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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. In the present study, we demonstrated that LNC CRYBG3, an ionizing radiation-inducible long noncoding RNA, directly binds with Bub3 and interrupts its interaction with CDC20 to result in aneuploidy. The 261–317 (S3) residual of the LNC CRYBG3 sequence is critical for its interaction with Bub3 protein. Overexpression of LNC CRYBG3 leads to aneuploidy and promotes tumorigenesis and metastasis of lung cancer cells, implying that LNC CRYBG3 is a novel oncogene. These findings provide a novel mechanistic basis for the pathogenesis of NSCLC after exposure to ionizing radiation as well as a potential target for the diagnosis, treatment, and prognosis of an often fatal disease.

Space exploration represents great challenge to astronauts’ health because of the uncertain risk of carcinogenesis caused by space radiation, in which high-charge and -energy (HZE) particles should be the most harmful components. Although there are a number of researches confirming that HZE particles have more severe biological effects including tumorigenesis than low-LET radiations, it is still very hard to accurately estimate the cancer risk of space HZE radiation due to the lack of suitable epidemiological data on exposures to low-dose HZE particle irradiation. Ground-based experiments on high-energy heavy ion accelerators might be appropriate complement for understanding the risk of space radiation. On the other hand, effective countermeasures to reduce the radiation damage are essential to manned space exploration. Up to now, shielding is still the most practical way to attenuate biological responses of space radiation. However, the knowledge on the biological effects of secondary particles produced by the interaction of HZE particles with shielding materials is required for space shielding design. This review will discuss the issues of space HZE particles and the biological effects of secondary particles produced by the interaction of space radiation and shielding materials.

During a long-term exploration in space, astronauts will be constantly exposed to space radiation which contains various types of low dose-rate heavy particles. Although the fluxes of these heavy ions are very small, the heavy ions can cause severe biological effects including early effects and late effects. This short review will discuss the biological effects induced by space radiation and introduce a new anti-radiation agent we have developed. We synthesized a class of reactive oxygen species scavengers called GANRA-5 with lowly toxic but high radio-protective effect to both heavy ions and X-rays. GANRA-5 can protect cells from X-rays and carbon ions induced cell killing by significantly reducing the amount of free radical production therefor reduce double-strand breaks and genomic instability. In vivo, GANRA-5 can effectively protect the mice from the damage induced by X-rays irradiation by enhancing superoxide dismutase activities. In brief, GANRA-5 is potentially applicable in space flight.

This paper presents a particle filter-based visual tracking method with online feature selection mechanism. In color-based particle filter algorithm the weights of particles do not always represent the importance correctly, this may cause that the object tracking based on particle filter converge to a local region of the object. In our proposed visual tracking method, the Bhattacharyya distance and the local discrimination between the object and background are used to define the weights of the particles, which can solve the existing local convergence problem. Experiments demonstrates that the proposed method can work well not only in single object tracking processes but also in multiple similar objects tracking processes.

Background B cell translocation gene 1 (BTG1) has long been recognized as a tumor suppressor gene. Recent reports demonstrated that BTG1 plays an important role in progression of cell cycle and is involved in cellular response to stressors. However, the microRNAs mediated regulatory mechanism of BTG1 expression has not been reported so far. MicroRNAs can effectively influence tumor radiosensitivity by preventing cell cycle progression, resulting in enhancement of the cytotoxicity of radiotherapy efficacy. This study aimed to demonstrating the effects of microRNAs on the BTG1 expression and cellular radiosensitivity. Methods The human renal carcinoma 786-O cells were treated with 5 Gy of X-rays. Expressions of BTG1 gene and miR-454-3p, which was predicted to target BTG1 by software algorithm, were analyzed by quantitative polymerase chain reaction. Protein expressions were assessed by Western blot. Luciferase assays were used to quantify the interaction between BTG1 3′-untranslated region (3′-UTR) and miR-454-3p. The radiosensitivity was quantified by the assay of cell viability, colony formation and caspase-3 activity. Results The expression of the BTG1 gene in 786-O cells was significantly elevated after treatments with X-ray irradiation, DMSO, or serum starvation. The up-regulation of BTG1 after irradiation reduced cellular radiosensitivity as demonstrated by the enhanced cell viability and colony formation, as well as the repressed caspase-3 activity. In comparison, knock down of BTG1 by siRNA led to significantly enhanced cellular radiosensitivity. It was found that miR-454-3p can regulate the expression of BTG1 through a direct interaction with the 3′-UTR of BTG1 mRNA. Decreasing of its expression level correlates well with BTG1 up-regulation during X-ray irradiation. Particularly, we observed that over-expression of miR-454-3p by transfection inhibited the BTG1 expression and enhanced the radiosensitivity. In addition, cell cycle analysis showed that over-expression of miR-454-3p shifted the cell cycle arrest from G2/M phase to S phase. Conclusions Our results indicate that BTG1 is a direct target of miR-454-3p. Down-regulation of BTG1 by miR-454-3p renders tumor cells sensitive to radiation. These results may shed light on the potential application in tumor radiotherapy. Electronic supplementary material The online version of this article (doi:10.1186/1748-717X-9-179) contains supplementary material, which is available to authorized users.