Method Profile

PPTN Response in Cervical Cancer Organoids

Compare organoid viability, membrane damage, proliferation-associated staining and cAMP-pathway responses after PPTN exposure.

Tumor ModelsOrganoids
Pap-stained cervical squamous cancer cells, with pink cytoplasm and dark nuclei.
Cervical squamous cell carcinoma, Pap stain. (National Cancer Institute, Public domain (US government work))

Research Applications

Exploratory pharmacological assessment of a P2Y14-antagonist hypothesis in a cervical cancer culture model.

Model & Design

Supplied cervical cancer organoids, with HeLa and SiHa cell-line experiments providing parallel evidence. A donor cohort size is not stated.

Experimental Format

Organoid PPTN exposure for 72 hours; dose-response IC50 and 17 μM follow-up treatment. Cell-line conditions are separately specified.

Model Components

  • Component

    Biological models

    Description

    AimingMed-supplied cervical cancer organoids; HeLa and SiHa cell lines.

  • Component

    Readouts

    Description

    Luminescent organoid viability, LDH release, Ki67/CK13 immunofluorescence, cAMP ELISA and PKA/CREB immunoblotting.

Measurements & Endpoints

  • Organoid viability and IC50
  • LDH release
  • Ki67 and CK13 staining
  • Protein-normalized cAMP
  • PKA and CREB phosphorylation

Analysis

Viability, membrane damage, proliferation/differentiation markers and signaling are assessed separately against same-passage control cultures.

Published Evidence

  • Study Design

    PPTN dose-response followed by organoid endpoint comparison at 17 μM for 72 hours.

    Study Sample

    Cervical cancer organoid cultures; endpoint assays report n = 3 samples per group. The organoid donor count is not stated.

    Comparison

    Matched untreated/control organoids; HeLa and SiHa experiments analyzed separately.

    Finding

    Organoid IC50 was 34.88 μM at 72 hours. PPTN reduced viability and Ki67 staining, increased LDH release, cAMP levels and PKA/CREB phosphorylation, without an obvious CK13 change.

    Interpretation & Limits
    • No receptor-specific genetic perturbation was performed.
    • No clinical response validation or in vivo tumor test is presented.
    • Micromolar PPTN activity and unspecified donor denominator constrain interpretation.

Sources

  1. Targeting P2Y14R inhibits proliferation of cervical cancer cells and organoids and activates cAMP/PKA/CREB signaling pathway. Purinergic Signalling. 2026-10-14. DOI: 10.1007/s11302-026-10192-0. ↗