Biology subjects

Rubin, E.

Publications and source records attributed to Rubin, E..

16 recordsLinked to original sources

bioRxiv2026

Skin microbiome mirrors habitat divergence in amphibious combtooth blenny fish (Teleostei, Blenniidae)

Host-associated microbiomes play vital roles in organismal health, ecological interactions, and evolution, yet little is known about how microbial communities shift during the transition from aquatic to increasingly terrestrial habitats. Here, we characterize the skin microbiomes of three combtooth blenny species (Blenniella paula, Praealticus labrovittatus, and Alticus arnoldorum) that occupy distinct positions along the intertidal gradient in Guam--from fully subtidal (and exclusively aquatic) to intertidal (amphibious) and supratidal environments (exclusively terrestrial). Using 16S rRNA amplicon sequencing, we compared skin-associated bacterial communities with those in surrounding seawater and substrate biofilms to assess habitat influences on microbiome structure. Skin microbiomes were distinct from environmental microbial communities, indicating strong ecological filtering by the host. The divergence between skin and substrate microbiomes in the three species parallels their distribution along progressively higher zones of the intertidal gradient. The most divergent skin microbiome was that of the supratidal fish A. arnoldorum, characterized by higher Gammaproteobacteria abundance and enrichment of epiphytic and mucus-associated taxa. Across all species, we identified 32 microbial orders significantly enriched on the skin relative to environmental samples, including taxa commonly associated with fish mucosa (e.g., Vibrio, Alteromonas, Cetobacterium) and others rarely reported in aquatic marine fish (e.g., Rubritalea, Granulosicoccus). Several rare taxa with potential pathogenicity were also detected at low abundances. Together, these findings suggest that habitat-specific selective pressures strongly shape fish skin microbiomes along subtidal (aquatic) to supratidal (terrestrial) habitats and suggest that microbial symbionts may contribute to the ecological and physiological adaptations enabling amphibious lifestyles. This study provides the first comparative assessment of skin microbiome divergence across amphibious fish species along an intertidal gradient and offers a framework for predicting microbiome responses to environmental change.

evolutionary biology↗

bioRxiv2026

Comparative genomics reveals modular virulence repertoires and extensive horizontal gene transfer in Vibrio species associated with white syndrome of Porites cylindrica

Coral white syndrome (WS) is a widespread condition characterized by tissue loss and skeletal exposure, with multiple bacterial pathogens--particularly Vibrio species--implicated in its etiology. To investigate the genomic basis of potential virulence in Vibrio associated with WS of Porites cylindrica, we isolated 57 Vibrio strains from healthy and diseased coral tissues collected from reefs in Guam. Thirteen representative strains from five dominant species--V. coralliilyticus, V. owensii, V. tubiashii, V. harveyi, and V. tetraodonis--were selected for whole-genome sequencing using Oxford Nanopore Technology. Comparative genomic analyses revealed a conserved repertoire of extracellular enzymes, including hemolysins, cytolysins, metalloproteases, and subtilisin-like peptidases, alongside lineage-specific toxin and regulatory modules. Variation in secretion systems (T1SS-T6SS), particularly in T3SS, T4SS, and T6SS subtypes, reflected diversification of host-interaction and competitive capacities across species. Mobile genetic elements, including plasmids and prophages, contributed additional virulence-associated genes and secretion clusters, underscoring the role of horizontal gene transfer in shaping the accessory genome content. Notably, V. coralliilyticus harbored cholera toxin-related genes (ace and zot), while conjugative plasmid systems indicated potential for gene dissemination across lineages. Together, these findings demonstrate that virulence potential in coral-associated Vibrio is broadly distributed and structured by a conserved ecological core overlaid with flexible, horizontally acquired modules. This study provides the first comparative genomic framework for Vibrio associated with P. cylindrica, advancing our understanding of how genomic plasticity and modular virulence repertoires may contribute to opportunistic disease dynamics in coral reef ecosystems.

microbiology↗

bioRxiv2026

White syndrome dynamics in Porites cylindrica: interactions among eutrophication, host structure, and microbial communities

