scholarly journals INTERCELLULAR COMMUNICATION AND TISSUE GROWTH

1968 ◽  
Vol 38 (3) ◽  
pp. 556-561 ◽  
Author(s):  
A. Jamakosmanović ◽  
W. R. Loewenstein
Keyword(s):  
Intercellular Communication ◽  
Tissue Growth ◽  
Membrane Potentials ◽  
Normal Cells ◽  
Thyroid Cancers ◽  
Normal Thyroid

Intercellular communication was examined in normal and cancerous isolated thyroids with an intracellular electrical technique. The cells of normal thyroid (rat, mouse, hamster, man) communicate, within any given follicle, through permeable junctions. The cells of a wide variety of thyroid cancers (rat, hamster) do not communicate to any detectable degree and have resting membrane potentials lower than those of normal cells.

scholarly journals INTERCELLULAR COMMUNICATION AND TISSUE GROWTH

1967 ◽  
Vol 33 (2) ◽  
pp. 235-242 ◽  
Author(s):  
Werner R. Loewenstein ◽  
Richard D. Penn
Keyword(s):  
Intercellular Communication ◽  
Wound Closure ◽  
Cell Movement ◽  
Normal Growth ◽  
Tissue Growth ◽  
Cellular Communication ◽  
Mechanical Contact ◽  
Cell Systems ◽  
Intact State ◽  
Striking Contrast

Intercellular communication was examined in regenerating rat liver and urodele skin, two tissues of fast but normal growth. In both, cellular communication is in general as good as in their respective normal intact state. This stands in striking contrast to the lack of cellular communication in tissues with cancerous growth. Upon wounding of the urodele skin, the normally permeable junctional membranes of cells near the wound border seal themselves off, thereby insulating the interiors of the communicated cell systems from the exterior. When the cells of two opposing borders make mechanical contact in the course of wound closure, communication between them ensues within 30 min. Within this period all cell movement also ceases ("contact inhibition"). The possible implications of these findings in the control of tissue growth are discussed.

scholarly journals The Emerging Role of Extracellular Vesicles in the Glioma Microenvironment: Biogenesis and Clinical Relevance

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1964
Author(s):  
Anjali Balakrishnan ◽  
Sabrina Roy ◽  
Taylor Fleming ◽  
Hon S. Leong ◽  
Carol Schuurmans
Keyword(s):  
Tumor Progression ◽  
Extracellular Vesicles ◽  
Intercellular Communication ◽  
Cell Types ◽  
Disease Diagnosis ◽  
Neural Cells ◽  
Cell Of Origin ◽  
Cell Type Specificity ◽  
Normal Cells ◽  
Mediate Cell

Gliomas are a diverse group of brain tumors comprised of malignant cells (‘tumor’ cells) and non-malignant ‘normal’ cells, including neural (neurons, glia), inflammatory (microglia, macrophage) and vascular cells. Tumor heterogeneity arises in part because, within the glioma mass, both ‘tumor’ and ‘normal’ cells secrete factors that form a unique microenvironment to influence tumor progression. Extracellular vesicles (EVs) are critical mediators of intercellular communication between immediate cellular neighbors and distantly located cells in healthy tissues/organs and in tumors, including gliomas. EVs mediate cell–cell signaling as carriers of nucleic acid, lipid and protein cargo, and their content is unique to cell types and physiological states. EVs secreted by non-malignant neural cells have important physiological roles in the healthy brain, which can be altered or co-opted to promote tumor progression and metastasis, acting in combination with glioma-secreted EVs. The cell-type specificity of EV content means that ‘vesiculome’ data can potentially be used to trace the cell of origin. EVs may also serve as biomarkers to be exploited for disease diagnosis and to assess therapeutic progress. In this review, we discuss how EVs mediate intercellular communication in glioma, and their potential role as biomarkers and readouts of a therapeutic response.

