Retinoic acid promotes phorbol ester-initiated macrophage differentiation in HL-60 leukemia cells without disappearance of protein kinase C

Zylber‐Katz, Ester; Knode, Marian C.; Glazer, Robert I.

doi:10.1016/0145-2126(86)90009-3

Cited by 7 publications

(3 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Using Calu-1 cells in serum-free medium, we obtained the exact opposite result because ATRA enhanced AP-1 activation and stimulated cell growth. Nonetheless, our results are in agreement with reports that ATRA and other retinoids can act synergistically with TPA, the classical activator of AP-1, to enhance HL-60 cell dierentiation (Zylber-Katz et al, 1986) and the proliferation of human skin ®broblasts (Zhang et al, 1992). Mechanistically, our results are similar to reports that the intact estrogen receptor, or its ligandbinding domain, stimulated transactivation of an AP-1 like sequence in the ovalbumin gene promoter or an authentic AP-1 sequence by c-Jun and c-Fos in chick embryo ®broblasts (Gaub et al, 1990).…”

Section: Discussionsupporting

confidence: 83%

Enhancement of Calu-1 human lung carcinoma cell growth in serum-free medium by retinoids: dependence on AP-1 activation, but not on retinoid response element activation

et al. 1997

View full text Add to dashboard Cite

Many lung cancer cell lines are resistant to the growth inhibitory eects of retinoids. However, some small-cell lung cancer cell lines were inhibited by all trans-retinoic acid (ATRA) in serum-free medium. We compared the responses of seven non-small cell lung cancer (NSCLC) cell lines to ATRA in serum-free medium and in medium supplemented with delipidized serum. Whereas the growth of four cell lines was inhibited more in serumfree medium, the growth of the Calu-1 cell line was stimulated by ATRA in a dose-dependent fashion with a maximum at 10 78 M. Delipidized serum (42.5%) but not bovine serum albumin (0.15%) suppressed growth stimulation by ATRA. Transcripts of RA receptors RARa and RARg but not of RARb were detected in Calu-1 cells. Receptor expression, the formation of a complex among receptors and a RA-responsive element (RARE), and the transcriptional activation RARE were not suppressed by serum. Natural retinoids and synthetic receptor class-or subtype-selective retinoid agonists, which activated RARs and RXRs for gene transcription from a RARE, and a RAR antagonist (CD2366), which was unable to do so, stimulated the growth of Calu-1 cells in serum-free medium but not in serum-containing medium. Both ATRA and CD2366 enhanced the transcriptional activation of an Activator Protein-1 (AP-1)-luciferase reporter construct in serum-free medium but not in delipidized serum. Transcriptional activation of the RARE by ATRA occurred both in the presence or absence of delipidized serum. These results demonstrate that retinoid-induced growth stimulation of Calu-1 cells is associated with enhanced AP-1 transactivation but not with RARE transactivation.

show abstract

Section: Discussionsupporting

confidence: 83%

Enhancement of Calu-1 human lung carcinoma cell growth in serum-free medium by retinoids: dependence on AP-1 activation, but not on retinoid response element activation

et al. 1997

View full text Add to dashboard Cite

show abstract

“…The combination of ATRA and the organic arsenical melarsoprol synergistically induced apoptosis in Du-145 and PC-3 cells in vitro and in immunodeficient mice (37). Although ATRA was shown to enhance TPA-induced differentiation of myeloid leukemia cells (14,38) and to enhance TPA-induced growth inhibition of breast and lung cancer cells (39), the effects of combinations of TPA and ATRA at clinically relevant concentrations on the growth and death of human prostate cancer cells were not reported previously. As indicated above, the present study demonstrates a synergistic inhibitory effect of TPA and ATRA on the growth of LNCaP prostate cancer cells.…”

