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Ovarian cancer (OC) is a fatal cancer in women, mainly due to its aggressive nature and poor survival rate. The lncRNA-miRNA-mRNA (long noncoding RNA-microRNAmessenger RNA) interaction is promising biomarkers for the improving prognosis of OC.Therefore, we explored the regulatory mechanism of WDFY3-AS2/miR-18a/RORA axis involved in the biological activities of OC cells. Microarray analysis predicted differentially expressed lncRNA, miRNA, and mRNA related to OC, followed by investigating the relationship among them. The expression patterns of the identified lncRNA WDFY3-AS2, miR-18a, and RORA were measured in OC tissue and cells. Gainand loss-of-function experiments were performed to characterize the effect of lncRNA WDFY3-AS2 on OC cells, as well as the involvement of miR-18a and RAR related orphan receptor A (RORA). The in vitro assays were validated by in vivo experiments. According to bioinformatics analysis, WDFY3-AS2 was speculated to affect OC by sponging miR-18a and modulating RORA. WDFY3-AS2 and RORA were underexpressed in OC, while miR-18a was highly expressed. Notably, WDFY3-AS2 acts as a competing endogenous RNA to sponge miR-18a and upregulate RORA. Upon overexpressing WDFY3-AS2 or inhibiting miR-18a, RORA expression was increased, thereby the OC cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) were suppressed, accompanied by enhanced apoptosis. In vivo experiments confirmed that the tumor growth was reduced in response to overexpressed WDFY3-AS2 or inhibited miR-18a.Taken together, the lncRNA WDFY3-AS2/miR-18a axis regulates the tumor progression of OC by targeting RORA, providing new insights for prevention and control of OC. K E Y W O R D Sepithelial-mesenchymal transition, invasion, lncRNA WDFY3-AS2, microRNA-18a, migration, ovarian cancer, proliferation, RORA

(2019) MicroRNA-23a depletion promotes apoptosis of ovarian cancer stem cell and inhibits cell migration by targeting DLG2,

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Background Smoking cessation is recommended as a key intervention for chronic obstructive pulmonary disease (COPD) smokers. However, in China, few COPD smokers quit successfully. The aim of this study was to explore in depth the barriers and facilitators for smoking cessation among smokers with COPD in China. Methods A purposive sample of 32 hospitalized smokers with COPD were included, 17 ex-smokers and 15 current smokers, participated in the semi-structured interviews. Interviews were analyzed thematically and using a deductive approach guided by Capability, Opportunity, Motivation-Behavior (COM-B) framework. Results Three inter-related themes were generated: smokers’ motivation was a prerequisite for quitting, maintaining capability to quit smoking, and opportunities that facilitated smokers to quit. Motivation to quit for most participants was activated by COPD-related symptoms, although they had a limited knowledge of COPD. Physical benefits from quitting and strong willpower were facilitators for maintaining quitting, while exposure to smoking environment and strong addiction to nicotine were frequent reasons for relapse. Most ex-smokers quit smoking by their own willpower rather than professionally delivered smoking cessation interventions. Smokers’ attitudes toward these interventions depended on their effectiveness and convenience. Very few participants had experienced pharmacotherapy or behavioral support from physicians. However, interviewees preferred auricular acupressure to pharmacotherapy. Conclusion Motivation to quit among smokers with COPD was usually initiated by COPD-related symptoms. Physical benefits observed by quitting and strong willpower facilitated smoking cessation, while exposure to smoking environment and strong addiction to nicotine led to relapse. COPD smokers in China preferred auricular acupressure to pharmacotherapy.

Highlights The study first reports the regulation of LINC01215 on methylation of RUNX3 promoter. LINC01215 is highly expressed while RUNX3 is reciprocal in EOC. LINC01215 overexpression promotes methylation of RUNX3 and reduces its expression. LINC01215 silencing suppresses LNM and EMT of EOC. This study may provide a new therapeutic target for EOC.

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