Coral white syndromes are among the most prevalent diseases affecting Indo-Pacific reefs, yet their etiology remains poorly understood, particularly in relation to eutrophication and microbial dynamics. Here, we investigated the drivers of Porites cylindrica white syndrome (PCYLWS) across two reef sites in Guam differing in nutrient enrichment and disease pressure. We combined 14 years of long-term disease monitoring with short-term lesion tracking, microbial community profiling of coral tissue and surrounding environments, and measurements of nutrient and environmental conditions. Long-term prevalence of PCYLWS was consistently higher at the oligotrophic site (Luminao) than at the eutrophic site (Tumon Bay), largely due to differences in host size structure and colony abundance. In contrast, lesions at Tumon Bay were larger and rapidly colonized by turf algae, whereas lesions at Luminao progressed faster but stabilized at smaller sizes. Microbial communities were strongly structured by sample type, with distinct assemblages in seawater, sediment, healthy tissue, and diseased tissue. Diseased tissues exhibited high spatial and temporal variability and signatures of microbial dysbiosis, characterized by reduced dominance of Parendozoicomonas and increased relative abundance of opportunistic taxa, including Ruegeria, Muricauda, and Vibrio. Environmental microbial communities and nutrient concentrations varied seasonally, particularly at the eutrophic site, suggesting transient environmental reservoirs of opportunistic bacteria. Together, these findings indicate that PCYLWS is shaped by context-dependent interactions among host population structure, environmental conditions, and dynamic microbial communities, supporting a multi-etiology framework for coral white syndromes. ImportanceCoral white syndromes are among the most common yet least mechanistically resolved coral diseases worldwide. By integrating 14 years of disease monitoring with lesion-scale dynamics, environmental microbiomes, and nutrient data, this study demonstrates that white syndrome expression in Porites cylindrica is shaped by context-dependent interactions among host population structure, eutrophication, and microbial dysbiosis rather than a single causative pathogen. These findings support a multi-etiology framework for coral disease and highlight the importance of environmental microbial reservoirs in modulating disease outcomes. This work provides a long-term, field-based perspective that is rarely available for coral disease systems and is broadly relevant to disease ecology in changing coastal environments.

microbiology↗

bioRxiv2025

TCUP: An Open Access Tool to Predict Tissue of Origin and Cancer of Unknown Primary (CUP)

IntroductionCancer of unknown primary (CUP) remains a major diagnostic hurdle, compromising therapies that depend on accurately identifying tissue of origin. We present TCUP, an ensemble learning framework that combines Contrastive Autoencoders (CAE) and Siamese Neural Networks (SNN) with base classifiers and a meta-learning layer to classify and interpret CUP, adding biological insight through Monte-Carlo ablations. MethodsGene-expression data from TCGA (tumour), GTEx (normal), and the Genome Sciences Centre (metastatic) were imputed, log-transformed, and SMOTE-balanced. A SNN and CAE learned pairwise and reconstruction embeddings. Multiple base classifiers (e.g., SVM, Random Forest) generated meta-features, which a meta-learner combined for final prediction. Monte-Carlo ablation iterations were performed to assess gene-level importance. ResultsTCUP achieved 98.3 % accuracy (F1 = 98.3) across all tissues. In metastatic BRCA, COAD, and PAAD it reached 86.7 % accuracy. Ablation highlighted 79 key contributors, including established tumour suppressors NKX6-1 and SOX30 and the less-studied SYTL1. PCA confirmed clearer separation in embedded space. ConclusionTCUP delivers high tissue-of-origin accuracy and CUP assignment while providing interpretable gene importance that clarifies tissue differences and metastatic drivers. By integrating advanced embeddings with systematic ablation TCUP supplies an accessible framework to advance CUP research and, ultimately, improve clinical outcomes. TCUP is freely available at https://fohs.bgu.ac.il/rubinlab/TCUP/

bioinformatics↗

bioRxiv2025

OptiRanker: an Advanced Tool for Simulation and Comparative Analysis of Drug Prioritization Algorithms in in-Vivo Trials

