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Study · In vitro (cells) · 1994

7 results

Cross-competition between vasoactive intestinal peptide and somatostatin for binding to tumor cell membrane receptors.

Virgolini I, Yang Q, Li S, Angelberger P, Neuhold N, Niederle B, Scheithauer W, Valent P

Cancer research1 Feb 1994Cited by 52 (Europe PMC)

PMID7905785 (opens in a new tab)PepBankPUB-07905785
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study7

4 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Activity measurement

    In tumor cells, VIP and somatostatin or octreotide cross-competed for binding to the cells.

    In plain wordsIn tumor cells grown in the lab, VIP and somatostatin or octreotide competed for the same binding sites.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    Not applicableCross-competition between VIP and SST/OCT for binding
    Study

    n: not reported in source

    tumor cell membranes, primary tumors and tumor cell lines
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Cross-competition between VIP and SST/OCT for binding to tumor cells was observed.
    1 context sentence
    Summary · context
    as well as on tumor cell lines (A431, HT29, PANC1, COLO320, HMC1, and KU812 cells)
  2. 02LabIn vitro (cells)Activity measurement

    In A431 cells, VIP was the most potent displacer of 123I-labeled VIP binding, with an IC50 of 2.9 nM.

    In plain wordsIn lab-grown A431 cells, VIP was the strongest competitor for its own binding site, at 2.9 nM.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    Not applicableVIP displacement of 123I-labeled VIP binding in A431 cells
    Study

    n: not reported in source

    A431 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Measurements

    IC50
    2.9 nM
    VIP displacing 123I-labeled VIP, A431 cells

    Source sentences

    Summary
    The rank-order of potency for displacement of 123I-labeled VIP binding to intact A431 cells was VIP [concentration causing half-maximal inhibition (IC50) = 2.9 +/- 1.9 (SD) nM] > OCT (IC50 = 9.3 +/- 1.7 nM) = SST > substance P = secretin (IC50 = 1 microM).
    1 context sentence
    Summary · context
    as well as on tumor cell lines (A431, HT29, PANC1, COLO320, HMC1, and KU812 cells)
  3. 03LabIn vitro (cells)Activity measurement

    In A431 cells, VIP inhibited binding of 123I-labeled Tyr-3-OCT with an IC50 of 4.9 nM, less potently than octreotide or somatostatin.

    In plain wordsIn lab-grown A431 cells, VIP blocked binding of labelled octreotide at 4.9 nM, less strongly than octreotide or somatostatin.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    Not applicableVIP inhibition of 123I-labeled Tyr-3-OCT binding in A431 cells
    Study

    n: not reported in source

    A431 cells
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Measurements

    IC50
    4.9 nM
    VIP inhibiting 123I-labeled Tyr-3-OCT binding, A431 cells

    Source sentences

    Summary
    Binding of 123I-labeled Tyr-3-OCT to A431 cells, in turn, was inhibited by OCT = Tyr-3-OCT (IC50 = 1.5 +/- 0.3 nM) = SST > VIP (IC50 = 4.9 +/- 1.1 nM).
    1 context sentence
    Summary · context
    as well as on tumor cell lines (A431, HT29, PANC1, COLO320, HMC1, and KU812 cells)
  4. 04LabIn vitro (cells)Activity measurement

    In primary tumors and tumor cell lines, the rank-order of potency seen in A431 cells for VIP and SST/OCT binding was also obtained.

    In plain wordsIn tumor samples and lab-grown tumor cells, VIP, somatostatin and octreotide showed the same strength order for binding as in A431 cells.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    Not applicableRank-order of binding potency in primary tumors and cell lines
    Study

    n: not reported in source

    tumor cell membranes, primary tumors and tumor cell lines
    Outcome group
    Receptor activity and mechanism · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    This rank-order of potency was also obtained for primary tumors and tumor cell lines.
    2 context sentences
    Summary · context
    The rank-order of potency for displacement of 123I-labeled VIP binding to intact A431 cells was VIP [concentration causing half-maximal inhibition (IC50) = 2.9 +/- 1.9 (SD) nM] > OCT (IC50 = 9.3 +/- 1.7 nM) = SST > substance P = secretin (IC50 = 1 microM).
    Summary · context
    as well as on tumor cell lines (A431, HT29, PANC1, COLO320, HMC1, and KU812 cells)

Studies that did not test the peptide alone3

In this study, Vasoactive intestinal peptide (VIP, aviptadil) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Vasoactive intestinal peptide (VIP, aviptadil).

