Trajectories of Early Adolescent Loneliness: Implications for Physical Health and Sleep

The current study examines the relationship between prolonged loneliness, physical health, and sleep among young adolescents (10–13 years; N = 1214; 53% girls). Loneliness was measured at 10, 12 and 13 years of age along with parent-reported health and sleep outcomes. Using growth mixture modelling, 6 distinct trajectories were identified: ‘low increasing to high loneliness’ (n = 23, 2%), ‘high reducing loneliness’ (n = 28, 3%), ‘medium stable loneliness’ (n = 60, 5%), ‘medium reducing loneliness’ (n = 185, 15%), ‘low increasing to medium loneliness’ (n = 165, 14%), and ‘low stable loneliness’ (n = 743, 61%). Further analyses found non-significant differences between the loneliness trajectories and parent-report health and sleep outcomes including visits to health professionals, perceived general health, and sleep quality. The current study offers an important contribution to the literature on loneliness and health. Results show that the relationship may not be evident in early adolescence when parent reports of children’s health are used. The current study highlights the importance of informant choice when reporting health. The implications of the findings for future empirical work are discussed

Estrogen mediated-activation of miR-191/425 cluster modulates tumorigenicity of breast cancer cells depending on estrogen receptor status.

MicroRNAs (miRNAs), single-stranded non-coding RNAs, influence myriad biological processes that can contribute to cancer. Although tumor-suppressive and oncogenic functions have been characterized for some miRNAs, the majority of microRNAs have not been investigated for their ability to promote and modulate tumorigenesis. Here, we established that the miR-191/425 cluster is transcriptionally dependent on the host gene, DALRD3, and that the hormone 17β-estradiol (estrogen or E2) controls expression of both miR-191/425 and DALRD3. MiR-191/425 locus characterization revealed that the recruitment of estrogen receptor α (ERα) to the regulatory region of the miR-191/425-DALRD3 unit resulted in the accumulation of miR-191 and miR-425 and subsequent decrease in DALRD3 expression levels. We demonstrated that miR-191 protects ERα positive breast cancer cells from hormone starvation-induced apoptosis through the suppression of tumor-suppressor EGR1. Furthermore, enforced expression of the miR-191/425 cluster in aggressive breast cancer cells altered global gene expression profiles and enabled us to identify important tumor promoting genes, including SATB1, CCND2, and FSCN1, as targets of miR-191 and miR-425. Finally, in vitro and in vivo experiments demonstrated that miR-191 and miR-425 reduced proliferation, impaired tumorigenesis and metastasis, and increased expression of epithelial markers in aggressive breast cancer cells. Our data provide compelling evidence for the transcriptional regulation of the miR-191/425 cluster and for its context-specific biological determinants in breast cancers. Importantly, we demonstrated that the miR-191/425 cluster, by reducing the expression of an extensive network of genes, has a fundamental impact on cancer initiation and progression of breast cancer cells