Changes in subcellular localization of visfatin in human colorectal HCT-116 carcinoma cell line after cytochalasin B treatment | Zendy

Rafał Jakub Bułdak | Zendy; Magdalena Skonieczna | Zendy; Łukasz Bułdak | Zendy; Natalia Matysiak | Zendy; Łukasz Mielańczyk | Zendy; Grzegorz Wyrobiec | Zendy; Michał Kukla | Zendy; Marek Michalski | Zendy; K Zwirska-Korczala | Zendy

Open Access

Changes in subcellular localization of visfatin in human colorectal HCT-116 carcinoma cell line after cytochalasin B treatment

Author(s) -

Rafał Jakub Bułdak,

Magdalena Skonieczna,

Łukasz Bułdak,

Natalia Matysiak,

Łukasz Mielańczyk,

Grzegorz Wyrobiec,

Michał Kukla,

Marek Michalski,

K Zwirska-Korczala

Publication year - 2014

Publication title -

european journal of histochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.754

H-Index - 42

eISSN - 2038-8306

pISSN - 1121-760X

DOI - 10.4081/ejh.2014.2408

Subject(s) - medicine , subcellular localization , cytochalasin d , cytochalasin b , cell culture , colorectal cancer , oncology , cancer research , cell , chemistry , endocrinology , biology , biochemistry , cancer , cytoskeleton , genetics , cytoplasm

The aim of the study was to assess the expression and subcellular localization of visfatin in HCT-116 colorectal carcinoma cells after cytokinesis failure using Cytochalasin B (CytB) and the mechanism of apoptosis of cells after CytB. We observed translocation of visfatin’s antigen in cytB treated colorectal carcinoma HCT-116 cells from cytosol to nucleus. Statistical and morphometric analysis revealed significantly higher area-related numerical density visfatin-bound nano-golds in the nuclei of cytB-treated HCT-116 cells compared to cytosol. Reverse relation to visfatin subcellular localization was observed in un-treated HCT-116 cells. The total amount of visfatin protein and visfatin mRNA level in HCT-116 cells was also decreased after CytB treatment. Additionally, CytB significantly decreased cell survival, increased levels of G2/M fractions, induced bi-nuclei formation as well as increased reactive oxygen species (ROS) level in HCT-116 cells. CytB treatment showed cytotoxic effect that stem from oxidative stress and is connected with the changes in the cytoplasmic/nuclear amount of visfatin in HCT-116 cells.

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