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

Jianwei Yu1, Xueqiong Deng1, Xueqin Lin1

  • 1Department of Gastroenterology, Longyan First Affiliated Hospital of Fujian Medical University, Longyan 364000, Fujian Province, China.

The Journal of Pharmacy and Pharmacology
|October 17, 2024
PubMed
Abstract

Insights

Dystonin (DST) is reduced in colorectal cancer (CRC) and its restoration inhibits tumor growth and chemoresistance. Upregulating DST may offer new therapeutic strategies for CRC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Dystonin (DST) is implicated in cancer cell proliferation and chemotherapy resistance.
  • The specific role of DST in colorectal cancer (CRC) and its modulation of cisplatin (DDP) resistance remains under-investigated.

Purpose of the Study:

  • To investigate the molecular role of DST in colorectal cancer (CRC).
  • To elucidate DST's function in modulating cisplatin (DDP) resistance in CRC.

Main Methods:

  • Analysis of DST expression in CRC tissues and cell lines.
  • In vitro studies using lentiviral overexpression and shRNA knockdown of DST to assess cell viability, apoptosis, invasion, migration, and proliferation.
  • In vivo evaluation in xenograft mouse models to determine DST's effect on tumor growth and DDP resistance.

Main Results:

  • DST expression was significantly lower in CRC and DDP-resistant tissues.
  • DST upregulation inhibited CRC cell viability, proliferation, invasion, and migration, while promoting apoptosis.
  • DST overexpression reduced angiogenesis, attenuated DDP-induced cytotoxicity, and suppressed DDP resistance via the PI3K/Akt pathway, both in vitro and in vivo.

Conclusions:

  • DST acts as a suppressor of CRC progression and a modulator of DDP resistance.
  • Targeting DST presents a potential therapeutic strategy for enhancing CRC treatment outcomes.
Keywords:
DSTPI3K/Akt pathwaycisplatincisplatin resistancecolorectal cancer

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