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Lithium effects on vesicular trafficking in hepatocellular carcinoma cells. / Taskaeva, Iuliia; Bgatova, Nataliya; Gogaeva, Izabella.

In: Ultrastructural Pathology, Vol. 43, No. 6, 09.12.2019, p. 301-311.

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Harvard

Taskaeva, I, Bgatova, N & Gogaeva, I 2019, 'Lithium effects on vesicular trafficking in hepatocellular carcinoma cells', Ultrastructural Pathology, vol. 43, no. 6, pp. 301-311. https://doi.org/10.1080/01913123.2019.1701167

APA

Vancouver

Taskaeva I, Bgatova N, Gogaeva I. Lithium effects on vesicular trafficking in hepatocellular carcinoma cells. Ultrastructural Pathology. 2019 Dec 9;43(6):301-311. doi: 10.1080/01913123.2019.1701167

Author

Taskaeva, Iuliia ; Bgatova, Nataliya ; Gogaeva, Izabella. / Lithium effects on vesicular trafficking in hepatocellular carcinoma cells. In: Ultrastructural Pathology. 2019 ; Vol. 43, No. 6. pp. 301-311.

BibTeX

@article{8debb18836e54d18a9e835439a42c99a,
title = "Lithium effects on vesicular trafficking in hepatocellular carcinoma cells",
abstract = "Hepatocellular carcinoma (HCC) is one of the most commonly malignant tumors worldwide, characterized by the presence of many heterogeneous molecular cell events that contribute to tumor growth and progression. Endocytic processes are intimately involved in various pathological conditions, including cancer, since they interface with various cellular signaling programs. The ability of lithium to induce cell death and autophagy and affect cell proliferation and intracellular signaling has been shown in various experimental tumor models. The aim of this study was to evaluate the effects of lithium on vesicular transport in hepatocellular carcinoma cells. Using transmission electron microscopy we have characterized the endocytic apparatus in hepatocellular carcinoma-29 (HCC-29) cells in vivo and detailed changes in endocytotic vesicles after 20 mM lithium carbonate administration. Immunofluorescent analysis was used to quantify cells positive for EEA1-positive early endosomes, Rab11-positive recycling endosomes and Rab7-positive late endosomes. Lithium treatment caused an increase in EEA1- and Rab11-positive structures and a decrease in Rab7-positive vesicles. Thus, lithium affects diverse endocytic pathways in HCC-29 cells which may modulate growth and development of hepatocellular carcinoma.",
keywords = "electron microscopy, endocytosis, Hepatocellular carcinoma, lithium, vesicular trafficking, RECEPTOR, MECHANISMS, DEATH, ENDOCYTOSIS, ENDOSOMES, LYSOSOMAL MEMBRANE PERMEABILIZATION, PATHWAY, CAVEOLAE, LEUKEMIA, EXPRESSION",
author = "Iuliia Taskaeva and Nataliya Bgatova and Izabella Gogaeva",
year = "2019",
month = dec,
day = "9",
doi = "10.1080/01913123.2019.1701167",
language = "English",
volume = "43",
pages = "301--311",
journal = "Ultrastructural Pathology",
issn = "0191-3123",
publisher = "Informa Healthcare",
number = "6",

}

RIS

TY - JOUR

T1 - Lithium effects on vesicular trafficking in hepatocellular carcinoma cells

AU - Taskaeva, Iuliia

AU - Bgatova, Nataliya

AU - Gogaeva, Izabella

PY - 2019/12/9

Y1 - 2019/12/9

N2 - Hepatocellular carcinoma (HCC) is one of the most commonly malignant tumors worldwide, characterized by the presence of many heterogeneous molecular cell events that contribute to tumor growth and progression. Endocytic processes are intimately involved in various pathological conditions, including cancer, since they interface with various cellular signaling programs. The ability of lithium to induce cell death and autophagy and affect cell proliferation and intracellular signaling has been shown in various experimental tumor models. The aim of this study was to evaluate the effects of lithium on vesicular transport in hepatocellular carcinoma cells. Using transmission electron microscopy we have characterized the endocytic apparatus in hepatocellular carcinoma-29 (HCC-29) cells in vivo and detailed changes in endocytotic vesicles after 20 mM lithium carbonate administration. Immunofluorescent analysis was used to quantify cells positive for EEA1-positive early endosomes, Rab11-positive recycling endosomes and Rab7-positive late endosomes. Lithium treatment caused an increase in EEA1- and Rab11-positive structures and a decrease in Rab7-positive vesicles. Thus, lithium affects diverse endocytic pathways in HCC-29 cells which may modulate growth and development of hepatocellular carcinoma.

AB - Hepatocellular carcinoma (HCC) is one of the most commonly malignant tumors worldwide, characterized by the presence of many heterogeneous molecular cell events that contribute to tumor growth and progression. Endocytic processes are intimately involved in various pathological conditions, including cancer, since they interface with various cellular signaling programs. The ability of lithium to induce cell death and autophagy and affect cell proliferation and intracellular signaling has been shown in various experimental tumor models. The aim of this study was to evaluate the effects of lithium on vesicular transport in hepatocellular carcinoma cells. Using transmission electron microscopy we have characterized the endocytic apparatus in hepatocellular carcinoma-29 (HCC-29) cells in vivo and detailed changes in endocytotic vesicles after 20 mM lithium carbonate administration. Immunofluorescent analysis was used to quantify cells positive for EEA1-positive early endosomes, Rab11-positive recycling endosomes and Rab7-positive late endosomes. Lithium treatment caused an increase in EEA1- and Rab11-positive structures and a decrease in Rab7-positive vesicles. Thus, lithium affects diverse endocytic pathways in HCC-29 cells which may modulate growth and development of hepatocellular carcinoma.

KW - electron microscopy

KW - endocytosis

KW - Hepatocellular carcinoma

KW - lithium

KW - vesicular trafficking

KW - RECEPTOR

KW - MECHANISMS

KW - DEATH

KW - ENDOCYTOSIS

KW - ENDOSOMES

KW - LYSOSOMAL MEMBRANE PERMEABILIZATION

KW - PATHWAY

KW - CAVEOLAE

KW - LEUKEMIA

KW - EXPRESSION

UR - http://www.scopus.com/inward/record.url?scp=85076438256&partnerID=8YFLogxK

U2 - 10.1080/01913123.2019.1701167

DO - 10.1080/01913123.2019.1701167

M3 - Article

C2 - 31826700

AN - SCOPUS:85076438256

VL - 43

SP - 301

EP - 311

JO - Ultrastructural Pathology

JF - Ultrastructural Pathology

SN - 0191-3123

IS - 6

ER -

ID: 23092342