CPT1A and fatty acid β-oxidation are essential for tumor cell growth and survival in hormone receptor-positive breast cancer.

Chromosome 11q13-14 amplification is a defining feature of high-risk hormone receptor-positive (HR+) breast cancer; however, the mechanism(s) by which this amplicon contributes to breast tumorigenesis remains unclear. In the current study, proteogenomic analyses of >3000 breast tumors from the TCGA, METABRIC and CPTAC studies demonstrated that carnitine palmitoyltransferase 1A (), which is localized to this amplicon, is overexpressed at the mRNA and protein level in aggressive luminal tumors, strongly associated with indicators of tumor proliferation and a predictor of poor prognosis. genetic studies demonstrated that is required for and can promote luminal breast cancer proliferation, survival, as well as colony and mammosphere formation.

lncRNA BORG:TRIM28 Complexes Drive Metastatic Progression by Inducing α6 Integrin/CD49f Expression in Breast Cancer Stem Cells.

Triple-negative breast cancer (TNBC) is the most lethal subtype of breast cancer, with its aggressive phenotype being attributed to chemotherapy resistance, metastatic dissemination, and rapid disease recurrence. Breast cancer stem cells (BCSC) are significant contributors to tumor initiation, as well as to the acquisition of aggressive tumorigenic phenotypes, namely due to their ability to self-replicate and to produce heterogeneous differentiated tumor cells. To elucidate the underlying mechanisms that drive BCSC tumorigenicity in TNBC, we identified the long noncoding RNA (lncRNA) MP/ P- esponsive ene (BORG) as an enhancer of BCSC phenotypes.

The role of RNA processing and regulation in metastatic dormancy.

Tumor dormancy is a major contributor to the lethality of metastatic disease, especially for cancer patients who develop metastases years-to-decades after initial diagnosis. Indeed, tumor cells can disseminate during early disease stages and persist in new microenvironments at distal sites for months, years, or even decades before initiating metastatic outgrowth. This delay between primary tumor remission and metastatic relapse is known as "dormancy," during which disseminated tumor cells (DTCs) acquire quiescent states in response to intrinsic (i.

Epigenetic plasticity in metastatic dormancy: mechanisms and therapeutic implications.

The overwhelming majority of cancer-associated morbidity and mortality can be ascribed to metastasis. Metastatic disease frequently presents in a delayed fashion following initial diagnosis and treatment, requiring that disseminated cancer cells (DCCs) spread early in tumor progression and persist in a dormant state at metastatic sites. To accomplish this feat, DCCs exhibit substantial phenotypic plasticity that is mediated by the epigenetic regulation of dormancy programs in response to intrinsic (i.

The IncRNA BORG: A novel inducer of TNBC metastasis, chemoresistance, and disease recurrence.

Although greater than 90% of breast cancer-related mortality can be attributed to metastases, the molecular mechanisms underpinning the dissemination of primary breast tumor cells and their ability to establish malignant lesions in distant tissues remain incompletely understood. Genomic and transcriptomic analyses identified a class of transcripts called long noncoding RNA (lncRNA), which interact both directly and indirectly with key components of gene regulatory networks to alter cell proliferation, invasion, and metastasis. We identified a pro-metastatic lncRNA BORG whose aberrant expression promotes metastatic relapse by reactivating proliferative programs in dormant disseminated tumor cells (DTCs).

Smoking and Tobacco-Free Policies in Women's Residential Substance Use Disorder Treatment Facilities: A Community-Engaged Approach.

Introduction: The purpose of this study was to (1) describe the role of smoking in the lives of women in residential substance use disorder (SUD) treatment and (2) explore perceptions of the facilitators and barriers to tobacco-free policy among women in residential SUD treatment.

Methods: This was a community-engaged study using qualitative descriptive methods. We first recruited women in a residential SUD treatment facility to participate on a community research team.

The role of functional, social, and mobility dynamics in facilitating older African Americans participation in clinical research.

Purpose: Older African Americans experience disproportionately higher incidence of morbidity and mortality related to chronic and infectious diseases, yet are significantly underrepresented in clinical research compared to other racial and ethnic groups. This study aimed to understand the extent to which social support, transportation access, and physical impediments function as barriers or facilitators to clinical trial recruitment of older African Americans.

Methods: Participants (N=221) were recruited from six African American churches in Atlanta and surveyed on various influences on clinical trial participation.

Inoculation's efficacy with young adults' risky behaviors: can inoculation confer cross-protection over related but untreated issues?

This investigation examined the potential of inoculation to protect young adults' attitudes from pressures to engage in risky behaviors (unprotected sex and binge drinking) as well as inoculation's efficacy in conferring umbrella protection (cross-protection) over related, but experimentally untreated, attitudes. A three-phase experiment was conducted involving 120 participants. The results revealed that inoculation can protect the attitudes of young adults from counterattitudinal pressures to engage in unprotected sex (treated issue) and binge drinking (untreated issue).

ENaC proteins are required for NGF-induced neurite growth.

Neurite growth is required for nervous system development and repair. Multiple signals, including neurotrophic factors and intact mechanosensing mechanisms, interact to regulate neurite growth. Degenerin/epithelial Na(+) channel (DEG/ENaC) proteins have been identified as putative mechanosensors in sensory neurons.

A comparison of whole-genome shotgun-derived mouse chromosome 16 and the human genome.

The high degree of similarity between the mouse and human genomes is demonstrated through analysis of the sequence of mouse chromosome 16 (Mmu 16), which was obtained as part of a whole-genome shotgun assembly of the mouse genome. The mouse genome is about 10% smaller than the human genome, owing to a lower repetitive DNA content. Comparison of the structure and protein-coding potential of Mmu 16 with that of the homologous segments of the human genome identifies regions of conserved synteny with human chromosomes (Hsa) 3, 8, 12, 16, 21, and 22.