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PubMedDate not supplied

Tumor-stroma interactions: their role in the control of tumor cell invasion.

The development and progression of tumors result from the concerted activity not only of tumor cells with neighboring cells e.g., fibroblasts and inflammatory cells. Host-tumor interactions are considered critical in tumor invasion and metastasis. In vitro studies as well as established in vivo models have analysed the reciprocal effects of tumor-host interactions for the tumor invasion process. These studies have shown that modifications in the extracellular matrix composition surrounding the tumors as well as alterations in the expression of tumor cell receptors or in the expression of growth factors/cytokines and proteases, are critical regulators of a developing tumor. We shortly review the most important and well characterized mechanisms involved in the progression of tumor cells through tissues, especially those participating in cellular communication, cell adhesion, and proteolysis.

Animals↗
PubMed1996

Cell adhesion receptors and gap junctions in normal and neoplastic transformed thyrocytes.

In the thyroid cell adhesion receptors and gap junctions establish a complex modular network defining the structural properties of cells, their interactions with neighboring cells and the extracellular matrix. Neoplastic alterations of this network can lead to an imbalance of cell to cell communication and allows transformed cells to escape from the tissue to generate metastases. The present manuscript summarizes general and thyroid-specific aspects of the molecular basis of cell-cell contacts, an expanding field of tumor biology.

Animals↗
PubMed1998

Atrial natriuretic factor reduces cell coupling in the failing heart, an effect mediated by cyclic GMP.

The influence of the atrial natriuretic factor (ANF) on heart-cell communication was investigated in cell pairs isolated from the ventricle of cardiomyopathic hamsters (BIO TO-2; 11 months old), and the results were compared with controls (F1B) of same age. The results indicated that ANF (10(-8) M) added to the bath caused a decline in junctional conductance (gj) of 48 +/- 2% (n = 15) within 90 s. The effect of ANF was suppressed by HS-142-1, a specific antagonist of guanylyl cyclase ANF receptor. Moreover, the decline in gj elicited by ANF was related to the synthesis of cyclic guanosine monophosphate (cGMP). Indeed, dibutyryl-cGMP (10(-4) M) decreased gj by 80 +/- 3.5% (n = 15) within 90 s, and zaprinast, a selective inhibitor of cGMP phosphodiesterase, enhanced the effect of ANF on gj. The possible relationship between ischemia, ANF release, and impairment of cell coupling is discussed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2001

Gastrointestinal development in the Drosophila embryo requires the activity of innexin gap junction channel proteins.

Cell to cell communication plays an essential role during pattern formation and morphogenesis of the diverse tissues and organs of the body. In invertebrates, such as the fruitfly Drosophila, the direct communication of closely apposed cells is mediated by gap junctions which are composed of oligomers of the innexin family of transmembrane channel proteins. Few data exist about the developmental role of the eight innexin genes which have been found in the Drosophila genome. We have investigated the role of the innexin 2 and ogre genes during gastrointestinal development of the fly embryo. Our findings suggest that innexins are involved in the formation of the proventriculus, an organ that develops at the foregut/midgut boundary by migration of primordial cells and subsequent infolding of epithelial tissue layers.

Animals↗
PubMed1990

[Effects of tumor promoters and related compounds on electric relations between giant cells of the salivary glands of Chironomus tentans larvae].

The action of 15 chemicals, being tumor-promoters and/or inhibitors of cell-to-cell communications in vitro upon electric relations between giant cells of salivary gland of the Chironomus tentans larvae are studied. It is shown that out of 11 compounds disturbing the intercellular contacts in this model, 10 chemicals are tumour-promoters (Aroclor 1254, butylated hydroxytoluene, di(ethylhexyl)phthalate, DDT, deoxycholic acid, lithocholic acid, oleic acid, anthralin, iodine-acetate, tween-80) and 1 compound (oleoyl-acetyl-glycerol) is not studied for the promoting activity. At the same time, two other tumor-promoters (phenobarbital and TPA) as well as two nontumor-promoters (phorbol and chlorpromazine) do not influence the electric relations. The possibilities of using the developed test-system for the screening of the tumour-promoters are discussed.

Animals↗
PubMed2026

Identification of Drug-resistant Cell Subpopulations in Colorectal Cancer Through Single-cell Analysis and Exploration of Potential Therapeutic Strategies.