A critical challenge in personalized medicine is identifying the optimal drug treatment for individual patients based on their unique biological profiles. While recent advancements have led to a surge in drug prioritization algorithms utilizing patient omics data, including regression, classification, multiple kernel learning, deep learning, and AI-based methods, objective validation remains essential to discern their effectiveness. This study introduces" OptiRanker," an innovative statistical framework designed to simulate and optimize the in vivo validation of these drug prioritization algorithms by ranking their predictive accuracy across varied conditions. OptiRanker not only mimics algorithmic predictions but also integrates them into ranked datasets, enabling the optimal selection of test subjects and drugs for trial setups. By providing a rigorous evaluation subset for ranking and comparison of high- and low-performing algorithms, OptiRanker facilitates the design of cost-effective in vivo trials tailored to efficiently assess predictive capability. This addresses a key bottleneck in personalized medicine: achieving a robust, scalable validation of computational models that can accelerate the clinical translation of promising algorithms. The efficient ranking provided by OptiRanker has the potential to advance personalized treatment strategies, ultimately leading to more effective, individualized patient care. The Python code for OptiRanker is available at the following GitHub repository: https://github.com/OhadLandau/OptiRanker.

bioinformatics↗

bioRxiv2024

Two methodologies and timescales show no promotion of antibiotic resistance from in-water coral disease treatments

The decimation of reefs caused by stony coral tissue loss disease prompted the use of a topical amoxicillin treatment to prevent coral mortality. Application of this treatment led to concerns about unintentional impacts such as potential alteration of the coral microbiome and possible spread of antibiotic resistance. We used two different methodologies - microbial RNA sequencing and microbial qPCR array - to assess these concerns and to establish a baseline of antimicrobial resistance genes in coral microbes. RNA sequencing was conducted on coral mucus samples collected before and 24 hours after amoxicillin application on wild Montastraea cavernosa. While diverse antibiotic resistance genes (ARGs) were expressed, no differences were detected in ARG expression after amoxicillin treatment. Additionally, there were no notable changes in the microbial communities between the before and after samples. Microbial qPCR array was used to assess differences in ARGs over longer timescales in wild Colpophyllia natans, comparing never-treated corals with ones treated a single time seven months prior and with those treated multiple times seven months and more prior. No clinically relevant ARGs represented in the arrays were detected across any samples. A small number of above-detection reads (4 in the never-treated corals, 2 in the once-treated corals, and 0 in the multi-treated corals) may indicate weak amplification of similar environmental (non-anthropogenic) ARGs in the corals. Results indicate that the localized topical application of amoxicillin to prevent mortality of SCTLD-affected corals is neither immediately disrupting the microbiome of treated corals at the colony level nor driving the development of ARGs over immediate or longer-term time scales.

microbiology↗

bioRxiv2024

Transcription Factor HNF4A is Involved in Breast Cancer Recurrence

Recurrence is a major challenge for breast cancer (BC) management, yet its mechanism is poorly understood. Although computational analysis of expression compendia has proved useful for studying BC recurrence, some recently developed methods have not been used for this purpose. Here we present a bioinformatics reanalysis of a compendium containing 1519 cases with documentation of expression and information about recurrence with >5y follow-up. A compendium of expression profiles were divided into sub-cohorts by time to recurrence, and genes were ranked by the relative significance of expression differences. The top 1% of the genes (131 genes) were used in enrichment and induced network module analyses. The findings were validated in two independent cohorts, E-MTAB-365 and GSE20685. HNF4A was found to be the major hub in the genes whose expression differs most strikingly between short and long/no recurrence patients: it is highly connected to differentially expressed genes, and high expression of HNF4A is associated with longer recurrence-free survival in the compendium, even when it was split by ER status. These results were further validated in two independent cohorts of ER+ + endocrine + chemotherapy-treated patients and found to be concordant. Here we re-analyze a previously published compendium and find that HNF4A is pivotal to expression differences between early and late/non-recurring BC patients. HNF4A has been reported to be associated with cancer risk in several cancers and is speculated to be recurrence-associated in BC. However, we establish for the first time an association between BC time-to-recurrence and HNF4A expression. Further research is required to check if HNF4A expression is causative or just correlative to recurrence. Yet since linoleic acid is a ligand of HNF4A, our finding may explain why consumption of linoleic acid was proposed to affect recurrence risk in BC.

