Dietary influence on the link between depression and muscle mass and muscle strength: exploring interaction and mediation effects.

Introduction: The present study aimed to investigate the associations of depression with muscle mass and muscle strength, and whether these associations were modified or mediated by dietary energy intake and dietary quality.

Methods: Our study included participants aged 40 and above from the 2011-2018 cycles of the National Health and Nutrition Examination Survey (NHANES). Depression was evaluated using the nine-item Patient Health Questionnaire.

Higher dietary intake of live microbes is inversely associated with accelerated biological aging.

: It remains unclear whether dietary live microbe intake is associated with biological aging. Therefore, the present study aimed to investigate the associations between dietary live microbe intake and biological aging. : Our study included 7719 participants aged 20 years and older from the 2007-2010 cycles of the National Health and Nutrition Examination Survey (NHANES).

FOXF1 promotes ovarian cancer metastasis by facilitating HMGA2-mediated USP30-dependent S100A6 deubiquitination.

Ovarian cancer is the most common type of gynecological malignant tumor, with the highest mortality rate among female genital malignant tumors. In this study, we initially identified forkhead box F1 (FOXF1) as a potential prognostic biomarker of ovarian cancer through bioinformatics analysis. FOXF1 expression was higher in ovarian cancer tissue samples and served as an unfavorable prognostic factor.

IMPA2 promotes basal-like breast cancer aggressiveness by a MYC-mediated positive feedback loop.

Basal-like breast cancer (BLBC) is the most aggressive subtype with poor prognosis; however, the mechanisms underlying aggressiveness in BLBC remain poorly understood. In this study, we showed that in contrast to other subtypes, inositol monophosphatase 2 (IMPA2) was dramatically increased in BLBC. Mechanistically, IMPA2 expression was upregulated due to copy number amplification, hypomethylation of IMPA2 promoter and MYC-mediated transcriptional activation.

IL11 signaling mediates piR-2158 suppression of cell stemness and angiogenesis in breast cancer.

Emerging evidence has indicated the aberrant expression of PIWI-interacting RNAs (piRNAs) in human cancer cells to regulate tumor development and progression by governing cancer cell stemness. Herein, we identified downregulation of piR-2158 in human breast cancer tumors, especially in ALDH+ breast cancer stem cells (BCSCs) from patients and cell lines, which was further validated in two types of genetically engineered mouse models of breast cancer (MMTV-Wnt and MMTV-PyMT). Enforced overexpression of piR-2158 in basal-like or luminal subtypes of breast cancer cells suppressed cell proliferation, migration, epithelial-mesenchymal transition (EMT) and stemness .

HIST1H1B Promotes Basal-Like Breast Cancer Progression by Modulating CSF2 Expression.

Background: Basal-like breast cancer (BLBC) is associated with a poor clinical outcome; however, the mechanism of BLBC aggressiveness is still unclear. It has been shown that a linker histone functions as either a positive or negative regulator of gene expression in tumors. Here, we aimed to investigate the possible involvement and mechanism of HIST1H1B in BLBC progression.

RNF20 Is Critical for Snail-Mediated E-Cadherin Repression in Human Breast Cancer.

Background: E-cadherin, a hallmark of epithelial-mesenchymal transition (EMT), is often repressed due to Snail-mediated epigenetic modification; however, the exact mechanism remains unclear. There is an urgent need to understand the determinants of tumor aggressiveness and identify potential therapeutic targets in breast cancer.

Experimental Design: We studied the association of RNF20 with Snail and G9a by co-immunoprecipitation.

Nuclear translocation of PLSCR1 activates STAT1 signaling in basal-like breast cancer.

Basal-like breast cancer (BLBC) is associated with high grade, distant metastasis, and poor prognosis; however, the mechanism underlying aggressiveness of BLBC is still unclear. Emerging evidence has suggested that phospholipid scramblase 1 (PLSCR1) is involved in tumor progression. Here, we aimed to study the possible involvement and molecular mechanisms of PLSCR1 contributing to the aggressive behavior of BLBC.

Meta-analytic method reveal a significant association of theBDNF Val66Met variant with smoking persistence based on a large samples.

Although numerous genetic studies have reported the link between Val66Met in BDNF gene with smoking, the findings remain controversial, mainly due to small-to-moderate sample sizes. The main aim of current investigation is to explore whether the variant of Val66Met has any genetic functions in the progress of smoking persistence. The Val-based dominant genetic model considering Val/* (namely, Val/Val + Val/Met) and Met/Met as two genotypes with comparison of the frequency of each genotype in current smokers and never smokers.

Loss of ABAT-Mediated GABAergic System Promotes Basal-Like Breast Cancer Progression by Activating Ca-NFAT1 Axis.

Basal-like breast cancer (BLBC) is the most aggressive subtype with a poor clinical outcome; however, the molecular mechanisms underlying aggressiveness in BLBC remain poorly understood. The effects of gamma-aminobutyrate aminotransferase (ABAT) on GABA receptors, Ca-NFAT1 axis, and cancer cell behavior were assessed by Ca imaging, Western blotting, immunostaining, colony formation, and migration and invasion assays. We elucidated the relationship between ABAT and Snail by luciferase reporter and ChIP assays.

ME1 promotes basal-like breast cancer progression and associates with poor prognosis.

Basal-like breast cancer (BLBC) is associated with a poor clinical outcome due to the few treatment options and absence of effective targeted agents. Here, we show that malic enzyme 1 (ME1) is dramatically upregulated in BLBC due to ME1 copy number amplification. ME1 expression increases glucose uptake and lactate production, and reduces oxygen consumption, leading to aerobic glycolysis.

Inhibition of UGT8 suppresses basal-like breast cancer progression by attenuating sulfatide-αVβ5 axis.

Basal-like breast cancer (BLBC) is associated with a poor clinical outcome as a result of the few treatment options and poor therapeutic response. Here, we report that elevated expression of urine diphosphate-galactose ceramide galactosyltransferase (UGT8) specifically occurs in BLBC and predicts poor prognosis in breast cancer patients. UGT8 expression is transcriptionally up-regulated by Sox10, triggering the sulfatide biosynthetic pathway; increased sulfatide activates integrin αVβ5-mediated signaling that contributes to BLBC progression.

AKR1B1 promotes basal-like breast cancer progression by a positive feedback loop that activates the EMT program.

Basal-like breast cancer (BLBC) is associated with high-grade, distant metastasis and poor prognosis. Elucidating the determinants of aggressiveness in BLBC may facilitate the development of novel interventions for this challenging disease. In this study, we show that aldo-keto reductase 1 member B1 (AKR1B1) overexpression highly correlates with BLBC and predicts poor prognosis in breast cancer patients.