INTRODUCTION: The therapeutic efficacy of Colorectal Cancer (CRC) is often compromised by resistance to the standard chemotherapy agent oxaliplatin. METHODS: This study obtained single-cell RNA sequencing (scRNA-seq) data from the Gene Expression Omnibus (GEO) database. Differentially Expressed Genes (DEGs) between resistant and sensitive epithelial subpopulations were identified, followed by enrichment analysis. Pseudotemporal trajectory and cell-cell communication were analyzed using Monocle2 and CellChat, respectively. The candidate drug was predicted by Connectivity Map (cMAP) analysis. External validation included assessment of the EpC2 signature in an oxaliplatin-resistant cell line dataset (GSE76092), survival analysis using The Cancer Genome Atlas (TCGA) cohorts, and re-analysis of the GSE179784 dataset to assess the reproducibility of EpC2-like subpopulations and their DNA Damage Repair (DDR) scores. RESULTS: Cell subpopulations were divided into 10 clusters. Among them, epithelial cells comprised 5 subpopulations, with EPC2 identified as a potential oxaliplatin-resistant subset. DEGs were enriched in the TNF and IL-17 pathways. External validation confirmed the enrichment of EpC2 in resistant cell lines and its association with poor survival. Pseudotemporal trajectory revealed that epithelial cells underwent state transitions, forming two distinct branches. The resistant group exhibited enrichment in RNA splicing and NF-κB pathways. Cell-cell communication analysis revealed interactions involving MDK- NCL and PPIA-BSG. Dasatinib was predicted as a candidate drug. DISCUSSION: We identified an oxaliplatin-resistant subpopulation of Epithelial Cells (EpC2) in CRC, elucidated its multi-layered resistance mechanisms, and integrated multi- omics and cMAP database analyses to predict a potential intervention drug. CONCLUSION: This study provided potential therapeutic possibilities for oxaliplatin resistance, contributing to CRC treatment.

Humans↗
PubMed2026

MetaCCI: meta cell-cell interaction inference and its application to CCIs characteristics of MDS.

MOTIVATION: Cell-cell interactions (CCIs) are fundamental to multicellular organisms and play crucial roles in diverse biological processes and disease mechanisms. Understanding CCIs is vital for deciphering disease pathogenesis and developing therapeutic strategies. Although numerous computational methods have been developed to infer CCIs from complex biological data, most existing approaches rely primarily on single-gene expression levels and ligand-receptor databases, often failing to capture the nuanced network-wide changes characteristic of disease states. RESULT: We propose MetaCCI, a novel computational strategy that integrates meta-information into CCI inference by extending the traditional gene expression-based analysis to a gene regulatory network framework. MetaCCI meticulously combines established ligand-receptor pairs with quantitative insights into gene behavior within complex gene networks, enabling the precise extraction of relevant targets for CCI inference. Subsequently, CCI inference was performed using an eigen cell co-expression network, providing a more holistic view of cell-cell communication. Monte Carlo simulations demonstrated that MetaCCI consistently outperforms existing methods in CCI inference. We applied MetaCCI to characterize cell-cell communication in Myelodysplastic Syndromes (MDS). Our results identified distinct interaction patterns in MDS compared with normal cell populations, specifically highlighting the loss of CCIs between "Dendritic cells and Hematopoietic precursor cells" and between "Dendritic cells and Hematopoietic multipotent progenitor cells" as characteristic features of MDS. Furthermore, FABP5, CD63, and HMGB1 were identified as MDS-specific markers. These findings suggest that diminished CCIs involving dendritic cells, hematopoietic precursor cells, and multipotent progenitor cells are pivotal to MDS pathogenesis. AVAILABILITY AND IMPLEMENTATION: The MetaCCI software is freely available at https://github.com/HeewonGitHub/MetaCCI. An archived version of the software and example datasets used in this study is available at Zenodo: https://doi.org/10.5281/zenodo.20101527.

Myelodysplastic Syndromes↗
PubMed2000

CD40-independent pathways of T cell help for priming of CD8(+) cytotoxic T lymphocytes.

In many cases, induction of CD8(+) CTL responses requires CD4(+) T cell help. Recently, it has been shown that a dominant pathway of CD4(+) help is via antigen-presenting cell (APC) activation through engagement of CD40 by CD40 ligand on CD4(+) T cells. To further study this three cell interaction, we established an in vitro system using dendritic cells (DCs) as APCs and influenza hemagglutinin (HA) class I and II peptide-specific T cell antigen receptor transgenic T cells as cytotoxic T lymphocyte precursors and CD4(+) T helper cells, respectively. We found that CD4(+) T cells can provide potent help for DCs to activate CD8(+) T cells when antigen is provided in the form of either cell lysate, recombinant protein, or synthetic peptides. Surprisingly, this help is completely independent of CD40. Moreover, CD40-independent CD4(+) help can be documented in vivo. Finally, we show that CD40-independent T cell help is delivered through both sensitization of DCs and direct CD4(+)-CD8(+) T cell communication via lymphokines. Therefore, we conclude that CD4(+) help comprises at least three components: CD40-dependent DC sensitization, CD40-independent DC sensitization, and direct lymphokine-dependent CD4(+)-CD8(+) T cell communication.

