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Peer-reviewedCC BY-NC-NDPurinergic signalling

Targeting P2Y₁₄R inhibits proliferation of cervical cancer cells and organoids and activates cAMP/PKA/CREB signaling pathway.

  • Rui Li1
  • Hai-Yun Xiong2
  • Shi-Yu Chen1
  • Yong Tang3
  • Wen-Bin Ma4
4 affiliations
  1. 1International Joint Research Centre On Purinergic Signalling, School of Health and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
  2. 2Sichuan Science City Hospital, Mianyang, 621999, China.
  3. 3International Joint Research Centre On Purinergic Signalling, School of Health and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. [email protected].
  4. 4International Joint Research Centre On Purinergic Signalling, School of Health and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. [email protected].
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Abstract

Purinergic signaling has been widely recognized as a critical regulator of tumor progression, yet the role of P2Y₁₄R in cervical cancer remains unclear. This study used the P2Y₁₄R antagonist PPTN in in vitro cell experiments; the results showed that it significantly inhibited cell proliferation and increased LDH release. The anti-tumor effect of P2Y₁₄R antagonism was further validated using a cervical cancer organoid model. Mechanistically, PPTN treatment elevated intracellular cAMP levels, enhanced the phosphorylation of PKA and CREB, and thereby activated the cAMP/PKA/CREB signaling axis. Moreover, PPTN intervention reduced Ki67 expression in cervical cancer organoids without affecting CK13 expression, suggesting that the anti-tumor effect of PPTN may not mediated through regulation of differentiation. Collectively, these findings identify P2Y₁₄R as a novel regulator of the cAMP/PKA/CREB signaling pathway in cervical cancer cells, providing a promising therapeutic target for cervical cancer.

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Cite

BibTeXRIS
BibTeX
@article{li2026targeting,
  title = {{Targeting P2Y₁₄R inhibits proliferation of cervical cancer cells and organoids and activates cAMP/PKA/CREB signaling pathway.}},
  author = {Rui Li and Hai-Yun Xiong and Shi-Yu Chen and Yong Tang and Wen-Bin Ma},
  journal = {Purinergic signalling},
  year = {2026},
  month = oct,
  doi = {10.1007/s11302-026-10192-0},
  url = {https://europepmc.org/article/MED/42873384},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Targeting P2Y₁₄R inhibits proliferation of cervical cancer cells and organoids and activates cAMP/PKA/CREB signaling pathway.
AU  - Rui Li
AU  - Hai-Yun Xiong
AU  - Shi-Yu Chen
AU  - Yong Tang
AU  - Wen-Bin Ma
PY  - 2026
DA  - 2026/10/14
JO  - Purinergic signalling
DO  - 10.1007/s11302-026-10192-0
UR  - https://europepmc.org/article/MED/42873384
AB  - Purinergic signaling has been widely recognized as a critical regulator of tumor progression, yet the role of P2Y₁₄R in cervical cancer remains unclear. This study used the P2Y₁₄R antagonist PPTN in in vitro cell experiments; the results showed that it significantly inhibited cell proliferation and increased LDH release. The anti-tumor effect of P2Y₁₄R antagonism was further validated using a cervical cancer organoid model. Mechanistically, PPTN treatment elevated intracellular cAMP levels, enhanced the phosphorylation of PKA and CREB, and thereby activated the cAMP/PKA/CREB signaling axis. Moreover, PPTN intervention reduced Ki67 expression in cervical cancer organoids without affecting CK13 expression, suggesting that the anti-tumor effect of PPTN may not mediated through regulation of differentiation. Collectively, these findings identify P2Y₁₄R as a novel regulator of the cAMP/PKA/CREB signaling pathway in cervical cancer cells, providing a promising therapeutic target for cervical cancer.
SN  - 1573-9538
SN  - 1573-9546
ER  -