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At least 37 records · Page 2Linked to original sources
PubMed2026

Harnessing Endogenous Plasticity Rather than Reprogramming of Mature Cells Will Advance Regenerative Medicine, Cancer Treatment and Rejuvenation.

The successful culture of human embryonic stem (hES) cells from inner cell mass cells of blastocyst stage 'spare' embryos in 1998, followed by induced pluripotent stem (iPS) cells in 2006, which allowed somatic cells to be reprogrammed to pluripotency using the Yamanaka factors, transformed regenerative biology and inspired extensive global efforts towards developing pluripotent stem cell-based applications. However, hES and iPS cells, as well as organoids generated from them, largely retain fetal-like characteristics, which limits their relevance for clinical translation. Concurrently, the prevailing assumption published in leading journals that adult tissues lack endogenous stem cells has led to the belief that mature cells dedifferentiate and reprogram during in vivo regeneration upon chronic injury, and that the appearance of embryonic/fetal markers in diabetes, heart failure, cancer, and many other chronic disease states reflects dedifferentiation of mature cells. We suggest that the prevailing concepts of dedifferentiation and reprogramming, both in vitro and in vivo, require careful re-evaluation. Adult somatic cells possibly do not truly dedifferentiate, neither in vitro nor in vivo. Instead, tissue-resident, pluripotent, very small embryonic-like stem cells (VSELs) in multiple organs account for the observed biology. In vitro "reprogramming" responses to Yamanaka factors likely reflect selective activation and expansion of VSELs/early progenitors rather than the dedifferentiation/ reprogramming of mature adult somatic cells. Likewise, the embryonic/fetal-like signatures reported in multiple disease states including cancer reflect expansion of immature tissue-specific progenitors that arise from VSELs but fail to differentiate normally due to a damaged microenvironment in vivo. Therapeutic strategies involving transplantation of MSCs, MUSE cells, or their secreted exosomes improve disease outcomes, possibly by restoring the damaged niche that supports functional tissue repair by VSELs. Although direct evidence to support this is lacking at present, recognising the central role of VSELs/progenitors and their niche in maintaining tissue homeostasis in vivo could resolve existing roadblocks and guide more effective endogenous regenerative therapies for diseased tissues and age-related dysfunctions.

Humans↗
PubMed1992

[Two cases of renal cell carcinoma accompanied with ossification].

We report two cases of renal cell carcinoma accompanied with ossification. Case 1: A 40-year-old male visited a physician with the complaint of epigastric pain. Examination of the stomach revealed compression of the greater curvature. Abdominal radiography and CT scan revealed a left renal mass with calcification, which was a hypovascular tumor on angiography. A transperitoneal left nephrectomy was performed. The resected kidney was 700g in weight and the tumor, which was 12 x 10 x 10 cm in size and located in the upper pole of the kidney, was enveloped with a hard capsule and was extensively necrotized. Histopathological diagnosis was renal cell carcinoma (papillary type, mixed subtype). Case 2: A 69-year-old female was occasionally pointed out to have a left renal mass in ultrasonic examination. It was accompanied with calcification in CT scan and a hypervascular tumor in angiography. A transperitoneal left nephrectomy was performed. The resected kidney was 320 g in weight and the tumor located in the lower pole of the kidney, was 6 x 6 x 6 cm in size and necrotized. Histopathological diagnosis was renal cell carcinoma (alveolar type, clear cell subtype). Microscopically in both cases, ossified tissue existed among the fibrous tissue in the necrotized lesion of the tumor, but not near the cancer cells and, it was accompanied by calcification. During the ossification process, the connective tissue proliferates after the necrosis of the tumor, and metaplasia occurred from its juvenile plastic cells to osteoblastic cells.

Adult↗
PubMed2026

Decoding context-dependent sirtuin pharmacology in cancer: Metabolic-epigenetic switches and precision therapeutic targeting.