  1. 05LabNot a test of Vasoactive intestinal peptide (VIP, aviptadil) aloneIn vitro (cells)Mechanism

    In tumor cells, somatostatin and octreotide inhibited VIP-induced [3H]thymidine incorporation with IC50 values below 10 nM.

    In plain wordsIn tumor cells, somatostatin and octreotide blocked a growth signal that VIP triggered.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    DecreaseSST/OCT inhibition of VIP-induced thymidine incorporation
    Study

    n: not reported in source

    tumor cell membranes, primary tumors and tumor cell lines
    Outcome group
    Receptor activity and mechanism · Cancer

    Measurements

    IC50
    < 10 nM
    SST and OCT inhibiting VIP-induced thymidine incorporation

    Source sentences

    Summary
    Furthermore, SST and OCT inhibited VIP-induced [3H]thymidine incorporation, cyclic AMP formation, and tyrosine kinase activity with IC50 values < 10 nM.
    1 context sentence
    Summary · context
    as well as on tumor cell lines (A431, HT29, PANC1, COLO320, HMC1, and KU812 cells)

    In this study, Vasoactive intestinal peptide (VIP, aviptadil) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Vasoactive intestinal peptide (VIP, aviptadil).

  2. 06LabNot a test of Vasoactive intestinal peptide (VIP, aviptadil) aloneIn vitro (cells)Mechanism

    In tumor cells, somatostatin and octreotide inhibited VIP-induced cyclic AMP formation with IC50 values below 10 nM.

    In plain wordsIn tumor cells, somatostatin and octreotide blocked the cAMP signal that VIP triggered.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    DecreaseSST/OCT inhibition of VIP-induced cAMP formation
    Study

    n: not reported in source

    tumor cell membranes, primary tumors and tumor cell lines
    Outcome group
    Receptor activity and mechanism · Cancer

    Measurements

    IC50
    < 10 nM
    SST and OCT inhibiting VIP-induced cAMP formation

    Source sentences

    Summary
    Furthermore, SST and OCT inhibited VIP-induced [3H]thymidine incorporation, cyclic AMP formation, and tyrosine kinase activity with IC50 values < 10 nM.
    1 context sentence
    Summary · context
    as well as on tumor cell lines (A431, HT29, PANC1, COLO320, HMC1, and KU812 cells)

    In this study, Vasoactive intestinal peptide (VIP, aviptadil) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Vasoactive intestinal peptide (VIP, aviptadil).

  3. 07LabNot a test of Vasoactive intestinal peptide (VIP, aviptadil) aloneIn vitro (cells)Mechanism

    In tumor cells, somatostatin and octreotide inhibited VIP-induced tyrosine kinase activity with IC50 values below 10 nM.

    In plain wordsIn tumor cells, somatostatin and octreotide blocked the tyrosine kinase activity that VIP triggered.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    DecreaseSST/OCT inhibition of VIP-induced tyrosine kinase activity
    Study

    n: not reported in source

    tumor cell membranes, primary tumors and tumor cell lines
    Outcome group
    Receptor activity and mechanism · Cancer

    Measurements

    IC50
    < 10 nM
    SST and OCT inhibiting VIP-induced tyrosine kinase activity

    Source sentences

    Summary
    Furthermore, SST and OCT inhibited VIP-induced [3H]thymidine incorporation, cyclic AMP formation, and tyrosine kinase activity with IC50 values < 10 nM.
    1 context sentence
    Summary · context
    as well as on tumor cell lines (A431, HT29, PANC1, COLO320, HMC1, and KU812 cells)

    In this study, Vasoactive intestinal peptide (VIP, aviptadil) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Vasoactive intestinal peptide (VIP, aviptadil).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    12 Oct 2026, 12:58 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 12:41 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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