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Updated: Oct 23, 2025
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
CALCR knockdown inhibits the development and progression of non-small-cell lung cancer
1Department of Cardio-thoracic Surgery, The Second Affiliated Hospital of Chengdu Medical College (China National Nuclear Corporation 416 Hospital), Chengdu, Sichuan, China.
Abstract:
G-protein-coupled receptors (GPCRs) have been reported to participate in the occurrence and development of a variety of human cancers. CALCR is one of the hundreds of GPCRs, but its expression level and functional importance have never been investigated in non-small-cell lung cancer (NSCLC). In the present study, the protein expression level of CALCR was detected by immunohistochemical staining and western blot analysis. The Celigo cell counting assay was used to assess cell proliferation. Both the wound-healing assay and the transwell assay were performed to evaluate cell migration. Flow cytometric analysis was utilized to detect cell apoptosis and cell cycle. A mouse xenograft model was constructed to conduct the in vivo experiments. The results indicated that the CALCR expression was abundantly up-regulated in NSCLC and positively related to tumor infiltrate. Besides, CALCR knockdown could significantly suppress cell proliferation, migration, enhance apoptosis and arrest cell cycle. The in vivo study verified the inhibitory effects of CALCR knockdown on NSCLC tumorigenesis. The abovementioned results provided a reference for the treatment of NSCLC, that was, CALCR knockdown might be a considerable therapeutic strategy.
Insights
CALCR, a G-protein-coupled receptor, is upregulated in non-small-cell lung cancer (NSCLC). Its reduction suppresses tumor growth, migration, and enhances apoptosis, suggesting CALCR as a potential therapeutic target for NSCLC.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- G-protein-coupled receptors (GPCRs) are implicated in various human cancers.
- The role of CALCR, a specific GPCR, in non-small-cell lung cancer (NSCLC) remains uninvestigated.
Purpose of the Study:
- To investigate the expression level and functional significance of CALCR in NSCLC.
- To explore the potential of CALCR as a therapeutic target for NSCLC.
Main Methods:
- Immunohistochemical staining and Western blot analysis for CALCR protein expression.
- Cell counting assays (Celigo) for proliferation, wound-healing and Transwell assays for migration.
- Flow cytometry for apoptosis and cell cycle analysis, and in vivo mouse xenograft models.
Main Results:
- CALCR expression is significantly upregulated in NSCLC tissues and correlates with tumor infiltrate.
- CALCR knockdown inhibits NSCLC cell proliferation and migration, induces apoptosis, and arrests the cell cycle.
- In vivo studies confirm that CALCR knockdown suppresses NSCLC tumor growth.
Conclusions:
- CALCR is a key driver in NSCLC progression.
- Targeting CALCR through knockdown presents a promising therapeutic strategy for NSCLC treatment.
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