It is well known that estrogen receptor α (ERα) participates in the pathogenic progress of breast cancer, hepatocellular carcinoma and head and neck squamous cell carcinoma. In neuroblastoma cells and related cancer clinical specimens, moreover, the ectopic expression of ERα has been identified. However, the detailed function of ERα in the proliferation of neuroblastoma cell is yet unclear. The transcriptional activity of ETS-1 (E26 transformation specific sequence 1) was measured by luciferase analysis. Western blot assays and Real-time RT-PCR were used to examine the expression of ERα, ETS-1 and its targeted genes. The protein-protein interaction between ERα and ETS-1 was determined by co-IP and GST-Pull down assays. The accumulation of ETS-1 in nuclear was detected by western blot assays, and the recruitment of ETS-1 to its targeted gene’s promoter was tested by ChIP assays. Moreover, SH-SY5Y cells’ proliferation, anchor-independent growth, migration and invasion were quantified using the MTT, soft agar or Trans-well assay, respectively. The transcriptional activity of ETS-1 was significantly increased following estrogen treatment, and this effect was related to ligand-mediated activation of ERα. The interaction between the ERα and ETS-1 was identified, and enhancement of ERα activation would up-regulate the ETS-1 transcription factor activity via modulating its cytoplasm/nucleus translocation and the recruitment of ETS-1 to its target gene’s promoter. Furthermore, treatment of estrogen increased proliferation, migration and invasion of neuroblastoma cells, whereas the antagonist of ERα reduced those effects. In this study, we provided evidences that activation of ERα promoted neuroblastoma cells proliferation and up-regulated the transcriptional activity of ETS-1. By investigating the role of ERα in the ETS-1 activity regulation, we demonstrated that ERα may be a novel ETS-1 co-activator and thus a potential therapeutic target in human neuroblastoma treatment.

MiR-122 is a novel tumor suppresser and its expression induces cell cycle arrest, or apoptosis, and inhibits cell proliferation in multiple cancer cells, including non-small cell lung cancer (NSCLC) cells. Radioresistance of cancer cell leads to the major drawback of radiotherapy for NSCLC and the induction of radiosensitization could be a useful strategy to fix this problem. The present work investigates the function of miR-122 in inducing radiosensitization in A549 cell, a type of NSCLC cells. MiR-122 induces the radiosensitization of A549 cells. MiR-122 also boosts the inhibitory activity of ionizing radiation (IR) on cancer cell anchor-independent growth and invasion. Moreover, miR-122 reduced the expression of its targeted genes related to tumor-survival or cellular stress response. These results indicate that miR-122 would be a novel strategy for NSCLC radiation-therapy.

Background: With the development of communication technology, the public is paying increasing attention to whether electromagnetic radiation is harmful to health. Mobile phone communication has entered the 5G era, and there are almost no reports on electromagnetic radiation at 2650 MHz. Therefore, it is necessary to evaluate the risk of adverse effects of 5G mobile phone EMR exposure on the human brain.Methods: Male animals were continuously exposed to 2650 MHz‐EMR for 28 days with a whole‐body averaged specific absorption rate (WBSAR) of 2.06 W/kg for 4 h per day. Mouse behavior was assessed using the open‐field test (OFT), elevated‐plus maze (EPM), and tail suspension test (TST). The Morris water maze (MWM), HE staining, and TUNEL staining were used to evaluate the spatial memory ability and pathological morphology of hippocampal dentate gyrus cells. Additionally, the expression levels of brain‐derived neurotrophic factor (BDNF), aminobutyric acid (GABA), and glucocorticoid (GR) in the hippocampus were detected by western blotting and immunohistochemistry, while the corticosterone (CORT) level in serum was detected by ELISA.Results: In the OFT, the total distance traveled, central distance traveled, and residence time significantly decreased in the EMR exposure group (p < .05). In EPM, the percentage of the number of times to open the arm and the percentage of time to open the arm significantly decreased in the EMR exposure group. However, in the TST, the two groups had no significant difference in the 4‐min immobility time. In the MWM, the escape latency of the EMR exposure group was shorter than that of the control group, with no significant difference. Furthermore, CORT levels in serum were significantly increased in the EMR exposure group (p < .05), while the expression of BDNF and GR proteins in the hippocampus was reduced (p < .05), but there was no significant difference in GABA expression.Conclusions: Our results indicate that exposure to 2650 MHz‐EMR (WBSAR: 2.06 W/kg, 28 days, 4 h per day) had no significant effect on the spatial memory ability of mice (in comparison to little effect). The exposure may be associated with anxiety‐like behavior in mice but not related to depression‐like behavior in mice.

Radiation therapy (RT) is essential for treating thoracic malignancies but often causes significant lung damage. FLASH‐RT, an ultra‐high dose rate irradiation technique, shows potential in reducing radiation‐induced lung injury (RILI) while maintaining tumor control. However, the underlying immune mechanisms remain poorly understood. This study investigates the immune and cellular responses to FLASH‐RT versus conventional dose rate (CONV) RT during the early phase of RILI. Using single‐cell RNA sequencing (scRNA‐seq), a dynamic landscape of the lung microenvironment is pictured during RILI within one‐week post‐irradiation. The analysis reveals that FLASH‐RT induces a more immediate but transient cellular response, while CONV‐RT causes sustained inflammation. FLASH irradiation significantly reduces neutrophil infiltration compared to CONV irradiation, particularly within the pro‐inflammatory Ccrl2 ⁺ subset. FLASH irradiation also triggers stronger activation of CD4 ⁺ CD40L ⁺ Th cells, which are critical for regulating immune responses and balancing inflammation. Moreover, FLASH irradiation attenuates pro‐inflammatory activation and intercellular signaling of Mefv⁺ monocytes, thereby restraining excessive macrophage‐driven inflammation. Additionally, FLASH irradiation enhances TGF‐β signaling and epithelial‐mesenchymal transition (EMT) in alveolar type 1 (AT1) cells, promoting tissue repair. These findings highlight FLASH‐RT's superior immune modulation and reparative potential, providing valuable insights into its clinical application for minimizing radiation damage and enhancing lung recovery.

To investigate the mechanism of ultra-high dose rate pulsed radiation in radiation-induced lung injury (RILI), providing an experimental and theoretical basis for the application of FLASH-RT (FLASH-radiotherapy) in radiotherapy. C57BL/6J mice were randomly divided into three groups: a sham group, a FLASH-irradiated group, and a CONV-irradiated group. A whole-body irradiation with a single dose of 3 Gy (200 Gy/s for FLASH group and 0.3 Gy/s for CONV group) using electron rays was used to establish models of lung injury. After 3 months, lung tissues were stained with HE and Masson stains to observe pathological changes in lung tissue and subjected to 4D-Fast DIA quantitative proteomics, with the sequencing data validated by Western blot and immunofluorescence. The mice in FLASH group had less lung tissue damage and lower levels of fibrosis compared to the CONV group. Proteomic sequencing showed significant differences in CCT6b protein expression between the two irradiation groups. As verified by the WB and immunofluorescence assays, the expression level of CCT6b was significantly reduced in the CONV group of mice compared with the SHAM and FLASH groups. With the down-regulation of CCT6b, there was a notable decrease in the expression of E-cadherin, accompanied by an increase in the expression of α-smooth muscle actin and Vimentin. The differential response in the level of lung fibrosis caused by the two types of radiation may be related to the level of CCT6b expression, but the specific mechanism of action needs to be further investigated.