Sirtuins (SIRT1-SIRT7) are a family of NAD+-dependent lysine deacetylases that possess mono-ADP-ribosyltransferase activity and integrate cellular metabolic status with chromatin regulation, genome maintenance, redox homeostasis, immune responses, and adaptation to cancer therapies. Their translational value has been obscured by a recurring paradox: the same isoform may constrain malignant transformation in one setting yet support metastatic competence, stemness, immune evasion, or drug resistance in another. This review reframes that paradox as a measurable problem of context. We define a SIRT context code in which NAD+ availability and compartmentalization, subcellular localization, PTM state, chromatin occupancy, oncogenic genotype, cell lineage, and tumor microenvironment jointly determine sirtuin output. Using recent mechanistic and translational evidence, we summarize how sirtuins regulate metabolic switching, histone acetylation and lactylation, genome stability, cancer-associated fibroblast programs, regulatory T-cell enrichment, cancer stem-cell plasticity, angiogenesis, and resistance to DNA-damaging, targeted, and immune therapies. We further argue that successful sirtuin pharmacology will require context matching rather than indiscriminate activation or inhibition. Priorities include spatial and single-cell biomarker discovery, compartment-specific NAD+ measurements, PTM-resolved activity assays, structure-guided isoform-selective agents, and degrader strategies targeting non-catalytic scaffolding functions. Sirtuins should therefore be viewed as metabolic-epigenetic decision nodes rather than fixed oncogenes or tumor suppressors. However, the evidence remains predominantly preclinical, and our search identified no clinical-stage oncology trials of direct sirtuin modulators using prospective biomarker stratification, underscoring that this framework remains translationally aspirational rather than clinically validated.

Humans↗
PubMed2025

Tumors hijack macrophages for iron supply to promote bone metastasis and anemia.

Bone marrow is both a primary site for hematopoiesis and a fertile niche for metastasis. The mechanism of the common occurrence of anemia among patients with bone metastasis remains poorly understood. Here, we show that a specialized population of VCAM1+CD163+CCR3+ macrophages, normally essential for erythropoiesis by transporting iron to erythroblasts, are highly enriched in the bone metastatic niche in mouse models. Tumor cells hijack these macrophages for iron supply, reducing iron availability for erythroblasts, impairing erythropoiesis, and contributing to anemia. Increased iron supply enables tumor cells to produce hemoglobin in response to hypoxia, mimicking erythroblasts. We identify macrophages with similar iron-transporting features in human bone metastases and show that elevated HBB expression correlates with increased risk of bone metastasis. These findings establish iron-transporting macrophages as an essential component of the metastatic bone niche, revealing a critical interplay between immune cells, metal metabolism, and tumor cell plasticity in driving metastasis and anemia.

Animals↗
PubMed1975

Intracytoplasmic filaments in pulmonary lymphatic endothelial cells. Fine structure and reaction after heavy meromyosin incubation.

The cytochemistry and ultrastructure of intracytoplasmic filaments of pulmonary lymphatic endothelial cells of neonatal rabbits were studied by comparison with myofilaments of the peribronchial and pulmonary vascular smooth muscle cells. Two types of endothelial filaments were observed: thin filaments (diameter: 50 A) which lie close to the abluminal cell membrane; and thick filaments (diameter: 90 A) which are dispersed throughout the cell cytoplasm. Following heavy meromyosin (HMM) treatment, characteristic arrowhead complexes formed in the thin lymphatic endothelial filaments as well as in the actin filaments of the smooth muscle cells. There was no detectable reaction of HMM with the thick filaments. After incubation with EDTA, the thin filaments were labile, and the thick filaments became the major filamentous component in the endothelial cells. In smooth muscle cells, the actin myofilaments were also labile while the 100 A filaments were stable. These observations support the hypothesis that the actin-like thin endothelial lymphatic filaments form part of a contractile system, while the thick filaments constitute a plastic cell skeleton. The significance of the contractile system in lymphatic endothelial cells might lie in a mechanism for the active regulation of the endothelial intercellular junction and gaps and hence the permeability of the lymphatic endothelial cell lining.

Actins↗
PubMed1992

Cytochalasin inhibits light-dependent synaptic plasticity of horizontal cells in teleost retina.

