4-Piperidinopiperidine-resistant lymphoma cells were resistant to dexamethasone- and A23187-induced apoptosis

Onishi, Yoshiaki; Oguro, M; Kizaki, Harutoshi

doi:10.1016/s0304-3835(98)00029-9

Cited by 8 publications

(11 citation statements)

References 10 publications

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“…Ikemoto et al demonstrated that calphositin C decreased bcl ‐2 transcript and protein in human glioma cell lines, and correlated bcl ‐2 levels with PKC inhibition 28. These findings have been supported by Onishi et al, who demonstrated that CPT‐11–resistant cells increase bcl ‐2 expression, leading them to propose that decreasing bcl ‐2 may decrease drug resistance 29. In addition to decreasing bcl ‐2, we found that PKC inhibition up‐regulates the proapoptotic protein bax.…”

Section: Discussionmentioning

confidence: 86%

“…To our knowledge, the possibility that inhibition of PKC may induce chemosensitivity to CPT‐11 via other mechanisms has not been tested. These mechanisms may include: 1) increasing glioma topoisomerase‐I activity; 2) improving glioma carboxylesterase activity, resulting in higher levels of SN‐38; and 3) increasing the accumulation of drugs, even in cells that overexpress P‐glycoprotein 29…”

Section: Discussionmentioning

confidence: 99%

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Combination therapy with irinotecan and protein kinase C inhibitors in malignant glioma

Chen

Fry

et al. 2003

Cancer

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The topoisomerase-I inhibitor irinotecan (CPT-11) is currently used in Phase I/II trials for the treatment of patients with recurrent malignant gliomas. Protein kinase C (PKC) inhibitors such as high-dose tamoxifen and hypericin also have been used in the treatment of malignant gliomas. The current study examined the role of PKC inhibitors as chemosensitizers for CPT-11 and their proposed mechanism of action. Two glioma cell lines (A-172 and U-87) and one primary glioma cell culture (LA-567) were used.Proliferation ( 3 H-thymidine) and cytotoxicity (methylthiotetrazole) studies were performed using CPT-11 (0 -100 M) alone, 7-ethyl-10-hydroxy camptothecin (SN-38) (0 -1000 nM) alone or in the presence of a PKC inhibitor, tamoxifen (10 M), hypericin (10 M), calphositin C (400 nM), or staurosporine (10 nM). The terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL) assay was used to determine apoptosis as the mechanism of cytotoxicity; alterations in bcl-2 and bax expression were determined using Western blot analysis. Conversion of CPT-11 to SN-38 by glioma cells was determined using high-performance liquid chromatography

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Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Combination therapy with irinotecan and protein kinase C inhibitors in malignant glioma

Chen

Fry

et al. 2003

Cancer

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“…The PCR fragments were analyzed by electrophoresis on 2% agarose gel, and the DNA was visualized using ethidium bromide staining. Measurements of the expression level of each sample adhered to guidelies established by Onishi et al . (1998).…”

Section: Methodsmentioning

confidence: 99%

Muscle-fiber characteristics in adult mouse-tongue muscles

et al. 2002

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To clarify functions of the mouse-tongue muscles, proteins such as myocin heavy chain (MHC) 2a and MHC-2b, which are isoforms of the fast-twitch fiber type myosin heavy chain, in the lateral margin of the tongue were observed by reverse transcription polymerase chain reaction and immunohistochemical analyses. The main MHC isoform in the superior longitudinal muscle of the tongue was MHC-2b, with the fastest function and the main MHC isoform in the transverse muscle of the tongue was MHC-2a. These findings suggested that the fastest function is necessary for the superior longitudinal muscle of the tongue, which is useful for moving the tongue in and out of the mouth in the sagittal direction, showing different cellular biological properties of the myofibers from those of the transverse muscle of the tongue.

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“…Thus, a large number of papers have been published in the literature concerning the medical application of the piperidine derivatives. Some of them are used as raw-material for antihistaminic agents [1], analgesic [2] and antibacterial drugs [3] or in the treatment of some illnesses: like the treatment of cancer [4], of the Parkinson [5] and Alzheimer [6] diseases, schizophrenia [6], HIV [7], as well as anti-inflammatory [2], for the treatment of drugs dependents [8], etc. In relation to piperidinemethanol derivatives, they are referenced as intermediates for antipsychotic drugs, 5-HT receptor antagonists and potential anxiolytics [9].…”

Section: Introductionmentioning

confidence: 99%

Standard molar enthalpies of formation of 2-, 3-, and 4-piperidinomethanol isomers

Silva

Cabral

2006

The Journal of Chemical Thermodynamics

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4-Piperidinopiperidine-resistant lymphoma cells were resistant to dexamethasone- and A23187-induced apoptosis

Cited by 8 publications

References 10 publications

Combination therapy with irinotecan and protein kinase C inhibitors in malignant glioma

Combination therapy with irinotecan and protein kinase C inhibitors in malignant glioma

Muscle-fiber characteristics in adult mouse-tongue muscles

Standard molar enthalpies of formation of 2-, 3-, and 4-piperidinomethanol isomers

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