CRISPLD1 promotes gastric cancer progression by regulating the Ca2+/PI3K-AKT signaling pathway
Liqiang Hu,
Jianghua Shi,
Zichen Zhu,
Xuemei Lu,
Huibo Jiang,
Hanyang Yu,
Hao Liu,
Wei Chen
Affiliations
Liqiang Hu
Graduate school of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China; Cancer Institute of Integrated Traditional Chinese and Western Medicine, Key Laboratory of Cancer Prevention and Therapy Combining Traditional Chinese and Western Medicine of Zhejiang Province, Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, Zhejiang, China
Jianghua Shi
Graduate school of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
Zichen Zhu
Graduate school of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
Xuemei Lu
Graduate school of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China; Cancer Institute of Integrated Traditional Chinese and Western Medicine, Key Laboratory of Cancer Prevention and Therapy Combining Traditional Chinese and Western Medicine of Zhejiang Province, Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, Zhejiang, China
Huibo Jiang
Graduate school of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China; Cancer Institute of Integrated Traditional Chinese and Western Medicine, Key Laboratory of Cancer Prevention and Therapy Combining Traditional Chinese and Western Medicine of Zhejiang Province, Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, Zhejiang, China
Hanyang Yu
School of Computer Science, University of Nottingham Ningbo China, Ningbo, China
Hao Liu
Graduate school of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China; Cancer Institute of Integrated Traditional Chinese and Western Medicine, Key Laboratory of Cancer Prevention and Therapy Combining Traditional Chinese and Western Medicine of Zhejiang Province, Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, Zhejiang, China; Corresponding author. Cancer Institute of Integrated Traditional Chinese and Western Medicine, Key Laboratory of Cancer Prevention and Therapy Combining Traditional Chinese and Western Medicine of Zhejiang Province, Zhejiang Academy of Traditional Chinese Medicine, No. 234, Gucui Road, Hangzhou, Zhejiang, 310012, China.
Wei Chen
Graduate school of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China; Cancer Institute of Integrated Traditional Chinese and Western Medicine, Key Laboratory of Cancer Prevention and Therapy Combining Traditional Chinese and Western Medicine of Zhejiang Province, Zhejiang Academy of Traditional Chinese Medicine, Hangzhou, Zhejiang, China; Corresponding author. Cancer Institute of Integrated Traditional Chinese and Western Medicine, Key Laboratory of Cancer Prevention and Therapy Combining Traditional Chinese and Western Medicine of Zhejiang Province, Zhejiang Academy of Traditional Chinese Medicine, No. 234, Gucui Road, Hangzhou, Zhejiang, 310012, China.
Gastric cancer (GC) is a malignant tumor with poor prognosis. Studies have shown that cysteine-rich secretory protein LCCL domain containing 1 (CRISPLD1) is associated with tumor progression. However, its role in GC is unclear. The present study aimed to determine the pathogenic mechanism of CRISPLD1 in GC. Analysis of public databases revealed high mRNA expression of CRISPLD1 in GC, which was associated with poor prognosis. Additionally, CRISPLD1 expression levels showed significant correlations with T stage, overall survival events, and stage. Knockdown of CRISPLD1 reduced cell proliferation, invasion, and migration. Furthermore, CRISPLD1 knockdown decreased intracellular calcium levels in GC cells and inhibited the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)-protein kinase B (AKT) signaling pathway. Treatment with an AKT activator reversed the inhibitory effect of CRISPLD1 knockdown on GC cell migration and invasion. Our findings suggest that CRISPLD1 promotes tumor cell progression in GC by mediating intracellular calcium levels and activating the PI3K-AKT pathway, highlighting CRISPLD1 as a potential therapeutic target for GC.