bioinformatics↗

bioRxiv2024

Antibiotics damage the colonic mucus barrier in a microbiota-independent manner

Antibiotic use is a risk factor for development of inflammatory bowel diseases (IBDs). IBDs are characterized by a damaged mucus layer, which does not properly separate the host intestinal epithelium from the microbiota. Here, we hypothesized that antibiotics might affect the integrity of the mucus barrier. By systematically determining the effects of different antibiotics on mucus layer penetrability we found that oral antibiotic treatment led to breakdown of the mucus barrier and penetration of bacteria into the mucus layer. Using fecal microbiota transplant, RNA sequencing followed by machine learning and ex vivo mucus secretion measurements, we determined that antibiotic treatment induces ER stress in the colonic tissue which inhibits colonic mucus secretion in a microbiota-independent manner. This mucus secretion flaw led to penetration of bacteria into the colonic mucus layer, translocation of microbial antigens into circulation and exacerbation of ulcerations in a mouse model of IBD. Thus, antibiotic use might predispose to development of intestinal inflammation by impeding mucus production.

immunology↗

bioRxiv2023

Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β

Acute gastrointestinal infection with intracellular pathogens like Salmonella Typhimurium triggers the inflammasome and the release of the proinflammatory cytokine interleukin 1{beta} (IL-1{beta}). However, the role of IL-1{beta} in intestinal defense against Salmonella remains unclear. Here, we show that IL-1{beta} production is detrimental during Salmonella infection. Mice lacking IL-1{beta} (IL-1{beta} -/-) failed to recruit neutrophils to the gut during infection, which reduced tissue damage and prevented depletion of short-chain fatty acid-producing commensals. Changes in epithelial cell metabolism that typically support pathogen expansion, such as switching energy production from fatty acid oxidation to fermentation, were absent in infected IL-1{beta}-/- mice which inhibited Salmonella expansion. Additionally, we found that IL-1{beta} induces expression of complement anaphylatoxins and suppresses the complement-inactivator Carboxypeptidase N (CPN1). Disrupting this process via IL-1{beta} loss completely prevented mortality in Salmonella-infected IL-1{beta}-/- mice and led to chronic infection. Thus, Salmonella exploits IL-1{beta} signaling to outcompete commensal microbes and establish gut colonization. Moreover, our findings identify the intersection of IL-1{beta} signaling and the complement system as key host factors involved in controlling mortality during invasive Salmonellosis.

immunology↗

bioRxiv2023

Binary classification machine-learning Unveils Sex-Dependent mutated gene Signatures in Melanoma

There are significant differences in the prevalence of cancer type, primary tumor body site, and mutation load between men and women, but the mechanisms underlying these sex-dependent differences is mostly unknown. Here we used binary classification machine-learning methodology to study sex-correlated somatic mutations signatures in cutaneous melanoma. We identified a number of genes that are more frequently mutated in females compared to males. Mutations in two genes, LAMA2 and TPTE, together with a set of specific genes that are not mutated, can predict sex of melanoma patients. Over representation analysis of genes clustered with LAMA2 revealed significant enrichment in androgen and estrogen biosynthesis and metabolism pathways, suggesting that mutation of LAMA2 might be involved in biased sex hormone synthesis in melanoma. Taken together, our analysis shows that gender can be predicted based on mutation status of genes in melanoma and that certain mutations are predictive of survival beyond sex differences. Our results will lead to better diagnosis and more effective personalized treatment of melanoma. SummaryIt was observed that between men and women there is a significant difference in the prevalence of cancer type, the primary tumor body site, and the number of mutations found in a given tumor type. However, the mechanisms behind these gender differences are mostly unknown. To investigate sex corelated somatic mutation signatures in cutaneous melanoma we used binary classification machine-learning methodology. We identified specific genes that are more frequently mutated in females compared to males, including LAMA2 and TPTE, which are predictive of gender. We also found a significant enrichment in androgen and estrogen biosynthesis and metabolism pathways clustered with LAMA2, suggesting that mutation of LAMA2 might be involved in biased sex hormone synthesis in melanoma. We showed that gender can be predicted based on mutation status of genes in melanoma and that certain mutations are predictive of survival. Our findings could lead to better diagnosis and more effective personalized treatment of melanoma.

bioinformatics↗

bioRxiv2022

Autophagy controls mucus secretion from intestinal goblet cells by alleviating ER stress

