substance-p--phe(5)-trp(7-9)-leu(11)- and Carcinoma--Squamous-Cell

substance-p--phe(5)-trp(7-9)-leu(11)- has been researched along with Carcinoma--Squamous-Cell* in 2 studies

Other Studies

2 other study(ies) available for substance-p--phe(5)-trp(7-9)-leu(11)- and Carcinoma--Squamous-Cell

Article	Year
[D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P induces apoptosis in lung cancer cell lines in vitro. Biochemical and biophysical research communications, 1994, Mar-30, Volume: 199, Issue:3 The broad spectrum antagonist [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P has been shown previously to inhibit the growth of small cell lung cancer cells both in vitro and in vivo. To elucidate further the pathways involved in the growth inhibitory actions of [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P we have examined the effect of this agent on cell viability and the induction of apoptosis in small cell and non-small cell lung cancer cells. Treatment of lung tumor cells with [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P caused a concentration-dependent loss of cell viability which was accompanied by the onset of apoptosis, as defined by cytological criteria and DNA fragmentation. This effect occurred in both small cell and non-small cell lung cancer cells and was not dependent on de novo protein synthesis. Such findings indicate that the antiproliferative action of [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P involves a signal transduction pathway for apoptosis. Topics: Adenocarcinoma; Antineoplastic Agents; Apoptosis; Carcinoma, Large Cell; Carcinoma, Non-Small-Cell Lung; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Cell Line; Cell Survival; DNA Damage; DNA, Neoplasm; Flow Cytometry; Humans; Kinetics; Lung Neoplasms; Substance P; Time Factors; Tumor Cells, Cultured	1994
In vitro effects of substance P analogue [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P on human tumour and normal cell growth. British journal of cancer, 1992, Volume: 65, Issue:3 Analogues of the neurotransmitter substance P (SP) can interact with neuropeptide receptors, and are reported to inhibit growth of small cell lung cancer cell lines (SCLC CLs). We found [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P (D-Phe5SP) significantly inhibited DNA synthesis by 10/10 human tumour CLs; six SCLC, one N-SCLC (squamous), two ovarian and one squamous cervical carcinoma, with inhibition to 50% control levels (IC50) of 20-50 microM. There was dose dependent inhibition of colony forming efficiency (CFE) in 3/3 SCLC and 1/1 N-SCLC CL, IC50s of 0.5-6.5 microM in 5% serum. Exposure of SCLC CL HC12 to 100 microM D-Phe5SP for 1-4 h caused a progressive fall in viable cell number; surviving cells, grown in the absence of peptide, showed a decreased growth rate. During 1 week's exposure of two SCLC CLs to 20 microM D-Ph5SP, growth was slower than control cultures, while 50-100 microM completely inhibited growth. These inhibitory effects were partially reversed by increasing serum concentration from 5 to 20%, but not by SP, vasopressin, bombesin or insulin-like growth factor 1. There was some inhibition of CFE by 3/3 normal human bone marrows, IC50s of 30-80 microM, compared with 8 microM for HC12 in 20% FCS. Therefore D-Phe5SP appears to have more potent antiproliferative effects in tumour cells than normal cells, suggesting a role for this analogue in tumour treatment. Topics: Analysis of Variance; Antineoplastic Combined Chemotherapy Protocols; Bombesin; Bone Marrow; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Cell Division; Cell Line; Colony-Forming Units Assay; DNA; Dose-Response Relationship, Drug; Female; Fibroblasts; Humans; In Vitro Techniques; Insulin-Like Growth Factor I; Lung Neoplasms; Ovarian Neoplasms; Substance P; Time Factors; Vasopressins	1992

Article

Year

[D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P induces apoptosis in lung cancer cell lines in vitro.

Biochemical and biophysical research communications, 1994, Mar-30, Volume: 199, Issue:3

The broad spectrum antagonist [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P has been shown previously to inhibit the growth of small cell lung cancer cells both in vitro and in vivo. To elucidate further the pathways involved in the growth inhibitory actions of [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P we have examined the effect of this agent on cell viability and the induction of apoptosis in small cell and non-small cell lung cancer cells. Treatment of lung tumor cells with [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P caused a concentration-dependent loss of cell viability which was accompanied by the onset of apoptosis, as defined by cytological criteria and DNA fragmentation. This effect occurred in both small cell and non-small cell lung cancer cells and was not dependent on de novo protein synthesis. Such findings indicate that the antiproliferative action of [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P involves a signal transduction pathway for apoptosis.

Topics: Adenocarcinoma; Antineoplastic Agents; Apoptosis; Carcinoma, Large Cell; Carcinoma, Non-Small-Cell Lung; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Cell Line; Cell Survival; DNA Damage; DNA, Neoplasm; Flow Cytometry; Humans; Kinetics; Lung Neoplasms; Substance P; Time Factors; Tumor Cells, Cultured

1994

In vitro effects of substance P analogue [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P on human tumour and normal cell growth.

British journal of cancer, 1992, Volume: 65, Issue:3

Analogues of the neurotransmitter substance P (SP) can interact with neuropeptide receptors, and are reported to inhibit growth of small cell lung cancer cell lines (SCLC CLs). We found [D-Arg1, D-Phe5, D-Trp7,9, Leu11] substance P (D-Phe5SP) significantly inhibited DNA synthesis by 10/10 human tumour CLs; six SCLC, one N-SCLC (squamous), two ovarian and one squamous cervical carcinoma, with inhibition to 50% control levels (IC50) of 20-50 microM. There was dose dependent inhibition of colony forming efficiency (CFE) in 3/3 SCLC and 1/1 N-SCLC CL, IC50s of 0.5-6.5 microM in 5% serum. Exposure of SCLC CL HC12 to 100 microM D-Phe5SP for 1-4 h caused a progressive fall in viable cell number; surviving cells, grown in the absence of peptide, showed a decreased growth rate. During 1 week's exposure of two SCLC CLs to 20 microM D-Ph5SP, growth was slower than control cultures, while 50-100 microM completely inhibited growth. These inhibitory effects were partially reversed by increasing serum concentration from 5 to 20%, but not by SP, vasopressin, bombesin or insulin-like growth factor 1. There was some inhibition of CFE by 3/3 normal human bone marrows, IC50s of 30-80 microM, compared with 8 microM for HC12 in 20% FCS. Therefore D-Phe5SP appears to have more potent antiproliferative effects in tumour cells than normal cells, suggesting a role for this analogue in tumour treatment.

Topics: Analysis of Variance; Antineoplastic Combined Chemotherapy Protocols; Bombesin; Bone Marrow; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Cell Division; Cell Line; Colony-Forming Units Assay; DNA; Dose-Response Relationship, Drug; Female; Fibroblasts; Humans; In Vitro Techniques; Insulin-Like Growth Factor I; Lung Neoplasms; Ovarian Neoplasms; Substance P; Time Factors; Vasopressins

1992