Regulation of M2, M3, and M4muscarinic receptor expression in K562 chronic myelogenous leukemic cells by carbachol

Cabadak, Hülya; Aydın, Banu; Kan, Beki

doi:10.3109/10799893.2010.506484

Cited by 21 publications

(22 citation statements)

References 37 publications

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“…Relative protein expression levels of α7-nAChR and M3-mAChR were calculated from the band intensities using computerized densitometry with ImageQuantTL software (GE Healthcare Life Sciences) . Notably, the M3-mAChR immunoblot had two bands, which were considered and quantified as M3-mAChR in accordance with a previous study (19).…”

Section: Methodsmentioning

confidence: 79%

Variation of nicotinic subtype α7 and muscarinic subtype M3 acetylcholine receptor expression in three main types of leukemia

et al. 2018

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Cholinergic receptors, such as α7-nicotinic acetylcholine receptor (α7-nAChR) and M3-muscarinic acetylcholine receptor (M3-mAChR), have been demonstrated to serve a significant role in the proliferation, differentiation and apoptosis of leukemic cells. However, the expression of these receptors in samples from patients with leukemia remains unclear. The present study aimed to determine the expression of M3-mAChR and α7-nAChR in the bone marrow or peripheral blood of 51 patients with leukemia, including acute myeloid leukemia (AML; n=33), acute lymphoblastic leukemia (ALL; n=13), and chronic myeloid leukemia (CML; n=5). Peripheral blood mononuclear cells (PBMCs) were also isolated from healthy subjects (n=5) for comparison. Western blot analysis was performed to determine the protein expression profiles, and a pattern of decreased α7-nAChR levels in patients with leukemia was observed. Among the leukemia types, the lowest expression of α7-nAChR and M3-mAChR were identified in patients with T-cell ALL/lymphoma (T-ALL). CML exhibited the highest level of M3-mAChR, which was significantly different from APL and AML-M4, yet not from healthy subjects (P<0.05). Therefore, different expression profiles of α7-nACR and M3-mAChR were detected amongst the leukemia types. Collectively, the present study supports the potential role of cholinergic signaling in mediating leukemogenesis. However, further studies in larger cohorts are required to validate these findings.

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Section: Methodsmentioning

confidence: 79%

Variation of nicotinic subtype α7 and muscarinic subtype M3 acetylcholine receptor expression in three main types of leukemia

et al. 2018

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“…We found that exposure of K562 cells supplemented with 10% serum to CCh led to an inhibition of DNA synthesis [3] and a decrease in cyclin D 1 expression. Inhibition of cyclin D 1 expression was fully reversed by the muscarinic antagonists atropine (non-selective), gallamine (M 2 /M 4 selective) and tropicamide (M 4 selective) but not by 4-DAMP (M 3 selective).…”

Section: Discussionmentioning

confidence: 90%

“…We have previously demonstrated the presence of M 2 , M 3 and M 4 mAChRs and M 3 subtype mediated NO signaling in K562 chronic myelogenous leukemic cells [8]. We also showed that collagenase clostridium histolyticum (CCh)-treatment leads to changes in muscarinic M 2 , M 3 and M 4 receptor transcripts as well as M 2 and M 3 protein levels [3] and enhances cyclic adenosine monophosphate (cAMP) accumulation in these cells [21].…”

Section: +mentioning

confidence: 99%

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confidence: 99%

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Muscarinic Agonist, Antagonists and Signaling Pathway Inhibitors Change c-Fos And Cyclin D1 Expression in K562 Cells

Cabadak¹,

Aydın²,

Kan³

2013

MMJ

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Acetylcholine is a neurotransmitter in the nervous system but it serves also as a paracrine or autocrine factor in different cell types, where it is linked to functions like proliferation and cell differentiation [1][2][3]. mAChRs mediate a wide array of cellular responses to acetylcholine in the central nervous system (CNS) and in non-nervous tissues innervated by the parasymphatic nervous system [4,5]. Muscarinic receptors are involved in diverse actions, including inhibition of adenylate cyclase, breakdown of phosphoinositide, regulation of nitric oxide (NO) synthesis, change of Ca 2+ levels and modulation of K channels [6][7][8]. Muscarinic cholinergic receptors can also induce cell proliferation, differentiation and transformation. These effects are cell type dependent and receptor subtype specific. Many cells express a mixture of muscarinic receptor

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“…A large number of studies have shown that many components of cholinergic signaling including Ach are present in a variety of non-neuronal tissues, such as lung cancer (21,22), colon (23), breast, ovarian carcinomas (24,25) and other common cancer cells. Interestingly, cholinergic signaling were found to increase further in the local tumor environment, representing a potential new pathway to target tumor growth (26).…”

Section: Discussionmentioning

confidence: 99%

Aclidinium bromide inhibits the growth and metastasis of gastric cancer MKN‑28 cells via the PI3K signaling pathway

et al. 2018

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The present study investigated the effect and underling mechanisms of aclidinium bromide, a novel, inhaled long‑acting muscarinic antagonist, on the development of gastric cancer. Human gastric cancer MKN‑28 cells, as a model in vitro, were treated with aclidinium bromide and dimethyl sulfoxide. Cell Counting Kit‑8 assay, transwell assay and flow cytometry were used to assess cell proliferation, invasion/migration and apoptosis, respectively. In addition, western blotting was performed to determine the relative expression of proteins associated with apoptosis and the phosphatidylinositol‑3‑kinase (PI3K) signaling pathway. Optical density values of MKN‑28 cells were decreased in a time‑ and dose‑dependent manner in the aclidinium bromide treated group. Matrigel invasion analysis demonstrated the number of invasive cells were significantly decreased in the aclidinium bromide‑treated group when compared with the control group. Furthermore, aclidinium bromide led to the marked reduction of the number of MKN‑28 cells passing though the microwells of the transwell chamber. The expression levels of the anti‑apoptotic protein B‑cell lymphoma 2 (Bcl‑2) decreased, and the expression of pro‑apoptotic proteins active Caspase3 and Bcl‑2‑associated X protein increased concurrently following aclidinium bromide stimulation using western blotting. The phosphorylation of protein kinase B and mechanistic target of rapamycin were significantly inhibited in MKN‑28 cells treated with aclidinium bromide; and the activity of the downstream proteins such as p70S6K and Cyclin D1 were also significantly decreased. In conclusion, aclidinium bromide could inhibit gastric cancer cell proliferation and metastasis, which may be associated with the enhancement of apoptosis induced by the PI3K signaling pathway.

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Regulation of M₂, M₃, and M₄muscarinic receptor expression in K562 chronic myelogenous leukemic cells by carbachol

Cited by 21 publications

References 37 publications

Variation of nicotinic subtype α7 and muscarinic subtype M3 acetylcholine receptor expression in three main types of leukemia

Variation of nicotinic subtype α7 and muscarinic subtype M3 acetylcholine receptor expression in three main types of leukemia

Muscarinic Agonist, Antagonists and Signaling Pathway Inhibitors Change c-Fos And Cyclin D1 Expression in K562 Cells

Aclidinium bromide inhibits the growth and metastasis of gastric cancer MKN‑28 cells via the PI3K signaling pathway

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