Colonic goblet cells are specialized epithelial cells that secrete mucus to form a barrier between the host and its microbiota, thus preventing bacterial invasion and inflammation. How goblet cells control the amount of mucus they secrete is unclear. We found that constitutive activation of autophagy in mice via Beclin 1 led to production of a thicker and less penetrable mucus layer by reducing endoplasmic reticulum (ER) stress. Accordingly, inhibiting Beclin 1-induced autophagy via Bcl-2 impaired mucus secretion. Furthermore, alleviating intestinal ER stress with a bile acid, or activating the unfolded protein response (UPR) pharmacologically via eIF2 phosphorylation, led to excessive mucus production. Over-production of mucus altered the gut microbiome, with expansion of mucus-utilizing bacteria, and protected from intestinal inflammation. Thus, ER stress is a cell-intrinsic switch that limits mucus secretion, while autophagy maintains proper mucus secretion and intestinal homeostasis by relieving ER stress.

immunology↗

bioRxiv2022

ATAC-Seq and RNA-Seq combined analysis elucidates the impact of BORIS/CTCFL on melanoma progression, mediated by chromatin accessibility and gene expression alterations

Melanoma is the deadliest form of skin cancer, due to its tendency to metastasize early. Brother of Regulator of Imprinted Sites (BORIS), also known as CCCTC binding factor-Like (CTCFL), is a transcription regulator that becomes ectopically expressed in melanoma. We recently showed that BORIS contributes to melanoma phenotype switching by altering the gene expression program of proliferative melanoma cells in favor of a more invasive phenotype. However, how BORIS alters the transcriptome remains unclear. Here, ATAC-seq was used to study BORIS-mediated chromatin accessibility alterations in proliferative melanoma cells. Genes that gained promoter accessibility following ectopic BORIS expression, were enriched for melanoma-specific invasive genes as well as invasion-associated biological processes, while promoters of genes associated with proliferation show reduce accessibility. Integration of ATAC-Seq and RNA-Seq data demonstrates that increased chromatin accessibility is associated with transcriptional upregulation of genes involved in tumor progression processes, and the aberrant activation of oncogenic transcription factors, while reduced chromatin accessibility and downregulated genes, were associated with repressed activity of tumor suppressors. Together, these findings indicate that BORIS mediates transcriptional reprogramming in melanoma cells by altering chromatin accessibility and gene expression, shifting the cellular transcription landscape of proliferative melanoma cells towards a pro-invasive genetic signature. SignificanceWe recently reported that BORIS contributes to melanoma phenotype switching by altering the transcriptional landscape of melanoma cells from a proliferative to an invasive state. In this study, using ATAC-Seq, we demonstrate that ectopic BORIS expression in proliferative melanoma cells leads to increased chromatin accessibility at promoters of upregulated invasion-associated genes. Importantly, by integrating the ATAC-Seq data with RNA-Seq data, we were able to identify key cancer-associated transcription factors that become aberrantly activated or repressed following ectopic BORIS expression. Taken together, this study sheds light on the mechanisms by which BORIS mediates phenotype switching in melanoma cells.

cancer biology↗

bioRxiv2021

Chemical-genetic interaction mapping links carbon metabolism and cell wall structure to tuberculosis drug efficacy

Current chemotherapy against Mycobacterium tuberculosis (Mtb), an important human pathogen, requires a multidrug regimen lasting several months. While efforts have been made to optimize therapy by exploiting drug-drug synergies, testing new drug combinations in relevant host environments remains arduous. In particular, host environments profoundly affect the bacterial metabolic state and drug efficacy, limiting the accuracy of predictions based on in vitro assays alone. In this study, we utilize conditional Mtb knockdown mutants of essential genes as an experimentally-tractable surrogate for drug treatment, and probe the relationship between Mtb carbon metabolism and chemical-genetic interactions (CGI). We examined the anti-tubercular drugs isoniazid, rifampicin and moxifloxacin, and found that CGI are differentially responsive to the metabolic state, defining both environment-independent and -dependent interactions. Specifically, growth on the in vivo-relevant carbon source, cholesterol, reduced rifampicin efficacy by altering mycobacterial cell surface lipid composition. We report that a variety of perturbations in cell wall synthesis pathways restore rifampicin efficacy during growth on cholesterol, and that both environment-independent and cholesterol-dependent in vitro CGI could be leveraged to enhance bacterial clearance in the mouse infection model. Our findings present an atlas of novel chemical-genetic-environmental interactions that can be used to optimize drug-drug interactions as well as provide a framework for understanding in vitro correlates of in vivo efficacy. SignificanceEfforts to improve tuberculosis therapy include optimizing multi-drug regimens to take advantage of drug-drug synergies. However, the complex host environment has a profound effect on bacterial metabolic state and drug activity, making predictions of optimal drug combinations difficult. In this study, we leverage a newly developed library of conditional knockdown Mycobacterium tuberculosis mutants in which genetic depletion of essential genes mimics the effect of drug therapy. This tractable system allowed us to assess the effect of growth condition on predicted drug-drug interactions. We found that these interactions can be differentially sensitive to the metabolic state and select in vitro-defined interactions can be leveraged to accelerate bacterial killing during infection. These findings suggest new strategies for optimizing tuberculosis therapy.

