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Abstract Background Radiation resistance is a major obstacle to the prognosis of cervical cancer (CC) patients. Many studies have confirmed that long non-coding RNAs (lncRNAs) are involved in the regulation of radiosensitivity of cancers. However, whether small nucleolar RNA host gene 12 (SNHG12) regulates the radiosensitivity of CC remains unknown. Methods Quantitative real-time polymerase chain reaction was used to measure the expression levels of SNHG12 and microRNA-148a (miR-148a). The radiosensitivity of cells was evaluated by clonogenic assay. Flow cytometry and caspase-3 activity assay were performed to assess the apoptosis ability and cell cycle distribution of cells. Besides, dual-luciferase reporter and RNA immunoprecipitation assay were used to verify the interaction between miR-148a and SNHG12 or cyclin-dependent kinase 1 (CDK1). Also, the protein levels of CDK1, CCND1 and γ-H2AX were detected by western blot analysis. Furthermore, in vivo experiments were conducted to verify the effect of SNHG12 on CC tumor growth. Ki-67 and TUNEL staining were employed to evaluate the proliferation and apoptosis rates in vivo. The hematoxylin and eosin (HE) staining were employed to evaluate the tumor cell morphology. Results SNHG12 was upregulated in CC tissues and cells, and its knockdown improved the radiosensitivity by promoting the radiation-induced apoptosis and cell cycle arrest of CC cells. Also, miR-148a could be sponged by SNHG12 and could target CDK1. MiR-148a inhibitor or CDK1 overexpression could invert the promotion effect of silenced-SNHG12 on CC radiosensitivity. Meanwhile, SNHG12 interference reduced the tumor growth of CC, increased miR-148a expression, and inhibited CDK1 level in vivo. Conclusion LncRNA SNHG12 promoted CDK1 expression to regulate the sensitivity of CC cells to radiation through sponging miR-148a, indicating that SNHG12 could be used as a potential biomarker to treat the radiotherapy resistance of CC patients.

Increasing evidence revealed that circular RNAs (circRNAs) play important roles in tumor progression. In the present study, we explored the roles and underlying mechanisms of hsa_circ_0075341 in cervical cancer development. Our data showed that the expression of hsa_circ_0075341 was significantly upregulated and associated with larger tumor size, advanced FIGO stage, and lymph-node metastasis in cervical cancer patients. Hsa_circ_0075341 inhibition reduced cervical cancer cell proliferation and invasion in vitro. In mechanism, hsa_circ_0075341 negatively regulated miR-149-5p in cervical cancer progression. In addition, AURKA was confirmed as a direct target of miR-149-5p in cervical cancer and positively regulated by hsa_circ_0075341. Collectively, our data suggested that hsa_circ_0075341 promoted cervical cancer cell proliferation and invasion through regulating the miR-149-5p/AURKA axis, which provided a novel therapeutic target for cervical cancer treatment.

Long non-coding RNAs (lncRNAs) play important roles in tumor initiation and progression, including cervical cancer (CC). However, the effects and underlying mechanisms of STXBP5-AS1 in CC are still unknown. The expression of STXBP5-AS1, miR-96-5p, and PTEN in CC was explored by qRT-PCR. CCK-8 and transwell assays were used to determine the roles of STXBP5-AS1 on CC progression. Luciferase report assay and RIP assay were used to explore the correction between STXBP5-AS1, miR-96-5p and PTEN in CC. In our study, we showed that the expression of STXBP5-AS1 and PTEN was reduced while miR-96-5p expression was upregulated in CC. STXBP5-AS1 overexpression significantly reduced CC cells proliferation and invasion ability by suppressing miR-96-5p expression. MiR-96-5p promoted CC cells progression via regulating PTEN expression. Furthermore, STXBP5-AS1 was identified as a ceRNA to upregulate PTEN via sponging miR-96-5p in CC. Taken together, our findings revealed that STXBP5-AS1 might function as a ceRNA to drive CC cells proliferation and invasion via regulating miR-96-5p/PTEN axis.

For the estimation of weak echo with low signal-to-noise ratio (SNR), a multilag estimator is developed, which has better performance than the conventional method. The performance of the multilag estimator is examined by theoretical analysis, simulated radar data and some specific observed data collected by a C-band polarimetric radar in previous research. In this paper, the multilag estimator is implemented and verified for Nanjing University C-band polarimetric Doppler weather radar (NJU-CPOL) during the Observation, Prediction and Analysis of Severe Convection of China (OPACC) field campaign in 2014. The implementation results are also compared with theoretical analysis, including the estimation of signal power, spectrum width, differential reflectivity, and copolar correlation coefficient. The results show that the improvement of the multilag estimator is little for signal power and differential reflectivity, but significant for spectrum width and copolar correlation coefficient when spectrum width is less than 2 ms−1, which implies a large correlation time scale. However, there are obvious biases from the multilag estimator in the regions with large spectrum width. Based on the performance analysis, a hybrid method is thus introduced and examined through NJU-CPOL observations. All lags including lag 0 of autocorrelation function (ACF) are used for moment estimation in this algorithm according to the maximum usable lag number. A case study shows that this hybrid method can improve moment estimation compared to both conventional estimator and multilag estimator, especially for weak weather echoes. The improvement will be significant if SNR decreases or the biases of noise power in the conventional estimator increase. In addition, this hybrid method is easy to implement on both operational and non-operational radars. It is also expected that the proposed hybrid method will have a better performance if applied to S-band polarimetric radars which have twice the maximum useable lags in the same conditions with C-band radars.