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  1. Home
  2. Crispld1 Promotes Gastric Cancer Progression By Regulating The Ca2+/pi3k-akt Signaling Pathway.
  1. Home
  2. Crispld1 Promotes Gastric Cancer Progression By Regulating The Ca2+/pi3k-akt Signaling Pathway.

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CRISPLD1 promotes gastric cancer progression by regulating the Ca2+/PI3K-AKT signaling pathway.

Liqiang Hu1,2, Jianghua Shi1, Zichen Zhu1

  • 1Graduate school of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.

Heliyon
|March 15, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Cysteine-rich secretory protein LCCL domain containing 1 (CRISPLD1) promotes gastric cancer (GC) progression by affecting calcium levels and the PI3K-AKT pathway. Targeting CRISPLD1 may offer a new therapeutic strategy for GC patients.

Keywords:
CRISPLD1CalciumCancerGastricPI3K-AKT

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Gastric cancer (GC) presents a significant global health challenge with a generally poor prognosis.
  • Cysteine-rich secretory protein LCCL domain containing 1 (CRISPLD1) has been implicated in tumor progression, but its specific role in GC remains largely undefined.

Purpose of the Study:

  • To elucidate the pathogenic mechanism of CRISPLD1 in gastric cancer.
  • To investigate the potential of CRISPLD1 as a therapeutic target for GC.

Main Methods:

  • Analysis of public gene expression databases to correlate CRISPLD1 mRNA levels with GC patient data (prognosis, clinical stage).
  • In vitro experiments involving CRISPLD1 knockdown in GC cells to assess effects on proliferation, invasion, and migration.
  • Measurement of intracellular calcium levels and assessment of the PI3K-AKT signaling pathway activity following CRISPLD1 modulation.
  • Pharmacological intervention using an AKT activator to evaluate its impact on GC cell behavior after CRISPLD1 knockdown.
  • Main Results:

    • High CRISPLD1 mRNA expression in GC correlates with advanced T stage, increased overall survival events, and poorer prognosis.
    • CRISPLD1 knockdown significantly inhibited GC cell proliferation, invasion, and migration.
    • Downregulation of CRISPLD1 led to decreased intracellular calcium levels and suppressed the PI3K-AKT signaling pathway in GC cells.
    • AKT pathway activation reversed the inhibitory effects of CRISPLD1 knockdown on GC cell migration and invasion.

    Conclusions:

    • CRISPLD1 promotes gastric cancer progression through the regulation of intracellular calcium levels and activation of the PI3K-AKT signaling pathway.
    • CRISPLD1 represents a promising molecular target for the development of novel therapeutic strategies against gastric cancer.