Animals↗
PubMed2002

[Phylogeny and evolution of hormone systems].

Classically hormones are defined as molecules that are secreted by endocrine glandular or neurosecretory cells into the blood stream and transported to their target tissue where they induce physiological processes at very low concentrations. Studies on the potential origin and the evolution of cell-to-cell communication systems suggest that exocrine pheromones (food signals and toxins) might have been the primitive bioregulatory molecules of unicellular organisms for chemical communication with each other and with the biosphere. The broad distribution and the structural diversity of pheromones suggests that these molecules and their receptors were predecessor modules of cell communication systems in metazoa. Neurosecretory cells, as we find them in Cnidarians, possibly served as basic modules for the evolution of neurohormonal systems of higher animals. Studies on genetic model organisms, such as Drosophila or the mouse, have demonstrated that chemical communication between neighbouring or more distant cells does not just involve endocrine and neurosecretory cells, but also unexpectedly tissues and organs such as the heart or the adipose tissue (e. g. the leptin signalling pathway). Comparative endocrinology could show that molecular components of hormonal systems represent signalling networks that are generally used during cellular communication processes and the differentiation of cell types during ontogenesis. Some of their functions are evolutionarily conserved, others not, as disscussion on steroid hormones and the prolactin signalling pathway will demonstrate.

Animals↗
PubMed2002

Na+/H+ exchange in primary, secondary and n-butyrate-treated cultures of ruminal epithelial cells: short communication.

Rate of amiloride-sensitive Na+ uptake into cultured rumen epithelial cells was studied in order to clarify the influence of culture conditions on Na+/H+ exchange (NHE). Cell cultures were exposed to Na-n-butyrate or not for seven days or subcultured. On the 14th day of culturing, primary cell cultures without butyrate exposure showed both non-stratified and stratified growth. Na-n-butyrate treated 14-day-old cultures and 3-day-old subcultures contained mostly non-stratified, i.e. non-keratinised cells. Both n-butyrate treatment and subculturing increased total and amiloride-sensitive Na+ uptake. Our results indicate that Na+ uptake via NHE is determined by the amount and the ratio of non-stratified (non-keratinised) cells.

Amiloride↗
PubMed1993

[Intercellular communication within the anterior pituitary].

Paracrine and autocrine interactions within the anterior pituitary have been studied in the last few years. The adaptation of novel methodology to the study of the physiology of the anterior pituitary has yielded convincing evidence for cell-cell communication. Another reason for expanded interest in this field is the discovery of a growing member of substances that likely play a role in cell-cell communication. The various types of secretory cells within the anterior pituitary, gonadotroph, thyrotroph, somatotroph, lactotroph and corticotroph, have been addressed as sources, and then targets of intercellular factors. We need have more a collection of observations than a system of delineated pathways. Moreover, care must be exercised in interpretations of these observations.

Activins↗
PubMed2001

Cellular communication and coupling within the suprachiasmatic nucleus.

In mammals, the part of the nervous system responsible for most circadian behavior can be localized to a pair of structures in the hypothalamus known as the suprachiasmatic nucleus (SCN). Importantly, when SCN neurons are removed from the organism and maintained in a brain slice preparation, they continue to generate 24h rhythms in electrical activity, secretion, and gene expression. Previous studies suggest that the basic mechanism responsible for the generation of these rhythms is intrinsic to individual cells in the SCN. If we assume that individual cells in the SCN are competent circadian oscillators, it is obviously important to understand how these cells communicate and remain synchronized with each other. Cell-to-cell communication is clearly necessary for conveying inputs to and outputs from the SCN and may be involved in ensuring the high precision of the observed rhythm. In addition, there is a growing body of evidence that a number of systems-level phenomena could be dependent on the cellular communication between circadian pacemaker neurons. It is not yet known how this cellular synchronization occurs, but it is likely that more than one of the already proposed mechanisms is utilized. The purpose of this review is to summarize briefly the possible mechanisms by which the oscillatory cells in the SCN communicate with each other.

Animals↗
PubMed2002

Regulation of antimicrobial peptide production by autoinducer-mediated quorum sensing in lactic acid bacteria.

Several lactic acid bacteria produce peptides with antimicrobial activity. During the last few years, cell-cell communication has emerged as the key regulatory mechanism that controls the production of many of these antimicrobial peptides via a regulatory strategy denominated quorum sensing. Quorum sensing allows populationwide synchronised production of antimicrobial peptides as a function of cell density. The cell-cell communication phenomenon required for sensing of the cell density is mediated by secreted signalling molecules. These 'molecular messengers' accumulate in the environment as the cell density increases and activate signal transduction cascades that result in the production of antimicrobial peptides by the stimulated bacterial cell.