Intercellular communication and tissue growth

1969 ◽  
Vol 1 (1) ◽  
pp. 274-293 ◽  
Author(s):  
Carmia Borek ◽  
S. Higashino ◽  
W. R. Loewenstein
Keyword(s):  
Intercellular Communication ◽  
Tissue Growth

Intercellular communication and tissue growth

1972 ◽  
Vol 10 (1) ◽  
pp. 247-258 ◽  
Author(s):  
R. Azarnia ◽  
W. Michalke ◽  
W. R. Loewenstein
Keyword(s):  
Intercellular Communication ◽  
Tissue Growth

Intercellular communication and tissue growth

1971 ◽  
Vol 6 (4) ◽  
pp. 368-385 ◽  
Author(s):  
R. Azarnia ◽  
W. R. Loewenstein
Keyword(s):  
Intercellular Communication ◽  
Tissue Growth

Isolation of a cDNA whose expression is markedly increased in malignantly transformed FRTL cells and neoplastic human thyroid tissues

1994 ◽  
Vol 12 (1) ◽  
pp. 85-92
Author(s):  
K Ohta ◽  
T Endo ◽  
K Gunji ◽  
T Onaya
Keyword(s):  
Northern Blot Analysis ◽  
Thyroid Tissue ◽  
Human Thyroid ◽  
Graves Disease ◽  
Mrna Levels ◽  
Thyroid Cells ◽  
Normal Cells ◽  
Normal Thyroid ◽  
Filter Hybridization ◽  
Rat Thyroid

ABSTRACT We have cloned a cDNA whose mRNA levels are increased in malignantly transformed rat thyroid FRTL cells (FRTL-Tc cells). We constructed a cDNA library from FRTL-Tc cells in λgt10 and screened the cDNAs by differential plaque filter hybridization. Twenty-five thousand clones were screened and one cDNA (C140) was selected which corresponded to a mRNA whose expression was 5·8 times higher in FRTL-Tc cells than in FRTL cells. A 0·8 kb specific C140 mRNA was detected by Northern blot analysis of FRTL-Tc and FRTL mRNAs. The C140 cDNA was sequenced and found to encode a protein of 227 amino acids. We have found that C140 mRNA is conserved in human thyroid cells, but it is encoded by a smaller 0·7 kb transcript. C140 mRNA was highly expressed in neoplastic thyroid tissues and weakly in normal thyroid tissues in the same patients. Additionally, we found that C140 mRNA was also increased in the thyroid tissue of a patient with Graves' disease. These results suggest that C140 expression might be higher in rapidly growing thyroid cells than in normal cells, and might provide a new aspect for the study of thyroid tumours.

scholarly journals INTERCELLULAR COMMUNICATION AND TISSUE GROWTH

1967 ◽  
Vol 33 (2) ◽  
pp. 225-234 ◽  
Author(s):  
Werner R. Loewenstein ◽  
Yoshinobu Kanno
Keyword(s):  
Cancer Cells ◽  
Membrane Permeability ◽  
Intercellular Communication ◽  
Surface Membrane ◽  
Cell Cancer ◽  
Normal Liver ◽  
Liver Cells ◽  
Tissue Growth ◽  
Liver Cancers ◽  
Strong Barrier

Intercellular communication was examined with intracellular electrical techniques in primary and transplanted rat liver cancers. Normal liver cells communicate rather freely with each other through permeable junctional membranes. Cancer liver cells show no communication at all; their surface membrane is a strong barrier to diffusion all around the cell. Cancer cells induce alterations in membrane permeability in normal liver cells; communication among the latter is markedly reduced when cancer cells grow near them.

scholarly journals Cell competition between anaplastic thyroid cancer and normal thyroid follicular cells exerts reciprocal stress response defining tumor suppressive effects of normal epithelial tissue

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249059
Author(s):  
Aidana Amrenova ◽  
Keiji Suzuki ◽  
Vladimir Saenko ◽  
Shunichi Yamashita ◽  
Norisato Mitsutake
Keyword(s):  
Thyroid Cancer ◽  
Stress Response ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
Epithelial Tissue ◽  
Follicular Cells ◽  
Cell Competition ◽  
Normal Cells ◽  
Normal Thyroid ◽  
Thyroid Follicular Cells

The microenvironment of an early-stage tumor, in which a small number of cancer cells is surrounded by a normal counterpart milieu, plays a crucial role in determining the fate of initiated cells. Here, we examined cell competition between anaplastic thyroid cancer cells and normal thyroid follicular cells using co-culture method. Cancer cells were grown until they formed small clusters, to which normal cells were added to create high-density co-culture condition. We found that co-culture with normal cells significantly suppressed the growth of cancer cell clusters through the activation of Akt-Skp2 pathway. In turn, cancer cells triggered apoptosis in the neighboring normal cells through local activation of ERK1/2. A bi-directional cell competition provides a suppressive mechanism of anaplastic thyroid cancer progression. Since the competitive effect was negated by terminal growth arrest caused by radiation exposure to normal cells, modulation of reciprocal stress response in vivo could be an intrinsic mechanism associated with tumor initiation, propagation, and metastasis.

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