Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Substance P (SP) immunoreactivity was demonstrated using the indirect immunofluorescence technique in one normal and one retinoblastomatous human retina. In the normal retina SP immunoreaction was located in nerve fibres but not in the neurons in the inner plexiform layer. A similar location was observed in the histologically normal areas of the retinoblastoma sample. SP immunoreactive neurons, probably amacrine cells, were, however, observed in the transitional area between the normal retina and the tumour. The tumour mass, although mainly SP negative, contained clusters of pleomorphic cells with an intense SP immunoreaction. The general distribution of SP immunoreaction in human retina resembles that of other mammals. The positive SP immunoreaction in retinoblastoma cells suggests that the tumour either may have its origin in the amacrine cells or that the retinoblasts are capable of redifferentiating in the direction of the amacrine cell population. The general problems concerning the origin and pathogenesis of retinoblastoma are discussed.
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PMID:Substance P immunoreactivity in normal human retina and in retinoblastoma. 619 10

In this study, expressions of cell-cycle-related genes: p53, retinoblastoma (Rb), p21, bcl-2(alpha), bcl-2(beta); protooncogene c-ski; glial cell marker protein gene S100beta; neurotransmitter gene, substance P and sexual-differentiation-related genes, androgen receptor (AR) and estrogen receptor beta (ER(beta)), are studied in the olfactory bulb of groups of both six female and six male rats at the ages of 3, 10, 20 and 40 days. Expressions of housekeeping genes such as beta-actin, cyclophilin and proliferating cell nuclear antigens (PCNA) are determined using reverse transcription polymerase chain reaction (RT-PCR) for the correction of unequal amount of cDNA added into the samples. Using labeled 32P-dCTP and Phosphorimager technology, relative abundance of radioactivities of the PCR products is obtained by dividing the radioactivity of each individual sample by the corresponding radioactivities of different housekeeping genes. Data evaluated by Two-way ANOVA indicate that only the bcl-2(alpha) gene expression is affected significantly by age, sex and their interactions no matter which of the three housekeeping genes is used for correction. When beta-actin was used for corrections, effects of age but not sex were found in the expressions of p53, Rb, p21, AR, ER(beta), substance P and S100beta genes, but not in bcl-2(beta), c-ski, cyclophilin and PCNA genes. While cyclophilin was used for corrections, only the p53, Rb, AR, ER(beta), substance P and S100beta but not the bcl-2(beta), p21, c-ski, PCNA and beta-actin genes are affected by age. They are all not influenced by sex of the animals. Only the AR, ER(beta) and S100beta genes are age-dependent when PCNA was used for the correction. The other gene expressions are not altered by sex, while the interactions of age and sex were found to be significantly affecting the bcl-2(beta) gene expression. Conclusively, developmental changes of the p53, Rb, AR, ER(beta), substance P and S100beta genes expressions are quite evidenced while only the bcl-2(alpha) gene seems to change significantly during the sexual differentiation of olfactory bulb in rats.
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PMID:Gene expressions during the development and sexual differentiation of the olfactory bulb in rats. 1067 68

Aprepitant is a selective high-affinity antagonist of human substance P (SP)/Neurokinin-1 (NK-1) receptors. Until now this drug has been used as anxiolytic, antidepressant and antiemetic. It has been demonstrated that SP induces cell proliferation and NK-1 receptor antagonists different to aprepitant inhibit growth in several human cancer cell lines, where NK-1 receptors are overexpressed. The purpose of this study is to demonstrate the antitumor action of aprepitant. We performed an in vitro study of the growth inhibition capacity of the NK-1 receptor antagonist aprepitant against glioma, neuroblastoma, retinoblastoma and pancreas, larynx, gastric and colon carcinomas cell lines. Coulter counter was used to determine viable cell numbers followed by application of the MTS colorimetric method. Furthermore, a DAPI method was applied to demonstrate apoptosis. We have demonstrated: aprepitant at (5-70 microM) concentration elicits growth cell inhibition in a concentration dependent manner in all tumor cell line studied. Maximum inhibition (100%) was observed when the aprepitant was administered at a concentration of > or = 70 microM in all tumor cell lines studied. The specific antitumor action of aprepitant occurs through the NK-1 receptor and tumor cells death was by apoptosis pathway. These findings reported here for the first time indicate that aprepitant is a new and promising broad spectrum antitumor drug in the treatment of cancer.
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PMID:The NK-1 receptor antagonist aprepitant as a broad spectrum antitumor drug. 1914 78

Cyclosporin A (CsA) is an immunosuppressive drug. In human cancer cells substance P (SP) and neurokinin-1 (NK-1) receptor antagonists, respectively, induce cell proliferation and inhibition. CsA is a tachykinin receptor antagonist that showed selectivity for both NK-1 and NK-2 receptors. CsA exerts antitumor action against gastric (AGS) and colon (HT29) carcinoma cell lines. However, the mechanisms involved in this action remain unknown, and it is unknown whether CsA exerts an antitumor action on other human cancer cell lines or not. To demonstrate that CsA exerts a broad-spectrum antitumor action, we carried out an in vitro study of the growth-inhibitory capacity of CsA against seven human cancer cell lines, namely GAMG glioma, SKN-BE(2) neuroblastoma, WERI-Rb-1 retinoblastoma, HEp-2 larynx carcinoma, CAPAN pancreas carcinoma, 23132/87 gastric carcinoma, and SW-403 colon carcinoma. A Coulter counter was used to determine viable cell numbers followed by application of the MTS colorimetric method. Micromolar concentrations of CsA inhibited the growth of these tumor cells, both with and without previous administration of nanomolar concentrations of SP; the inhibition occurred in a dose-dependent manner. Moreover, CsA blocks SP-induced mitogen stimulation of tumor cells, suggesting that the NK-1 receptor is involved in such action. Following administration of CsA apoptosis was observed in the above seven tumor cell lines. These findings suggest that the antitumor action of CsA is at least due to its NK-1 receptor antagonist pharmacological profile, since the involvement of NK-2 receptors in the mentioned action must not be discarded, and that CsA has a broad-spectrum antitumor action.
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PMID:The broad-spectrum antitumor action of cyclosporin A is due to its tachykinin receptor antagonist pharmacological profile. 2054 69