Bacterial Proteins↗
PubMed2003

Vascular morphogenesis: tales of two syndromes.

Advances in our understanding of fundamental biological processes can be made by the analysis of defects manifested in inherited diseases. The genes responsible for these genetic syndromes often encode proteins that act at critical points of the pathways that control biological processes such as cell proliferation, cell-cell communication, cellular differentiation, and cell death. This approach has lead to the discovery of novel gene products and/or biochemical pathways involved in disease, genes that in turn play a fundamental role in normal biological processes. This forward genetic approach, focusing on Mendelian disorders of vascular anomalies, has been particularly fruitful for the study of genetic regulation of angiogenesis. This review summarizes the ongoing saga of two genetic syndromes involving disruption of normal vascular morphogenesis. Each inherited disorder involves the focal development of a distinct vascular anomaly. In hereditary hemorrhagic telangiectasia (HHT), the hallmark vascular lesion is termed an arteriovenous malformation, which involves the direct communication of an artery with a vein (arteriovenous shunt), without an intervening capillary bed. For cerebral cavernous malformations (CCM), the lesions are grossly-dilated, closely-packed, capillary-like sinusoidal chambers. The autosomal dominant mode of inheritance of each of these distinct syndromes suggested that the underlying genes might regulate critical aspects of vascular morphogenesis. Emerging but intriguing tales are being told by the genes (and their protein products) mutated in these disorders.

Activin Receptors, Type I↗
PubMed2003

Gap junctional intercellular communication in cells isolated from urethane-induced tumors in A/J mice.

Studies using normal or neoplastically transformed established mouse lung epithelial cell lines revealed a reduction in gap junctional, intercellular communication (GJIC) with transformation. To determine the stage in tumor development at which GJIC is interrupted, we used the well-established model of lung tumors induced in strain A/J mice by urethane. In this system, tumor development follows a well-characterized pattern; hyperplasias, adenomas, and carcinomas are manifested at approximately 8, 16, and 40 weeks after urethane treatment, respectively. GJIC levels were examined using a novel technique where cells are grown on a glass slide, half of which is coated with electrically conductive, optically transparent, indium-tin oxide. An electric pulse that opens transient pores on the plasma membrane is applied in the presence of the fluorescent dye, Lucifer yellow, causing dye penetration into cells growing on the conductive part of the slide. Migration of the dye through gap junctions to nonelectroporated cells growing on the nonconductive area is then microscopically observed under fluorescence illumination. Unexpectedly, primary cells cultured from urethane-induced tumors, even late stage carcinomas, possessed extensive GJIC immediately upon isolation. Upon passage for several months however, these cells lost GJIC. These results suggest that the molecular changes that lead to the formation of the tumor in vivo are not sufficient to interrupt gap junctions. Propagation of tumor cells in culture induces additional alterations that can lead to gap junction closure.

Animals↗
PubMed1990

Intracellular regulation of ion channels in cell membranes.

Cells communicate with their environment through receptor proteins on the cell membrane. Some ion channels are receptors, whereas others are linked to receptors through guanine nucleotide-binding proteins (G proteins). Ion channels control intracellular concentrations of ions such as calcium, and these concentrations control cell functions such as secretion and cell division. This review summarizes the current state of knowledge about the control of ion channels.

Cell Communication↗
PubMed1983

The electrical coupling of epithelium and fibers in the frog lens.

Electrical coupling has been measured between central epithelial cells and fiber cells in the frog lens following the removal of the lens capsule with collagenase. Current passed from a microelectrode inserted in a lens fiber cell was found to induce a potential difference in epithelial cells which was indistinguishable from that measured in nearby fiber cells. The measurements were made under circumstances where the current and voltage microelectrodes could be shown to be in different cells and an intraepithelial location of the voltage-measuring microelectrode could be verified. The electrical coupling appears to be direct from superficial fiber cells to epithelial cells, rather than indirect through equatorial epithelial cells. The epithelial cells and surface fiber cells each had resting potentials of -61.8 +/- 2.1 mV in this collagenase-treated preparation. Scanning electron microscopy (SEM) of mechanically decapsulated frog lenses showed specialized junction-like plaques on the expanded anterior ends of fiber cells which made contact with epithelial cells. Such specialized plaques were not found on the expanded posterior ends of these fibers where they contracted the posterior capsule. The studies provide direct evidence for cell-to-cell communication between frog lens epithelial cells and fibers.

Animals↗
PubMed1976

Sodium pump: its importance to intercellular communication in heart fibres.

The effect of ouabain on the electrical coupling of canine Purkinje cells was investigated. It was found that the glycoside decreases cell communication through an increase in junctional resistance, what supports the view that the sodium pump has an important role on the control of cell communication.

Animals↗