microbiology↗

bioRxiv2020

Whole exome precision oncology targeting synthetic lethal vulnerabilities across the tumor transcriptome

Precision oncology has made significant advances in the last few years, mainly by targeting actionable mutations in cancer driver genes. However, the proportion of patients whose tumors can be targeted therapeutically remains limited. Recent studies have begun to explore the benefit of analyzing tumor transcriptomics data to guide patient treatment, raising the need for new approaches for systematically accomplishing that. Here we show that computationally derived genetic interactions can successfully predict patient response. Assembling a broad repertoire of 32 datasets spanning more than 1,500 patients and including both tumor transcriptomics and response data, we predicted the response in 17 out of 21 targeted and 8 out of 11 checkpoint therapy datasets across 8 different cancer types with considerable accuracy, without ever training on these datasets. Analyzing the recently published multi-arm WINTHER trial, we show that the fraction of patients benefitting from transcriptomic-based treatments could potentially be markedly increased from 15% to about 85% by targeting synthetic lethal vulnerabilities in their tumors. In summary, this is the first computational approach to obtain considerable predictive performance across many different targeted and immunotherapy datasets, providing a promising new way for guiding cancer treatment based on the tumor transcriptomics of cancer patients.

cancer biology↗

bioRxiv2019

Gray whale transcriptome reveals longevity adaptations associated with DNA repair, autophagy and ubiquitination

One important question in aging research is how differences in genomics and transcriptomics determine the maximum lifespan in various species. Despite recent progress, much is still unclear on the topic, partly due to the lack of samples in non-model organisms and due to challenges in direct comparisons of transcriptomes from different species. The novel ranking-based method that we employ here is used to analyze gene expression in the gray whale and compare its de novo assembled transcriptome with that of other long- and short-lived mammals. Gray whales are among the top 1% longest-lived mammals. Despite the extreme environment, or maybe due to a remarkable adaptation to its habitat (intermittent hypoxia, Arctic water, and high pressure), gray whales reach at least the age of 77 years. In this work, we show that long-lived mammals share common gene expression patterns between themselves, including high expression of DNA maintenance and repair, ubiquitination, apoptosis, and immune responses. Additionally, the level of expression for gray whale orthologs of pro- and anti-longevity genes found in model organisms is in support of their alleged role and direction in lifespan determination. Remarkably, among highly expressed pro-longevity genes many are stress-related, reflecting an adaptation to extreme environmental conditions. The conducted analysis suggests that the gray whale potentially possesses high resistance to cancer and stress, at least in part ensuring its longevity. This new transcriptome assembly also provides important resources to support the efforts of maintaining the endangered population of gray whales.

evolutionary biology↗

bioRxiv2019

BORIS/CTCFL promotes a switch from a proliferative towards an invasive phenotype in melanoma cell lines

Melanoma is among the most aggressive cancers due to its tendency to metastasize early. Phenotype switching between a proliferative and an invasive state has been suggested as a critical process for metastasis. The mechanisms that regulate these transitions are poorly understood, but are associated with transcriptional changes. Brother of Regulator of Imprinted Sites (BORIS), also known as CCCTC binding factor-Like (CTCFL), is a transcriptional modulator that becomes aberrantly expressed in melanoma. Here, we provide the first evidence that BORIS is involved in phenotype switching in melanoma. Genetic modification of BORIS expression in melanoma cells combined with whole transcriptome analysis indicated that BORIS expression contributes to an invasion-associated transcriptome. In agreement with this finding, inducible BORIS overexpression in melanoma cells reduced proliferation and increased migration and invasion, demonstrating that the transcriptional switch is accompanied by a phenotypic switch. Overall, our study indicates a pro-invasive role for BORIS in melanoma via transcriptional reprogramming.

cancer biology↗