Inhibition of protein kinase C is associated with a decrease in <i>c‐myc</i> expression in human myeloid leukemia cells

Bernstein, Steven H.; Kharbanda, Surender; Sherman, Matthew L.; Stone, Richard; Küfe, Donald

doi:10.1016/0014-5793(91)81346-a

Cited by 13 publications

(4 citation statements)

References 27 publications

(16 reference statements)

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“…14 This finding suggests that c-Myc may be a transcription factor for GRK4. In addition, phorbol esters can transiently increase c-Myc mRNA expression in human myeloid leukemia cells 15 and have been shown to increase promoter activity of GRK4 in transfected HEK-293 cells. 9 In cells other than renal proximal tubule, phorbol esters have also been shown to increase phospho-c-Myc, suggesting that phospho-c-Myc may activate GRK4 expression.…”

Section: Introductionmentioning

confidence: 99%

A Novel Role for c-Myc in G Protein–Coupled Receptor Kinase 4 (GRK4) Transcriptional Regulation in Human Kidney Proximal Tubule Cells

et al. 2013

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The G coupled-protein receptor kinase 4 (GRK4) negatively regulates the dopaminergic system by desensitizing the dopamine-1-receptor (D1R). The expressional control of GRK4 has not been reported, but here, we show that the transcription factor c-Myc binds to the promoter of GRK4 and positively regulates GRK4 protein expression in human renal proximal tubule cells (RPTCs). Addition of phorbol esters (PMA) to RPTCs not only increased c-Myc binding to the GRK4 promoter, but also increased both phospho-c-Myc and GRK4 expression. The PMA-mediated increase in GRK4 expression was completely blocked by the c-Myc inhibitor, 10074-G5, indicating that GRK4 is downstream of phospho-c-Myc. The autocrine production of angiotensin II (Ang II) in RPTCs increased the phosphorylation and activation of c-Myc and subsequently GRK4 expression. 3-Amino-4-thio-butyl sulfonate (EC-33), an inhibitor of aminopeptidase A (APA), increased RPTC secretion of Ang II. EC-33 or Ang II increased the expression of both phospho-c-Myc and GRK4, which was blocked by 10074-G5. Blockade of the angiotensin II type 1 receptor (AT1R) with losartan decreased phospho-c-Myc and GRK4 expression. Both inhibition of c-Myc activity and blockade of AT1R restored the coupling of D1R to adenylyl cyclase (AC) stimulation in uncoupled RPTCs (uRPTCs) while PMA or Ang II caused the uncoupling of normally coupled RPTCs (nRPTCs). We suggest that the AT1R impairs D1R function via c-Myc activation of GRK4. This novel pathway may be involved in the increase in blood pressure in hypertension that is mediated by increased activity of the renin-angiotensin system and decreased activity of the renal dopaminergic system.

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Section: Introductionmentioning

confidence: 99%

A Novel Role for c-Myc in G Protein–Coupled Receptor Kinase 4 (GRK4) Transcriptional Regulation in Human Kidney Proximal Tubule Cells

et al. 2013

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“…In contrast, activation of PKC in resting cells induced expression of c‐ myc . In addition to StSp, H7 reduces c‐ myc expression to undetectable levels within 60 min in HL‐60 and U‐937 cells [14, 26, 28]. Inhibitors related to cyclic nucleotide‐dependent protein kinases have no effect on c‐ myc mRNA levels [26].…”

Section: Discussionmentioning

confidence: 97%

“…(2) A dual effect of PKC on c‐ myc expression has been described. PKC activation by phorbol esters induces HL‐60 and U‐937 cells to differentiate along the monocytic lineage [5, 25]and the expression of c‐ myc is reduced [26, 27]. In contrast, activation of PKC in resting cells induced expression of c‐ myc .…”

Section: Discussionmentioning

confidence: 99%

Nuclear accumulation of c‐myc mRNA in phytohaemagglutinin‐activated T lymphocytes treated with anti‐HLA class I monoclonal antibody

et al. 1998

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Anti-HLA class I monoclonal antibody 01.65 inhibits the proliferative response of PHA-activated human T lymphocytes from peripheral blood mononuclear cells. The recruitment rate in the cell cycle is slack and the G1 and S phases are prolonged. Among the early events after PHA activation, only the calcium-dependent PKC activity appears to be modified: particulate PKC is completely depleted while cytosolic residual PKC is reduced by 80% after MAb 01.65 treatment. We have carried out in greater detail the study of c-myc gene regulation by MAb 01.65 and the results are as follows: (i) c-myc RNA transcription is normally initiated and finished, suggesting a post-transcriptional regulation of c-myc gene expression; (ii) no alteration in c-myc mRNA stability has been documented; (iii) steady-state levels of c-myc mRNA expression by Northern blot analysis and PCR amplification are decreased in the cytoplasmic compartment, while in the nuclear compartment they appear to be increased. Nuclear accumulation of mature mRNA after MAb 01.65 and PKC inhibitor (H7 and StSp) treatment appears to be the most probable mechanism involved. The possible implications of this are discussed.z 1998 Federation of European Biochemical Societies.

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“…Classical isoenzymes of the protein kinase C (PKC) family can also be involved in cell cycle regulation and cell growth by influencing its downstream targets such as Myc, cyclins, CDKs, CKIs [52,53], or NF-κB [54].…”

Section: Ellagic Acid and Sustaining Proliferative Signalingmentioning

confidence: 99%

Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence

Čižmáriková,

Michalková,

Mirossay

et al. 2023

Biomolecules

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Cancer is a complex and multifaceted disease with a high global incidence and mortality rate. Although cancer therapy has evolved significantly over the years, numerous challenges persist on the path to effectively combating this multifaceted disease. Natural compounds derived from plants, fungi, or marine organisms have garnered considerable attention as potential therapeutic agents in the field of cancer research. Ellagic acid (EA), a natural polyphenolic compound found in various fruits and nuts, has emerged as a potential cancer prevention and treatment agent. This review summarizes the experimental evidence supporting the role of EA in targeting key hallmarks of cancer, including proliferation, angiogenesis, apoptosis evasion, immune evasion, inflammation, genomic instability, and more. We discuss the molecular mechanisms by which EA modulates signaling pathways and molecular targets involved in these cancer hallmarks, based on in vitro and in vivo studies. The multifaceted actions of EA make it a promising candidate for cancer prevention and therapy. Understanding its impact on cancer biology can pave the way for developing novel strategies to combat this complex disease.

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Inhibition of protein kinase C is associated with a decrease in c‐myc expression in human myeloid leukemia cells

Cited by 13 publications

References 27 publications

A Novel Role for c-Myc in G Protein–Coupled Receptor Kinase 4 (GRK4) Transcriptional Regulation in Human Kidney Proximal Tubule Cells

A Novel Role for c-Myc in G Protein–Coupled Receptor Kinase 4 (GRK4) Transcriptional Regulation in Human Kidney Proximal Tubule Cells

Nuclear accumulation of c‐myc mRNA in phytohaemagglutinin‐activated T lymphocytes treated with anti‐HLA class I monoclonal antibody

Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence

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