Previous studies have shown that the horizontal cell-->cone photoreceptor negative feedback synapse in teleost fish retinae is 'plastic', being suppressed in the dark and potentiated by light adaptation. The possible involvement of filamentous actin in ultrastructural and electrophysiological aspects of this plasticity has been investigated using cytochalasins, which inhibit actin turnover, in the cyprinid fish (roach) retinae. Cytochalasin B or D (40 microM) inhibited both the light-dependent formation and maintenance of spinules, and enhancement of the feedback interaction involved in generation of biphasic spectral responses in horizontal cells. The results suggest that actin turnover is essential for both ultrastructural and electrophysiological plasticity of horizontal cell feedback and that spinules could mediate this dynamic interaction.

Animals↗
PubMed1978

Neoplasms produced from C3H/10T 1/2 cells attached to plastic plates; saturation density, anchorage dependence and serum requirement of in vitro lines correlated with growth aggressiveness in vivo.

The C3H/10T 1/2 embryo cell line, which is nontumorigenic when inoculated subcutaneously in saline suspension, produces tumors when implanted subcutaneously attached to 1 X 5 X 10 mm plastic plates. Under these in vivo conditions there is direct selection for "spontaneous" transformants that have undergone the specific cellular alterations required for neoplastic behavior. This is in contrast to the conventional situation where transformants are obtained in vitro and are only secondarily tested in vivo for neoplastic behavior. Early passages of cell lines from four different C3H/10T 1/2 tumors explanted back in culture were quantitatively examined for tumorigenicity and for alteration in the properties of density inhibition, anchorage dependence, serum requirement, and plasminogen activator production. A fairly consistent quantitative relationship was found between the degree of growth aggressiveness in vivo and the degree of expression of these phenotypic markers of the transformed state in vitro during early passages of the cell lines after tumor explantation.

Animals↗
PubMed1992

Inhibition of cell adhesion to plastic substratum by phosphorothioate oligonucleotide.

Antisense oligonucleotides have been widely used to achieve specific inhibition of targeted gene expression. However, the mechanism of action is not well understood and in many systems sequence-independent effects occur. We have recently shown that chronic administration of an antisense c-myc phosphorothioate oligonucleotide can specifically inhibit expression of the c-myc protein and growth in human breast cancer cells. We now identify an additional effect of the same oligonucleotide on cell adhesion. Transient delivery through electroporation of 2.5 microM antisense-myc oligonucleotide to MCF-7 cells results in 85% inhibition of adhesion to plastic substratum within 24 h. Both the onset of this effect and the subsequent recovery occur without a change in cell viability, growth, or alteration of adhesion to Matrigel, collagen IV, laminin, or fibronectin. However, no parallel changes in c-myc mRNA or protein expression are detectable, suggesting that in this instance inhibition of adhesion caused by antisense-myc oligonucleotide may involve a mechanism independent of the target sequence.

Base Sequence↗
PubMed1992

[The functional plasticity of the cells of the paraventricular nucleus in surviving slices of the hypothalamus].

In surviving cuts of the hypothalamus, stimulation of the supraoptic nucleus induced focal potentials in the paraventricular nucleus. A repeated stimulation was followed by a reduction of the descending of the focal potentials. Tetanization of the supraoptic nucleus induced an additional wave at the descending phase of focal potentials preserving for 15 min. The data obtained suggest a functional plasticity of the hypothalamus paraventricular nucleus' cells.

Action Potentials↗
PubMed2026

Engineering CRISPR nanoplatforms to deplete cancer stem cells: Delivery checkpoints, target plasticity, and clinical viability.

Cancer stem cells (CSCs) sustain tumor initiation, therapy resistance, and relapse, yet evade durable control because they switch phenotype, enter quiescence, shelter within protective niches, resist drug efflux, and share markers with normal stem cells. Programmable CRISPR editing can disable intracellular self-renewal dependencies that antibodies and small molecules cannot reach, whereas only nanoscale carriers can confine such editing to intended cells; neither component alone solves the CSC problem. This review reframes CSC-directed CRISPR nanomedicine as an integrated design problem. We examine why target plasticity defeats static single-marker targeting; the sequential delivery checkpoints spanning blood stability, organ selection, tumor penetration, CSC recognition, endosomal escape, and productive editing; and advanced architectures including organ-selective lipid nanoparticles, biomimetic and vesicle carriers, metal-organic frameworks, and logic-gated systems. Genotoxicity, immunogenicity, incomplete depletion, manufacturing reproducibility, and absent CSC-specific clinical evidence remain limiting. Clinical viability, not imminent cure, is the realistic near-term objective.

