Irradiation-responsive PRDM10-DT modulates the angiogenic response in human NSCLC cells in an SP1-dependent manner via the miR-663a/TGF-β1 axis.

Background: Photon radiation has been shown to stimulate the secretion of radioresistant factors from tumor cells, ultimately promoting tumor angiogenesis and metastasis. On the other hand, heavy-ion radiotherapy has been demonstrated to control tumor angiogenesis and metastasis levels. The molecular mechanisms responsible for the different angiogenic responses to photon and heavy-ion irradiation are not fully understood.

Tetramethylpyrazine attenuates sodium arsenite-induced acute kidney injury by improving the autophagic flux blockade via a YAP1-Nrf2-p62-dependent mechanism.

With increased application, sodium arsenite (AS III)-induced acute kidney injury (AI-AKI) is becoming a new clinical challenge, but its potential pathogenesis remains poorly studied. Our previous data demonstrated that inducing autophagy and mitochondrial dysfunction in renal tubular cells are important links of AI-AKI and could be inhibited by tetramethylpyrazine (TMP). Recently, co-transcription factor YAP1 is reported to control autophagy and is mandatory to stimulate autophagic flux.

Immune Response following FLASH and Conventional Radiation in Diffuse Midline Glioma.

Purpose: Diffuse midline glioma (DMG) is a fatal tumor traditionally treated with radiation therapy (RT) and previously characterized as having a noninflammatory tumor immune microenvironment (TIME). FLASH is a novel RT technique using ultra-high dose rate that is associated with decreased toxicity and effective tumor control. However, the effect of FLASH and conventional (CONV) RT on the DMG TIME has not yet been explored.

The Tumorigenic Effect of lncRNA AFAP1-AS1 is Mediated by Translated Peptide ATMLP Under the Control of m A Methylation.

Long noncoding RNAs (lncRNAs) in eukaryotic transcripts have long been believed to regulate various aspects of cellular processes, including carcinogenesis. Herein, it is found that lncRNA AFAP1-AS1 encodes a conserved 90-amino acid peptide located on mitochondria, named lncRNA AFAP1-AS1 translated mitochondrial-localized peptide (ATMLP), and it is not the lncRNA but the peptide that promotes the malignancy of nonsmall cell lung cancer (NSCLC). As the tumor progresses, the serum level of ATMLP increases.

Single-Cell Transcriptome Analysis of Radiation Pneumonitis Mice.

Radiation-induced lung injury (RILI), especially radiation pneumonitis (RP), is a common clinical complication associated with thoracic radiotherapy for malignant tumors. However, the specific contributions of each cell subtype to this process are unknown. Here, we provide the single-cell pathology landscape of the RP in a mouse model by unbiased single-cell RNA-seq (scRNA-seq).

Smurf2 inhibition enhances chemotherapy and radiation sensitivity in non-small-cell lung cancer.

Lung cancer has been the most common cancer worldwide for several decades. The outcomes of patients with locally advanced lung cancer remain dismal, and only a minority of patients survive more than 5 years. However, tumor therapeutic resistance mechanisms are poorly studied.

Mitochondrial Damage Response and Fate of Normal Cells Exposed to FLASH Irradiation with Protons.

Radiation therapy (RT) plays an important role in cancer treatment. The clinical efficacy of radiation therapy is, however, limited by normal tissue toxicity in areas surrounding the irradiated tumor. Compared to conventional radiation therapy (CONV-RT) in which doses are typically delivered at dose rates between 0.

Ionizing radiation-induced long noncoding RNA CRYBG3 regulates YAP/TAZ through mechanotransduction.

Mechanotransduction sensing of tissue architecture and cellular microenvironment is a fundamental regulator of cell fate, including cancer. Meanwhile, long noncoding RNAs (lncRNAs) play multifunctions during cancer development and treatment. However, the link between lncRNAs and cellular mechanotransduction in the context of cancer progression has not yet been elucidated.

A proposed change to astronaut exposures limits is a giant leap backwards for radiation protection.

Addressing the uncertainties in assessing health risks from cosmic ray heavy ions is a major scientific challenge recognized by many previous reports by the National Academy of Sciences (NAS) and the National Council on Radiation Protection and Measurements (NCRP) advising the National Aeronautics and Space Administration (NASA). These reports suggested a series of steps to pursue the scientific basis for space radiation protection, including the implementation of age and sex dependent risk assessments and exposure limits appropriate for a small population of radiation workers, the evaluation of uncertainties in risk projections, and developing a vigorous research program in heavy ion radiobiology to reduce uncertainties and discover effective countermeasures. The assessment of uncertainties in assessing risk provides protection against changing assessments of risk, reveals limitations in information used in space mission operations, and provides the impetus to reduce uncertainties and discover the true level of risk and possible effectiveness of countermeasures through research.

Androgen Receptor, Although Not a Specific Marker For, Is a Novel Target to Suppress Glioma Stem Cells as a Therapeutic Strategy for Glioblastoma.

Targeting androgen receptor (AR) has been shown to be promising in treating glioblastoma (GBM) in cell culture and flank implant models but the mechanisms remain unclear. AR antagonists including enzalutamide are available for treating prostate cancer patients in clinic and can pass the blood-brain barrier, thus are potentially good candidates for GBM treatment but have not been tested in GBM orthotopically. Our current studies confirmed that in patients, a majority of GBM tumors overexpress AR in both genders.

Silver nanoparticles protect against arsenic induced genotoxicity via attenuating arsenic bioaccumulation and elevating antioxidation in mammalian cells.

Arsenic (As) and its compounds have been classified as Group I carcinogenic agents by the International Agency for Research on Cancer (IARC); however, there is few specific and efficient antidotes used for As detoxification. The present study aimed to investigate the protective effects of silver nanoparticles (AgNPs) at non-toxic concentrations on As(Ⅲ) induced genotoxicity and the underlying mechanism. Our data showed that AgNPs pretreatment significantly inhibited the generation of phosphorylated histone H2AX (γ-H2AX, marker of nuclear DNA double strand breaks) and the mutation frequencies induced by As(Ⅲ) exposure.

The long noncoding RNA CRYBG3 induces aneuploidy by interfering with spindle assembly checkpoint via direct binding with Bub3.

Aneuploidy is a hallmark of genomic instability that leads to tumor initiation, progression, and metastasis. CDC20, Bub1, and Bub3 form the mitosis checkpoint complex (MCC) that binds the anaphase-promoting complex or cyclosome (APC/C), a crucial factor of the spindle assembly checkpoint (SAC), to ensure the bi-directional attachment and proper segregation of all sister chromosomes. However, just how MCC is regulated to ensure normal mitosis during cellular division remains unclear.

Radiation Exposure-Induced Changes in the Immune Cells and Immune Factors of Mice With or Without Primary Lung Tumor.

Recent studies have demonstrated that radiation activates in situ antitumor immunity and consequently induced a synergistic effect of radiotherapy and immunotherapy. However, studies related to radiation-induced changes in immune system of tumor-bearing mice are limited, which are of great significance to improve the efficacy of radioimmunotherapy. In this study, we first established a primary lung tumor mouse model using urethane.

Inhibition of autophagic flux differently modulates cannabidiol-induced death in 2D and 3D glioblastoma cell cultures.

Radiotherapy combined with chemotherapy is the major treatment modality for human glioblastoma multiforme (GBM). GBMs eventually relapse after treatment and the average survival of GBM patients is less than two years. There is some evidence that cannabidiol (CBD) can induce cell death and increases the radiosensitivity of GBM by enhancing apoptosis.