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calmodulin/neoplasms
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A study on the levels of calmodulin and DNA in human lung cancer cells.
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In order to study the role of calmodulin (CaM) in the proliferation of lung cancer cells, the CaM level of the specimens of 40 cases of primary lung cancers and the DNA content of the specimens of 35 cases of primary lung cancers were determined with phosphodiesterase assay and flow cytometry
Calmodulin-androgen receptor (AR) interaction: calcium-dependent, calpain-mediated breakdown of AR in LNCaP prostate cancer cells.
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Chemotherapy of prostate cancer targets androgen receptor (AR) by androgen ablation or antiandrogens, but unfortunately, it is not curative. Our attack on prostate cancer envisions the proteolytic elimination of AR, which requires a fuller understanding of AR turnover. We showed previously that
The effect of calmodulin antagonists on the activation of RAW-264 macrophage-like cells for tumor cell killing.
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The effects of several calmodulin antagonists on the activation of RAW-264 macrophage-like cells for tumor cell killing were investigated. At concentrations ranging from 5 X 10(-8) to 5 X 10(-7) M, calmidazolium, trifluoperazine, chlorprothixene, chlorpromazine and W-13 inhibited the development of
Response of estrogen receptor containing tumour cells to pure antiestrogens and the calmodulin inhibitor, calmidzolium chloride.
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Cell survival is dependent on both external and internally generated signalling processes and current strategies for medical intervention in neoplastic disease are directed towards signal transduction blockade. Redundancy in signalling pathways may mean, however, that a combination of agents is
Cloning and characterization of a p53 and DNA damage down-regulated gene PIQ that codes for a novel calmodulin-binding IQ motif protein and is up-regulated in gastrointestinal cancers.
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We have identified a p53 and DNA damage-regulated gene that encodes a novel IQ motif protein, which we have named p53 and DNA damage-regulated IQ motif protein (PIQ). PIQ has two isoforms, long (PIQ-L) and short (PIQ-S), and both bind to calmodulin in the presence and absence of calcium. PIQ
Calmodulin antagonists promote TRA-8 therapy of resistant pancreatic cancer.
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Pancreatic cancer is highly malignant with limited therapy and a poor prognosis. TRAIL-activating therapy has been promising, however, clinical trials have shown resistance and limited responses of pancreatic cancers. We investigated the effects of calmodulin(CaM) antagonists, trifluoperazine(TFP)
Calmodulin antagonist W 13 prevents DNA repair after bleomycin treatment of human urological tumor cells growing on extracellular matrix.
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1. The combined application of DNA strand-scission agents (bleomycin) and inhibitors of recovery from lethal damage (calmodulin antagonist W-13) could be a novel and potentially important approach to cancer therapy. 2. As determined by alkaline elution, both DNA-DNA and DNA-protein cross-links in
Stimulation of free radical generation in human leukocytes by various agents including tumor necrosis factor is a calmodulin dependent process.
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The mechanism(s) involved in the generation of free radicals in human leukocytes by phorbol myristate acetate (PMA), formyl-methionyl-leucyl-phenylalanine (FMP), lipopolysaccharide (LPS), arachidonic acid (AA), and recombinant-tumor necrosis factor-1-alpha (r-TNF-1 alpha) was investigated.
PTPRZ1 regulates calmodulin phosphorylation and tumor progression in small-cell lung carcinoma.
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BACKGROUND
Small-cell lung carcinoma (SCLC) is a neuroendocrine tumor subtype and comprises approximately 15% of lung cancers. Because SCLC is still a disease with a poor prognosis and limited treatment options, there is an urgent need to develop targeted molecular agents for this
Calmodulin: a potential target for cancer chemotherapeutic agents.
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Calmodulin is a ubiquitous, calcium-binding protein that is responsible for many of the intracellular actions of calcium. Recent evidence suggests that calmodulin may regulate cellular proliferation and that its function may be altered in malignancy. The discovery that drugs such as phenothiazines
Digoxin and ouabain induce P-glycoprotein by activating calmodulin kinase II and hypoxia-inducible factor-1alpha in human colon cancer cells.
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Digoxin and ouabain are cardioactive glycosides, which inhibit the Na+/K+-ATPase pump and in this way they increase the intracellular concentration of cytosolic calcium ([Ca2+](i)). They are also strong inducers of the P-glycoprotein (Pgp), a transmembrane transporter which extrudes several drugs,
Triptolide induces apoptosis through the calcium/calmodulin‑dependent protein kinase kinaseβ/AMP‑activated protein kinase signaling pathway in non‑small cell lung cancer cells
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Triptolide, a triterpene extracted from the Chinese herb Tripterygium wilfordii, has been reported to exert multiple bioactivities, including immunosuppressive, anti‑inflammatory and anticancer effects. Although the anticancer effect of triptolide has attracted significant attention, the specific
Interaction between quercetin and Ca2+-calmodulin complex: possible mechanism for anti-tumor-promoting action of the flavonoid.
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Quercetin was found to have similar inhibitory effects on tumor promoter-induced phenomena to those of N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, a calmodulin antagonist. Moreover, quercetin was shown to interact directly with the Ca2+-calmodulin complex. These results suggest that
Isolation and characterization of calmodulin from an insulin-secreting tumour.
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A major protein constituent of a rat islet cell tumour that exhibited Ca2+-dependent changes in electrophoretic mobility has been purified to homogeneity and compared in its physicochemical and biological properties with bovine brain and rat brain calmodulin (synonymous with phosphodiesterase
Effects of calmodulin antagonists on human ovarian cancer cell proliferation in vitro.
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Examined were effects of calmodulin antagonists (W-5 and W-7) on proliferation of two kinds of human cell lines, designated HR and KF, derived from serous cystadecarcinoma of the ovary. Although both W-5 and W-7 inhibited their cell proliferation in vitro, the degree of inhibition was more marked
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