Entangled cellular and molecular relationships at the sensory neuron-cancer interface.

Peripheral sensory neurons, once regarded merely as a passive route for nociceptive signals, are now acknowledged as active participants in solid tumor progression. This review explores how sensory neurons influence and are influenced by the tumor microenvironment (TME) through both chemical and electrical signaling, underscoring their pivotal role in the emerging field of cancer neuroscience. We summarize recent findings indicating that cancer-neuron interactions vary among different organs and experimental models, highlighting the ways in which various tumors recruit and reprogram sensory neurons to establish mutual communication loops that foster malignancy.

Personality-based intergenerational effects of prenatal THC exposure in an inherited mouse model of social dominance and submissiveness.

This study examines how stress-coping phenotypes influence the effect of prenatal [Formula: see text]-tetrahydrocannabinol (THC) exposure (PTE) on selectively bred Dominant (Dom) and Submissive (Sub) mice offspring exhibiting stress resilience and vulnerability, respectively. Pregnant Dom and Sub dams of generation 54 received THC (20 mg/kg, intraperitoneally) on gestation days 13, 15, and 17. Our findings indicate that PTE significantly reduced body weight (measured at postnatal day (PND) 7 and 30), increased anxiety-like behaviors in two-month-old Dom offspring, and enhanced sociability and reduced anxiety-like behaviors in Sub offspring.

Maternal oral sodium propionate supplementation restores gut integrity and mitigates stress-induced metabolic and behavioral outcomes in offspring.

Maternal attachment is a critical determinant of offspring's postnatal development, significantly influencing their later-life metabolic and behavioral patterns. We previously showed that stress-vulnerable, socially submissive (Sub) mice exhibit significant disruptions in gut physiology including distorted microbiome composition, lower colonic propionate levels, and increased gut permeability. These alterations exacerbated chronic inflammation, caused metabolic imbalances and reduced maternal care.

Colon impairments and inflammation driven by an altered gut microbiota leads to social behavior deficits rescued by hyaluronic acid and celecoxib.

Background: The exact mechanisms linking the gut microbiota and social behavior are still under investigation. We aimed to explore the role of the gut microbiota in shaping social behavior deficits using selectively bred mice possessing dominant (Dom) or submissive (Sub) behavior features. Sub mice exhibit asocial, depressive- and anxiety-like behaviors, as well as systemic inflammation, all of which are shaped by their impaired gut microbiota composition.

Nurture outpaces nature: fostering with an attentive mother alters social dominance in a mouse model of stress sensitivity.

Maternal care is critical for epigenetic programming during postnatal brain development. Stress is recognized as a critical factor that may affect maternal behavior, yet owing to high heterogeneity in stress response, its impact varies among individuals. We aimed here to understand the connection between inborn stress vulnerability, maternal care, and early epigenetic programming using mouse populations that exhibit opposite poles of the behavioral spectrum (social dominance [Dom] and submissiveness [Sub]) and differential response to stress.

Targeted Modulation of Interferon Response-Related Genes with IFN-Alpha/Lambda Inhibition.

Interferon (IFN) signaling resulting from external or internal inflammatory processes initiates the rapid release of cytokines and chemokines to target viral or bacterial invasion, as well as cancer and other diseases. Prolonged exposure to IFNs, or the overexpression of other cytokines, leads to immune exhaustion, enhancing inflammation and leading to the persistence of infection and promotion of disease. Hence, to control and stabilize an excessive immune response, approaches for the management of inflammation are required.

Robust expression of LINE-1 retrotransposon encoded proteins in oral squamous cell carcinoma.

Background: Oral Squamous Cell Carcinoma (OSCC) results from a series of genetic alteration in squamous cells. This particular type of cancer considers one of the most aggressive malignancies to control because of its frequent local invasions to the regional lymph node. Although several biomarkers have been reported, the key marker used to predict the behavior of the disease is largely unknown.

LINE-1 retrotransposon encoded ORF1p expression and promoter methylation in oral squamous cell carcinoma: a pilot study.

Oral squamous cell carcinoma (OSCC) is highly predominant in India due to excessive use of tobacco. Here we investigated Long INterpersed Element 1 (LINE or L1) retrotransposon activity in OSCC samples in the same population. There are almost 500,000 copies of L1 occupied around 30%  of the human genome.

Detection of the LINE-1 retrotransposon RNA-binding protein ORF1p in different anatomical regions of the human brain.

Background: Recent reports indicate that retrotransposons - a type of mobile DNA - can contribute to neuronal genetic diversity in mammals. Retrotransposons are genetic elements that mobilize via an RNA intermediate by a "copy-and-paste" mechanism termed retrotransposition. Long Interspersed Element-1 (LINE-1 or L1) is the only active autonomous retrotransposon in humans and its activity is responsible for ~ 30% of genomic mass.