Digital interventions empowering mental health reconstruction among students after the COVID-19 pandemic.

With the gradual end of the coronavirus disease 2019 (COVID-19) pandemic, the reconstruction of students' mental health is urgently necessary. Digital interventions offer advantages such as high accessibility, anonymity, and accurate identification, which can promote the reconstruction of students' mental health through the provision of psychological support platforms, psychological assessment tools, and online mental health activities. However, we recognize that digital interventions must undergo many adjustments, and corresponding ethical norms require further clarification. It is crucial for different stakeholders to collaborate and work toward maximizing the effectiveness of digital interventions for the reconstruction of mental health after the COVID-19 pandemic.

Shikonin reduces tamoxifen resistance through long non-coding RNA uc.57.

Tamoxifen resistance is a serious problem in the endocrine therapy of breast cancer. Long non-coding RNAs play important roles in tumor development. In this study, we revealed the involvement of lncRNA uc.57 and its downstream gene BCL11A in TAM resistance. Tamoxifen-resistant MCF-7R cells showed lower expression of uc.57 and higher expression of BCL11A mRNA and protein than the parental MCF-7 cells. Moreover, levels of uc.57 mRNA were lower and BCL11A mRNA were higher in breast cancer tissues than in precancerous breast tissues. Shikonin treatment reduced tamoxifen resistance in MCF-7R cells both in vitro and in vivo, targeting uc.57/BCL11A. Fluorescence in situ hybridization and RNA immunoprecipitation analyses showed that uc.57 binds to BCL11A. Uc.57 overexpression downregulated BCL11A and reduced tamoxifen resistance in MCF-7R cells both in vitro and in vivo. BCL11A knockdown also reduced tamoxifen resistance by inhibiting PI3K/AKT and MAPK signaling pathways. It thus appears shikonin reduces tamoxifen resistance of MCF-7R breast cancer cells by inducing uc.57, which downregulates BCL11A to inhibit PI3K/AKT and MAPK signaling pathways.

uc.38 induces breast cancer cell apoptosis via PBX1.

Long non-coding RNAs (lncRNAs) are transcripts longer than 200 bp with no protein-coding capacity. Transcribed ultraconserved regions (T-UCRs) are a type of lncRNA and are conserved among human, chick, dog, mouse and rat genomes. These sequences are involved in cancer biology and tumourigenesis. Nevertheless, the clinical significance and biological mechanism of T-UCRs in breast cancer remain largely unknown. The expression of uc.38, a T-UCR, was down-regulated in both breast cancer tissues and breast cancer cell lines. However, uc.38 was expressed at significantly lower levels in larger tumours and tumours of more advanced stages. Based on the results of in vitro and in vivo experiments, up-regulation of uc.38 expression inhibited cell proliferation and induced cell apoptosis. Thus, uc.38 suppressed breast cancer. Additional experiments revealed that uc.38 negatively regulated the expression of the pre-B-cell leukaemia homeobox 1 (PBX1) protein and subsequently affected the expression of Bcl-2 family members, ultimately inducing breast cancer cell apoptosis. Describing the uc.38/PBX1 axis has improved our understanding of the molecular mechanisms involved in breast cancer apoptosis and has suggested that this axis is a potential therapeutic target for breast cancer.