Search

Dianhui Xiu,1 Lin Liu,1 Min Cheng,1 Xiaosong Sun,2 Xibo Ma3 1Department of Radiology, China-Japan Union Hospital of Jilin University, Changchun 130021, Jilin, People’s Republic of China; 2Department of Thyroid-Head and Neck Surgery, Jilin Cancer Hospital, Changchun 130021, Jilin, People’s Republic of China; 3Department of Otolaryngology, Jilin Provincial People’s Hospital, Changchun 130021, Jilin, People’s Republic of ChinaCorrespondence: Lin Liu; Min ChengDepartment of Radiology, China-Japan Union Hospital of Jilin University, No. 126, Sendai Street, Changchun City, Jilin Province, People’s Republic of ChinaEmail uyigtl@163.com; nrwpne@163.comBackground: Prostate cancer (PCa) is a common malignant tumor of the urinary system in males. LncRNA taurine-upregulated gene 1 (TUG1) has been verified to play a crucial role in progression and prognosis of PCa. However, the functional mechanism of TUG1 remains unclear with radiosensitivity of PCa.Methods: Quantitative real-time PCR (qRT-PCR) was conducted to measure the transcription levels of genes. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were employed to assess cell proliferation and apoptosis, respectively. Moreover, colony formation assay was used to measure colony survival. Western blot was performed to detect the relative proteins expression. The interaction among variables was predicted by online tool starbase, and then confirmed using the dual luciferase reporter assay. A xenograft mouse model was constructed to investigate the effect of TUG1 on tumor growth in vivo.Results: The levels of lncRNA TUG1 and SMC1A were remarkably increased, while miR-139-5p was downregulated in PCa. Patients with high expression of TUG1 showed a lower survival rate and poor prognosis. Knockdown of TUG1 inhibited PCa cell proliferation and colony survival fraction, and promoted apoptosis. Downregulation of miR-139-5p reversed the effects of TUG1 deletion on proliferation, apoptosis and colony survival fraction in PCa cells treated with 4 Gy of X-ray radiation. Moreover, TUG1 sponged miR-139-5p to regulate SMC1A expression. SMC1A deletion blocked the effects of TUG1 on the progression of PCa cells treated with 4 Gy of X-ray radiation. The tumor volume and weight were illustriously reduced with radiation and TUG1 silencing in xenograft model.Conclusion: Knockdown of lncRNA TUG1 enhanced radiosensitivity in PCa via the TUG1/miR-139-5p/SMC1A axis. It may become a promising target for PCa treatment.Keywords: TUG1, miR-139-5p, SMC1A, prostate cancer, radiosensitivity

Fluorescence molecular tomography (FMT), as a powerful imaging technique in preclinical research, can offer the three-dimensional distribution of biomarkers by detecting the fluorescently labelled probe noninvasively. However, because of the light scattering effect and the ill-pose of inverse problem, it is challenging to develop an efficient reconstruction method, which can provide accurate location and morphology of the fluorescence distribution. In this research, we proposed a novel adaptive Gaussian weighted Laplace prior (AGWLP) regularization method, which assumed the variance of fluorescence intensity between any two voxels had a non-linear correlation with their Gaussian distance. It utilized an adaptive Gaussian kernel parameter strategy to achieve accurate morphological reconstructions in FMT. To evaluate the performance of the AGWLP method, we conducted numerical simulation and in vivo experiments. The results were compared with fast iterative shrinkage (FIS) thresholding method, split Bregman-resolved TV (SBRTV) regularization method, and Gaussian weighted Laplace prior (GWLP) regularization method. We validated in vivo imaging results against planar fluorescence images of frozen sections. The results demonstrated that the AGWLP method achieved superior performance in both location and shape recovery of fluorescence distribution. This enabled FMT more suitable and practical for in vivo visualization of biomarkers.

Fluorescence molecular tomography (FMT), as a promising imaging modality in preclinical research, can obtain the three-dimensional (3-D) position information of the stem cell in mice. However, because of the ill-posed nature and sensitivity to noise of the inverse problem, it is a challenge to develop a robust reconstruction method, which can accurately locate the stem cells and define the distribution. In this paper, we proposed a sparsity adaptive correntropy matching pursuit (SACMP) method. SACMP method is independent on the noise distribution of measurements and it assigns small weights on severely corrupted entries of data and large weights on clean ones adaptively. These properties make it more suitable for in vivo experiment. To analyze the performance in terms of robustness and practicability of SACMP, we conducted numerical simulation and in vivo mice experiments. The results demonstrated that the SACMP method obtained the highest robustness and accuracy in locating stem cells and depicting stem cell distribution compared with stagewise orthogonal matching pursuit and sparsity adaptive subspace pursuit reconstruction methods. To the best of our knowledge, this is the first study that acquired such accurate and robust FMT distribution reconstruction for stem cell tracking in mice brain. This promotes the application of FMT in locating stem cell and distribution reconstruction in practical mice brain injury models.

The last couple of decades have seen brilliant progress in stem cell therapies, including native, genetically modified, and engineered stem cells, for osteonecrosis of the femoral head (ONFH). In vitro studies evaluate the effect of endogenous or exogenous factor or gene regulation on osteogenic phenotype maintenance and/or differentiation towards osteogenic lineage. The preclinical and clinical outcomes accelerate the clinical translation. Bone marrow mesenchymal stem cells and adipose-derived stem cells have demonstrated better effects in the treatment of femoral head necrosis. Various materials have been used widely in the ONFH treatment in both preclinical and clinical trials. In a word, in vivo and multiscale efforts are expected to overcome obstacles in the approaches for treating ONFH and provide clinical relevance and commercial strategies in the future. Therefore, we will discuss the above aspects in this paper and present our opinions.