At 24 h postirradiation, a considerable difference was only observed in the expression of the β-catenin gene. Conclusion This study showed that the TRIM29 and TRIM37 genes are involved in the cell response to radiation and proposed that these genes may be biomarkers for predicting RS in normal and tumoral cell lines.Background Growing evidence demonstrated that long noncoding RNAs (lncRNAs) were involved in the progression of diverse cancers, including breast cancer (BC). Recent studies indicated that lncRNA nuclear enriched abundant transcript 1 (NEAT1) was overexpressed and facilitated tumor processes in many cancers. Nevertheless, the underlying mechanism of NEAT1 in regulating BC progression is still largely unknown. Materials and Methods The abundance of NEAT1, microRNA-138-5p (miR-138-5p), and zinc finger protein X-linked (ZFX) was assessed by quantitative real-time polymerase chain reaction. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, and transwell assay were utilized to evaluate cell proliferation, apoptosis, migration, and invasion, respectively. Western blot analysis was applied to detect the protein expression of CyclinD1, Bax, E-cadherin, and ZFX. The interaction between miR-138-5p and NEAT1 or ZFX was predicted by starBase v3.0 and validated by dual-luciferase reporter, RNA pull-down, and RNA immunoprecipitation assays. The mice xenograft model was established to investigate the roles of NEAT1 in vivo. Results NEAT1 was highly expressed and miR-138-5p was lowly expressed in BC tissues and cells. NEAT1 interference or miR-138-5p restoration repressed cell proliferation, migration, and invasion but accelerated apoptosis in BC cells. Moreover, miR-138-5p directly interacted with NEAT1 and its knockdown reversed the suppressive impact of NEAT1 downregulation on the progression of BC cells. In addition, ZFX was a downstream target of miR-138-5p and its upregulation attenuated the antitumor role of miR-138-5p in BC cells. Besides, ZFX expression was positively regulated by NEAT1 and inversely modulated by miR-138-5p. Furthermore, interference of NEAT1 inhibited tumor growth by upregulating miR-138-5p and downregulating ZFX. Conclusion NEAT1 affected BC progression through modulating miR-138-5p/ZFX axis, providing a vital theoretical basis for BC treatment.Background Non-small cell lung cancer (NSCLC) is the most prevalent cancer in the world. Chemotherapy resistance is a major obstacle to NSCLC therapy. This study aimed to explore the role and molecular mechanism of circular RNA 0011292 (circ_0011292) in tumorigenesis and chemoresistance of NSCLC. Methods The levels of circ_0011292, miR-379-5p, and tripartite motif-containing protein 65 (TRIM65) were measured by quantitative real-time polymerase chain reaction or Western blot assay. Cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was monitored by flow cytometry. Cell migration and invasion were detected by transwell assay. The levels of apoptosis-related and epithelial-mesenchymal transition-related proteins were examined by Western blot. The half-inhibition concentration (IC50) of paclitaxel (PTX) was evaluated by CCK-8 assay. Xenograft model was established to analyze the effect of circ_0011292 on PTX resistance of NSCLC in vivo. PIK-III ic50 The interaction among circ_0011292, miR-379-5p, and TRIM65 was verified by dual-luciferase reporter assay and RNA immunoprecipitation assay. Results Circ_0011292 and TRIM65 were upregulated, while miR-379-5p was downregulated in NSCLC tissues and cells. Circ_0011292 knockdown hindered NSCLC progression and enhanced PTX sensitivity of NSCLC. Circ_0011292 silencing reduced PTX resistance in vivo. Besides, miR-379-5p potentiated PTX sensitivity by targeting TRIM65. Also, circ_0011292 increased PTX resistance by sponging miR-379-5p. Conclusion Circ_0011292 facilitated tumorigenesis and PTX resistance in NSCLC by regulating the miR-379-5p/TRIM65 axis, suggesting that circ_0011292 was a promising therapeutic target for NSCLC chemotherapy.Background Temozolomide (TMZ) resistance is a serious hindrance in clinical chemotherapy for glioma. Circular RNA homeodomain interacting protein kinase 3 (circHIPK3) can be involved in regulating the progression of glioma, but the molecular mechanism of circHIPK3 in TMZ-resistant-glioma is completely unclear. Materials and Methods The levels of circRNA, miRNA, and mRNA were examined using quantitative real-time polymerase chain reaction. 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide assay was used for assessing the half inhibitory concentration (IC50) of TMZ and cell proliferation. Cell apoptosis and metastasis (migration and invasion) were detected by flow cytometry and transwell assay, respectively. Western blot and dual-luciferase reporter assay were performed several times to analyze the expression levels of associated proteins and the targeted relation. Results The upregulation of circHIPK3 was found in TMZ-resistant glioma tissues and cells. Both circHIPK3 knockdown and kinesin family member 2A (KIF2A) inhibition could facilitate TMZ sensitivity and apoptosis but repress proliferation and metastasis in TMZ-resistant glioma cells. CircHIPK3 targeted microRNA-524-5p (miR-524-5p) and KIF2A functioned as a downstream target of miR-524-5p. Decrease of miR-524-5p relieved the effects of si-circHIPK3 on TMZ-resistant glioma cells by upregulating KIF2A. Downregulation of circHIPK3 refrained the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signal pathway partly through miR-524-5p/KIF2A axis. Conclusions Knockdown of circHIPK3 promoted TMZ sensitivity in glioma by modulating proliferation, metastasis, and apoptosis through miR-524-5p/KIF2A-mediated PI3K/AKT pathway. CircHIPK3 may be the potential target for the diagnosis and therapy of TMZ-resistant glioma.We present the hypothesis that microorganisms can change the freezing/melting curve of cold salty solutions by protein expression, as it is known that proteins can affect the liquid-to-ice transition, an ability that could be of ecological advantage for organisms on Earth and on Mars. We tested our hypothesis by identifying a suitable candidate, the well-known psycrophile and halotolerant bacteria Rhodococcus sp. JG3, and analyzing its response in culture conditions that included specific hygroscopic salts relevant to Mars-that is, highly concentrated magnesium perchlorate solutions of 20 wt % and 50 wt % Mg(ClO4)2 at both end members of the eutectic concentration (44 wt %)-and subfreezing temperatures (263 K and 253 K). Using a combination of techniques of molecular microbiology and aqueous geochemistry, we evaluated the potential roles of proteins over- or underexpressed as important players in different mechanisms for the adaptability of life to cold environments. We recorded the changes observed by micro-differential scanning calorimetry.