Section: Discussionmentioning

confidence: 73%

Inhibitory Effect of 12- O -Tetradecanoylphorbol-13-acetate Alone or in Combination with All- trans -Retinoic Acid on the Growth of LNCaP Prostate Tumors in Immunodeficient Mice

et al. 2004

View full text Add to dashboard Cite

The percentage of animals with some tumor regression after 21 days of treatment was 0% for the control group, 31% for the ATRA group, 62% for the TPA group, and 100% for the TPA؉ATRA group (13 mice/ group). Although treatment of the mice with TPA or TPA؉ATRA continued to inhibit tumor growth for the duration of the 46-day study, treatment of the mice with ATRA alone did not inhibit tumor growth beyond 28 days of daily injections (6 mice/group). Mechanistic studies indicated that treatment of the mice with TPA or TPA؉ATRA for 46 days increased apoptosis in the tumors, and treatment with TPA؉ATRA also decreased the mitotic index. Because the dose of TPA used in this study was effective and resulted in clinically achievable blood levels, clinical trials with TPA alone or in combination with ATRA in patients with prostate cancer may be warranted.

show abstract

“…Because DMSO can affect the fluidity of plasma membranes, it can activate several biological functions of cells by removing surface water from phospholipid bilayers [150,151]. AMP-dependent and phospholipid/Ca 2+ -dependent protein kinases are thought to be involved in the early stages of regulation of the phosphorylation/dephosphorylation status in cells [152,153]. Surprisingly, however, little is known about the detailed mechanisms regulating the myeloid differentiation of HL-60 cells.…”

Section: Wt-kras Engages With Wnt/β-catenin Signaling Pathway In the ...mentioning

confidence: 99%

Novel Insights into the Role of Kras in Myeloid Differentiation: Engaging with Wnt/β-Catenin Signaling

Yokoyama

Nakayama

Iwabuchi

2023

Cells

View full text Add to dashboard Cite

Cells of the HL-60 myeloid leukemia cell line can be differentiated into neutrophil-like cells by treatment with dimethyl sulfoxide (DMSO). The molecular mechanisms involved in this differentiation process, however, remain unclear. This review focuses on the differentiation of HL-60 cells. Although the Ras proteins, a group of small GTP-binding proteins, are ubiquitously expressed and highly homologous, each has specific molecular functions. Kras was shown to be essential for normal mouse development, whereas Hras and Nras are not. Kras knockout mice develop profound hematopoietic defects, indicating that Kras is required for hematopoiesis in adults. The Wnt/β-catenin signaling pathway plays a crucial role in regulating the homeostasis of hematopoietic cells. The protein β-catenin is a key player in the Wnt/β-catenin signaling pathway. A great deal of evidence shows that the Wnt/β-catenin signaling pathway is deregulated in malignant tumors, including hematological malignancies. Wild-type Kras acts as a tumor suppressor during DMSO-induced differentiation of HL-60 cells. Upon DMSO treatment, Kras translocates to the plasma membrane, and its activity is enhanced. Inhibition of Kras attenuates CD11b expression. DMSO also elevates levels of GSK3β phosphorylation, resulting in the release of unphosphorylated β-catenin from the β-catenin destruction complex and its accumulation in the cytoplasm. The accumulated β-catenin subsequently translocates into the nucleus. Inhibition of Kras attenuates Lef/Tcf-sensitive transcription activity. Thus, upon treatment of HL-60 cells with DMSO, wild-type Kras reacts with the Wnt/β-catenin pathway, thereby regulating the granulocytic differentiation of HL-60 cells. Wild-type Kras and the Wnt/β-catenin signaling pathway are activated sequentially, increasing the levels of expression of C/EBPα, C/EBPε, and granulocyte colony-stimulating factor (G-CSF) receptor.

show abstract

Retinoic acid promotes phorbol ester-initiated macrophage differentiation in HL-60 leukemia cells without disappearance of protein kinase C

Cited by 7 publications

References 16 publications

Enhancement of Calu-1 human lung carcinoma cell growth in serum-free medium by retinoids: dependence on AP-1 activation, but not on retinoid response element activation

Enhancement of Calu-1 human lung carcinoma cell growth in serum-free medium by retinoids: dependence on AP-1 activation, but not on retinoid response element activation

Inhibitory Effect of 12- O -Tetradecanoylphorbol-13-acetate Alone or in Combination with All- trans -Retinoic Acid on the Growth of LNCaP Prostate Tumors in Immunodeficient Mice

Novel Insights into the Role of Kras in Myeloid Differentiation: Engaging with Wnt/β-Catenin Signaling

Contact Info

Product

Resources

About