Background. Circular RNAs (circRNAs) are frequently dysregulated in cancers and are implicated in tumorigenesis and tumor progression. In this study, we investigated the role of circZNF91 in regulating the malignant phenotype of chronic lymphocytic leukemia (CLL) cells and the underlying molecular mechanism. Material/Methods. The expression of circZNF91 was determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The binding sequences between circZNF91/miR-1283 and miR-1283/WEE1 were predicted by the bioinformatic database. The functional interactions were confirmed by the dual-luciferase reporter, RT-qPCR, and Western blot assays. The functional roles of the circZNF91/miR-1283/WEE1 axis in CLL progression were examined by cell proliferation, apoptosis, and EdU incorporation assays. Results. circZNF91 was upregulated in CLL samples. Silencing circZNF91 attenuated CLL cell proliferation and induced apoptosis and cell cycle arrest. circZNF91 could sponge miR-1283 to suppress its activity, which in turn upregulated WEE1 expression. Silencing circ-TTBK2 reduced WEE1 expression, while the inhibitor of miR-1283 enhanced WEE1 expression. The miR-1283/WEE1 axis mediated the effects of circZNF91 on cell proliferation and apoptosis, as well as induced cell cycle regulation. Conclusions. The circZNF91/miR-1283/WEE1 axis is engaged in the pathological phenotypes of CLL cells, which could serve as potential targets for future therapy development.
A meta‐analysis study to assess the effect of honey dressing (HD) in the management of diabetic foot ulcer (DFU). A comprehensive literature examination till January 2023 was implemented and 1794 linked studies were appraised. The picked studies contained 882 subjects with DFUs were in the picked studies' baseline, 424 of them were using HD, and 458 were using a control. Odds ratio (OR) in addition to 95% confidence intervals (CIs) were used to calculate the consequence of HD in the management of DFUs after DFU by the dichotomous and continuous styles and a fixed or random model. The HD applied to DFUs caused a significantly higher wound healing rate (OR, 2.06; 95% CI, 1.45‐2.93, P < .001) and lower wound healing time (MD, −10.42; 95% CI, −16.27‐ −4.58, P < .001) compared with the control. The HD applied to DFUs caused a significantly higher wound healing rate and lower wound healing time compared with the control. Although precautions should be taken when commerce with the consequences since most of the picked studies for this meta‐analysis was with low sample sizes.
BackgroundRadiation resistance poses a major clinical challenge in breast cancer (BC) treatment, but little is known about how long noncoding RNA (lncRNA) may regulate this phenomenon. We aimed to explore the role and possible mechanisms of lncRNA DUXAP8 in radiotherapy resistance of BC. Methods We used gain-of-function and loss-of-function assays to examine the impact of DUXAP8 on the radiosensitivity of BC cells. We performed RNA immunoprecipitation and chromatin immunoprecipitation assays to determine the potential mechanisms of DUXAP8. Results Here, we reported that DUXAP8 was highly expressed in radioresistant BC tissues, and high expression of DUXAP8 was associated with poor prognosis. We found that the overexpression of DUXAP8 promoted radioresistance, while inhibition of DUXAP8 expression increased radiosensitivity. Further studies revealed that DUXAP8 enhanced the radioresistance of BC cells by activating the PI3K/AKT pathway and by repressing the expression of E-cadherin and RHOB through interaction with EZH2. Moreover, DUXAP8 depletion significantly improved the radiosensitivity of BC in vivo. Conclusions Together, our work demonstrates for the first time, the ability of DUXAP8 to promote radiation resistance through modulating the PI3K/AKT pathway and the EZH2-E-cadherin/RHOB pathway.
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