The effect of G-CSF on F-actin reorganization in HL-60 and K562 cell lines

Abstract

The aim of this investigation was to show the influence of G-CSF (G-CSF) on the F-actin cytoskeleton and the morphology of G-CSFR-proficient HL-60 and G-CSFR-deficient K562 cell lines. In the present study, we show changes in F-actin distribution in HL-60 cells after treatment with 5 and 10 ng/ml concentration of G-CSF but also changes in the organization and fluorescence intensity of F-actin in the K562 cell line. After treatment of HL-60 cells with 5 ng/ml concentration of G-CSF we observed an increase in F-actin levels. Additionally, a higher labeling of nuclear F-actin under TEM was observed. Moreover, changes in the cell cycle indicate cell differentiation. On the other hand, in the K562 cell line we observed an increase in the percentage sub-G1 cells following treatment with both concentration of G-CSF. Furthermore, an increase in the percentage of late apoptotic cells after G-CSF treatment was observed. A statistically significant difference in the cytoplasmic F-actin levels was not detected, but nuclear levels were decreased. In conclusion, we suggest that the G-CSF-based reorganization of actin filaments in HL-60 cells is involved in the differentiation process. Moreover, we suggest that the G-CSF-induced changes observed in K562 cells are associated with a G-CSF receptor-independent pathway or its binding to other similar receptors.

The interactions between SATB1 and F-actin are important for mechanisms of active cell death

“…Also the results of our studies obtained by a modification of both confocal and transmission electron microscopy (TEM) and combination of pre-and post-embedding labeling techniques demonstrated the presence of actin filaments in cell nuclei of various cell lines [19][20][21][22][23]. In the present study we have also detected the presence of SATB1 protein in nuclei of MCF-7 cells, a human breast cancer cell line widely used to investigate SATB1 expression [13,28,29].…”

“…Our previous studies indicated the presence of F-actin in nuclei of different cell lines after induction of the active cell death process due to cells' treatment with anti-cancer drugs [19][20][21][22][23]. Moreover, we observed the colocalization of SATB1 and F-actin in the transcriptional active regions of the cell nucleus during active cell death of the Chinese hamster ovary cell line (CHO AA8 cell line) following treatment with doxorubicin [24].…”

“…Many authors showed that actin may translocate into the cell nucleus to function as a transcriptional modulator of gene expression [1,3,[32][33][34][35][36]. We have previously demonstrated not only the translocation of F-actin into the nucleus, but also its involvement in chromatin remodeling during cell death [19][20][21][22][23]. Our current findings together with results of the previous report on CHO AA8 cells [24] collectively suggest that SATB1 may not only provide the structural background for chromatin organization but also it may play a significant role in the reorganization of chromatin during cell death.…”

The alterations in SATB1 and nuclear F-actin expression affect apoptotic response of the MCF-7 cells to geldanamycin

“…Our earlier studies have demonstrated not only the translocation of actin into the nucleus but also the involvement of nuclear F-actin in chromatin remodeling during cell death processes [32][33][34][35][36]. The results presented in this paper suggest that SATB1 may be involved together with F-actin in chromatin reorganization during cell death.…”

“…We have previously shown that SATB1/nuclear F-actin complex is localized at the border of condensed and decondensed chromatin, which suggests its involvement in the process of transcription [31]. We have also demonstrated F-actin presence in the cell nucleus of different cell lines treated with anti-cancer drugs and speculated that nuclear F-actin may be involved in chromatin remodeling processes during apoptosis and mitotic catastrophe [32][33][34][35][36]. To date, no studies have described the possible association between the apoptotic process and the alterations in SATB1 expression.…”