50% established in 15 min. The absence of effect in recA- and lex- is explainable by the fact that these cells cannot be induced, for example, for prophage or the inducible inhibitor of post-irradiation DNA degradation. We suggest that the inducible inhibitor of postirradiation DNA degradation is one factor in a recovery system possessed by E. coli cells.

Cell Division↗
PubMed1977

A study on fungal radioresistance and sensitivity.

Lower doses of gamma and X-rays (5 and 1 Krad, respectively) stimulated the spore germination and growth of 7 tested fungi. Higher doses (500 and 100 Krad, respectively) revealed that Epicoccum nigrum was the most radioresistant, while Alternaria humicola, Stemphylium verruculosum, Rhizopus nigricans, and Cladosporium herbarum were of moderate resistance. Aspergillus niger and Penicillium oxalicum were the most radiosensitive. Protein and polysaccharide synthesis were inhibited in the mycelium developed from irradiated spores; the inhibition was a function of dose. Study of the different factors (morphological, biological, and biochemical) indicates that variability in fungal resistance to ionizing radiation is, most probably, an inherent character, connected with mycelial water content and the natural production of a chemical substance(s) that acts as a radioprotector(s).

Amino Acids↗