Neoplastic Stem Cells↗
PubMed2025

Sustained NF-κB activation allows mutant alveolar stem cells to co-opt a regeneration program for tumor initiation.

Disruptions to regulatory signals governing stem cell fate open the pathway to tumorigenesis. To determine how these programs become destabilized, we fate-map thousands of murine wild-type and KrasG12D-mutant alveolar type II (AT2) stem cells in vivo and find evidence for two independent AT2 subpopulations marked by distinct tumorigenic capacities. By combining clonal analyses with single-cell transcriptomics, we unveil striking parallels between lung regeneration and tumorigenesis that implicate Il1r1 as a common activator of AT2 reprogramming. We show that tumor evolution proceeds through the acquisition of lineage infidelity and reversible transitions between mutant states, which, in turn, modulate wild-type AT2 dynamics. Finally, we discover how sustained nuclear factor κB (NF-κB) activation sets tumorigenesis apart from regeneration, allowing mutant cells to subvert differentiation in favor of tumor growth.

Animals↗
PubMed1977

Procedure for the embedment and ultrastructural visualization of cells cultured on plastic microtest plates.

The polystyrene Microtest plate has served as an excellent means of quantitation in the interaction of immunological, chemotherapeutic and radiobiological treatments with cultured cells. In order to assess the accompanying ultrastructural changes it was necessary to develop a technique which allowed cells grown in the wells of the plates to be embedded for electron microscopy. Conventional epoxy resin embedding techniques require the use of propylene oxide as a clearing agent. Unfortunately propylene oxide is a solvent of the polystyrene plates. By the substitution of absolute ethanol for propylene oxide, toluidine blue staining during the procedure and other preparative techniques it was feasible to prepare reacted cells grown in Microtest plates for electron microscopy.

Cells, Cultured↗
PubMed1977

Altered morphology and increased cell adhesiveness of chinese hamster ovary cells cultured on fibrin.

Chinese hamster ovary cells cultivated on fibrin exhibited different characteristic from cells growing on plastic. While sparsely plated cells on plastic dishes had an epithelioid morphology, cells on fibrin assumed a round shape and then converted to a stretched form with protruded processes that increased with cell density. Within a few days, cells fibrinolysed adjacent fibrin and returned to the morphology seen in plastic dishes. When fibrinolysis was inhibited by epsilon-aminocaproic acid (EACA), cells continued to grow on the fibrin for a longer period and showed dense, criss-crossed fibroblast-type congestion. Whereas, cells on plastic maintained pavement-like epitheloid appearance when they grew to a confluent monolayer. The other altered characteristics on fibrin was increased accumulation of cells in multilayers. Normally as Chinese hamster cells on plastic proliferate, many cells float into the medium instead of piling up after they form a monolayer. On the other hand, cells on fibrin, being maintained by the addition of EACA, remained adherent, piling up multilayers instead of floating into the medium. A possible explanation of these findings is that the surface properties of the stretched cells on fibrin are altered to make them more adhesive. A possible link of these characteristics of the cells on fibrin to tumor cell behavior in vivo is dicussed.

Aminocaproates↗
PubMed1978

Assay method for Vibrio cholerae and Escherichia coli enterotoxins by automated counting of floating chinese hamster ovary cells in culture medium.

As Chinese hamster ovary (CHO) cells on plastic proliferate, many cells float off into the medium instead of piling up after they form a monolayer. Fewer cells were floating in the medium when CHO cells were incubated with cholera toxin at a concentration as low as 10 pg/ml. The toxin increased the adhesiveness of the cells forming confluent monolayers so that the floating cells accumulated on the adherent monolayers. On the basis of this finding, a simple, quantitative assay method for cholera and Escherichia coli enterotoxins was devised by cultivating CHO cells in a Linbro multidish and counting the cells in the medium with a Coulter Counter. The method was sensitive enough to detect toxins in 100- to 200-fold-diluted culture media of toxigenic E. coli strains. Little or no activity was detected by this method in the culture medium of nontoxigenic E. coli.

Animals↗