JOURNAL ARTICLE

DST regulates cisplatin resistance in colorectal cancer via PI3K/Akt pathway.

  • Published In: Journal of Pharmacy & Pharmacology, 2025, v. 77, n. 5. P. 698 1 of 3

  • Database: Academic Search Ultimate 2 of 3

  • Authored By: Yu, Jianwei; Deng, Xueqiong; Lin, Xueqin; Xie, Li; Guo, Sisi; Lin, Xiaoliang; Lin, Dong 3 of 3

Abstract

This article investigates the role of dystonin (DST), a potential tumor suppressor gene, in colorectal cancer (CRC) progression and resistance to cisplatin (DDP) chemotherapy. The study found that DST expression is significantly reduced in CRC tumors and DDP-resistant CRC tissues compared to normal and paracancerous tissues. Experimental upregulation of DST in CRC and DDP-resistant cell lines inhibited cell proliferation, invasion, migration, and angiogenesis while promoting apoptosis, effects mediated through suppression of the PI3K/Akt signaling pathway. In vivo, DST overexpression reduced tumor growth and mitigated DDP resistance in xenograft mouse models, suggesting DST as a promising therapeutic target for overcoming chemoresistance in CRC.

Additional Information

  • Source:Journal of Pharmacy & Pharmacology. 2025/05, Vol. 77, Issue 5, p698
  • Document Type:Article
  • Subject Area:Health and Medicine
  • Publication Date:2025
  • ISSN:0022-3573
  • DOI:10.1093/jpp/rgae104
  • Accession Number:185322015
  • Copyright Statement:Copyright of Journal of Pharmacy & Pharmacology is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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