LncRNA SBF2-AS1 has been reported to be implicated in the deterioration of multiple human cancers. However, the roles and underlying mechanisms of SBF2-AS1 in acute myeloid leukemia (AML) are still unclear. In the present study, the online GEPIA database showed that SBF2-AS1 expression was significantly increased in AML samples. QRT-PCR results showed that SBF2-AS1 expression was upregulated in AML cells. CCK-8 assay revealed that SBF2-AS1 inhibition decreased AML cells proliferation ability in vitro. Flow cytometry assays showed that SBF2-AS1 inhibition induced AML cells apoptosis and arrested AML cells in G0/G1 phase. Mechanistically, miR-188-5p was identified as a direct target of SBF2-AS1. SBF2-AS1 upregulated the expression level of ZFP91 by sponging miR-188-5p. And the effects of SBF2-AS1 suppression on AML cells progression could be abolished by miR-188-5p inhibitors. Moreover, we found that SBF2-AS1 inhibition reduced tumor growth in vivo. Taken together, our findings elucidated that SBF2-AS1 could act as a miRNA sponge in AML progression, and provided a potential therapeutic strategy for AML treatment.

Abstract. Neuroblastoma (NB) is the most common solid extracranial tumor in children. However, the molecular mechanism of NB remains to be elucidated. In the present study, reverse transcription quantitative polymerase chain reaction data demonstrated that the expression of Sam68 was significantly upregulated in NB tissues compared with their matched adjacent normal tissues. Furthermore, it was revealed that reduced expression of miR-203 and increased expression of Sam68 co-existed in NB tissues. Knockdown of Sam68 reduced the proliferation, migration and invasion of human SK-N-SH and SH-SY5Y NB cells. Similarly, overexpression of miR-203 also inhibited the proliferation, migration and invasion of these two cell lines. It was further demonstrated that the protein expression level of Sam68 was negatively mediated by miR-203 in the SK-N-SH and SH-SY5Y NB cells. Additionally, data from a dual luciferase reporter assay confirmed that miR-203 directly targeted Sam68 by binding to its 3'-untranslated region. In conclusion, the present study suggested for the first time, to the best of our knowledge, that the aberrant downregulation of miR-203 may contribute to the aberrant upregulation of Sam68 in NB and that miR-203 has an inhibitory role in malignant progression of NB by targeting Sam68. The present study provided evidence to support miR-203/Sam68 as a novel diagnostic or therapeutic targets for NB.

Background Chemotherapy of nasopharyngeal carcinoma (NPC) can lead to significant side effects and complications. Exercises during chemoradiotherapy have potential to reduce complications and fatigue and improve quality of life. The aim of the randomised clinical study was to investigate the benefits of resistance exercise during chemoradiotherapy in NPC patients. Methods A total of 146 patients were randomised to perform resistance or relaxation exercises during chemoradiotherapy. Resistance exercise consisted of eight machine‐based progressive resistance exercises, and relaxation control consisted of progressive muscle relaxation. Side effects and complications were analysed, and fatigue was assessed by Multidimensional Fatigue Symptom Inventory‐Short Form (MFSI‐SF) scores. The European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core‐30 (EORTC QLQ30) scale was used to evaluate the effects of resistance exercise or relaxation control on quality of life. Per‐protocol analysis was performed on the collected data. Results Resistance exercise has stronger effects than relaxation in reducing complications, including oral mucositis, mouth‐opening difficulties, xerostomia, hearing loss and nasal congestion, and alleviating both physical fatigue and mental fatigue. The improvement in quality of life was also more prominent among patients performing resistance exercise. Conclusions For NPC patients undergoing chemoradiotherapy, resistance exercise has a better efficacy in reducing complications, alleviating fatigue and improving quality of life.

Objective: We conducted a cohort study to investigate the association of three common SNPs of vascular endothelial growth factors (VEGF) gene (+1612G/A, -634C/G and +936G/C) with clinical outcome of osteosarcoma in a Chinese population. Methods: A prospective study was conducted. Genotyping analyses of VEGF -2578C/A, +1612G/A, -634C/G and +936G/C were conducted using polymerase chain reaction-restriction fragment length of polymorphism. Multivariate Cox proportional hazards models were used to calculate hazard ratio (HR) and 95% CI of effect of each genotype of VEGF+1612G/A, -634C/G and +936G/C on PFS and osteosarcoma of osteosarcoma. Results: The good response rate was 52.29%, and 116 (68.7%) died during the follow-up period. Patients carrying the +936 CC genotype and C allele showed a significantly more response to chemotherapy than those carrying the wild-type genotype. In the Cox proportional hazards model, patients carrying the VEGF -634 T allele was associated with a significantly decreased risk of PFS and Osteosarcoma (OS). Patients carrying the +936 CC genotype and C allele were associated with a significantly decreased risk of presenting progressive disease or death from osteosarcoma when compared with those carrying the wild-type genotype. However, we observed no significant association between the VEGF -2578C/A and +1612A/G polymorphisms and PFS and Osteosarcoma (OS) in gastric cancer patients. Conclusions: We found that VEGF -634G/C and +936T/C polymorphisms may affect the prognosis of osteosarcoma patients. These finding may be useful for predicting the clinical outcome of patients with Osteosarcoma (OS). Further studies are greatly needed to confirm the clinical significance of these results.

Background Hypoxia-mediated radioresistance is the main obstacle to the successful treatment of glioblastoma (GBM). Enhancing hypoxic radiosensitivity and alleviating tumor hypoxia are both effective means to improve therapeutic efficacy, and the combination of the two is highly desirable and meaningful. Results Herein, we construct a low-dose pleiotropic radiosensitive nanoformulation consisting of a high-Z atomic nanocrystal core and mesoporous silica shell, surface-modified with angiopep-2 (ANG) peptide and loaded with nitric oxide (NO) donor and hypoxia-activated prodrug (AQ4N). Benefiting from ANG-mediated transcytosis, this nanoformulation can efficiently cross the BBB and accumulate preferentially in the brain. Low-dose radiation triggers this nanoformulation to exert a three-pronged synergistic therapeutic effect through high-Z-atom-dependent dose deposition enhancement, NO-mediated hypoxia relief, and AQ4N-induced hypoxia-selective killing, thereby significantly inhibiting GBM in situ growth while prolonging survival and maintaining stable body weight in the glioma-bearing mice. Meanwhile, the proposed in vivo 9.4 T BOLD/DWI can realize real-time dynamic assessment of local oxygen supply and radiosensitivity to monitor the therapeutic response of GBM. Conclusions This work provides a promising alternative for hypoxia-specific GBM-targeted comprehensive therapy, noninvasive monitoring, and precise prognosis. Graphical Abstract