Accumulating evidence suggests that circular RNAs (circRNAs) may be a key contributor to oncogenesis. Yet, the function of circRNAs in laryngeal squamous cell carcinoma (LSCC) is still not clear. In this study, we examined the function of circRNA_103862 in LSCC progression by analyzing the tissue specimens collected from a patient with LSCC by using different LSCC cell models in vitro and an LSCC xenograft model in nude mice. We found that circRNA_103862 was frequently upregulated in the tissues of LSCC and was correlated with metastasis and prognosis of LSCC patients. Furthermore, circRNA_103862 downregulation could reduce proliferation, migration, and invasion ability of LSCC cells. In terms of mechanism exploration, miR-493-5p was sponged by circRNA_103862. Rescue experiments also showed that circRNA_103862 could achieve a carcinogenic effect by regulating miR-493-5p. Moreover, a luciferase reporter analysis showed that Golgi membrane protein 1 (GOLM1) is a downstream effector of miR-493-5p. In conclusion, our data suggested that circRNA_103862 promotes the proliferation of LSCC through targeting the miR-493-5p/GOLM1 axis, and it might serve as a potential prognosis marker and therapy target for LSCC.
Laryngeal cancer, more than 95% of which are squamous cell carcinomas (SCC), is the second most common malignant neoplasm in head and neck. Its incidence has remarkably increased over the recent years due to the high smoking rates, industrialization and ageing. 1,2 Despite considerable progress in surgical techniques, as well as chemotherapy and radiotherapy, the prognosis of advanced laryngeal cancer remains poor. [3][4][5] Also, the exact molecular mechanisms underlying the carcinogenesis or progression of LSCC remain poorly
Long non-coding RNAs (lncRNAs) play important roles in various biological progresses of carcinogenesis. However, the function of lncRNAs in human sinonasal squamous cell carcinoma (SNSCC) remains greatly unclear. In the current study, lncRNA AC091729.7 expression was examined in SNSCC samples by using microarray, RNA in situ hybridization (ISH) and real-time fluorescence quantitative PCR (qRT-PCR). Cell viability, colony-formation, wound-healing, and transwell assays were applied to SNSCC cells. Xenograft mouse models were employed to evaluate the role of AC091729.7 in growth of SNSCC in vivo. Human protein microarray (Huprot TM Protoarray) and RNA immunoprecipitation (RIP) were used for identifying AC091729.7 binding proteins in SNSCC. Results showed AC091729.7 was upregulated and closely connected with the survival of the SNSCC patients. Knockdown of AC091729.7 suppressed SNSCC cell migration, proliferation, invasion in vitro. Furthermore, downregulation of AC091729.7 could inhibit the growth of SNSCC in vivo. Moreover, Human protein microarray and RIP suggested that AC091729.7 directly combine with the serine/arginine rich splicing factor 2 (SRSF2). Our results suggest that in the cell progression of SNSCC, lncRNA AC091729.7 plays a carcinogenic role and serves as a novel biomarker and latent curative target in SNSCC patients.
Background
BrainWear is a phase II observational clinical trial which collects data on patient activity levels, fatigue, Quality of Life (QoL) and imaging in patients with brain tumours
Methods
Newly diagnosed patients were offered wrist worn accelerometers (Axivity AX3) to be worn continuously throughout their treatment (surgery, chemoradiotherapy or radiotherapy) to monitor physical activity. We collected standardised measures of QoL, fatigue, MRI imaging data and disease progression. Here, we report early results on activity data 5 days before and after treatment.
Results
Of 23 patients recruited, we report complete pre and post treatment data in 4 patients (2 HGG, 2 metastatic) who underwent craniotomy (2), fractionated radiotherapy (1) and SRS (1). Both craniotomy patients experienced an immediate 60 – 70% reduction in activity, and were successfully discharged at day 2 post-op even though their activity was still significantly reduced. Both patients recovered another 10% in their activity levels following discharge. Radiotherapy patients experienced no early change within 5 days of starting treatment.
Conclusion
As expected craniotomy results in much larger changes in activity levels than SRS and radical radiotherapy. Activity levels recover post craniotomy, but this takes > 5 days.
Using wearable activity monitors in brain tumour patients is feasible, although there are multiple practical problems. Interpreting such data will require consideration of inpatient vs. outpatient settings.
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