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Id2 exerts tumor suppressor properties in lung cancer through its effects on cancer cell invasion and migration
Jian-Ting Chen1, Yuan-Ling Hsu2, Yi-Chiung Hsu3
1Graduate Institute of Biomedical and Pharmaceutical Science, Fu Jen Catholic University, New Taipei City, Taiwan.
Background:
Despite advances in prognosis and treatment of lung adenocarcinoma (LADC), a notable non-small cell lung cancer subtype, patient outcomes are still unsatisfactory. New insight on novel therapeutic strategies for LADC may be gained from a more comprehensive understanding of cancer progression mechanisms. Such strategies could reduce the mortality and morbidity of patients with LADC. In our previous study, we performed cDNA microarray screening and found an inverse relationship between inhibitor of DNA binding 2 (Id2) expression levels and the invasiveness of LADC cells.
Materials And Methods:
To identify the functional roles of Id2 and its action mechanisms in LADC progression, we successfully established several Id2-overexpressing and Id2-silenced LADC cell clones. Subsequently, we examined in vitro the effects exerted by Id2 on cell morphology, proliferation, colony formation, invasive, and migratory activities and examined in vivo those exerted by Id2 on cell metastasis. The mechanisms underlying the action of Id2 were investigated using RNA-seq and pathway analyses. Furthermore, the correlations of Id2 with its target gene expression and clinical outcomes were calculated.
Results:
Our data revealed that Id2 overexpression could inhibit LADC cells' migratory, invasive, proliferation, and colony formation capabilities. Silencing Id2 expression in LADC cells reversed the aforementioned inhibitory effects, and knockdown of Id2 increased LADC cells' metastatic abilities in vivo. Bioinformatics analysis revealed that these effects of Id2 on cancer progression might be regulated by focal adhesion kinase (FAK) signaling and CD44/Twist expression. Furthermore, in online clinical database analysis, patients with LADC whose Id2 expression levels were high and FAK/Twist expression levels were low had superior clinical outcomes.Conclusion: Our data indicate that the Id2 gene may act as a metastasis suppressor and provide new insights into LADC progression and therapy.
Insights
Inhibitor of DNA binding 2 (Id2) suppresses lung adenocarcinoma (LADC) metastasis by inhibiting cell migration and invasion. High Id2 expression correlates with better patient outcomes, suggesting Id2 as a therapeutic target for LADC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Lung adenocarcinoma (LADC) remains a significant health concern with unsatisfactory patient outcomes despite treatment advances.
- Understanding cancer progression mechanisms is crucial for developing novel therapeutic strategies for LADC.
- Previous studies indicated an inverse relationship between inhibitor of DNA binding 2 (Id2) expression and LADC cell invasiveness.
Purpose of the Study:
- To elucidate the functional roles and mechanisms of Id2 in LADC progression.
- To investigate the impact of Id2 on LADC cell behavior both in vitro and in vivo.
- To explore the potential of Id2 as a therapeutic target for LADC.
Main Methods:
- Establishment of Id2-overexpressing and Id2-silenced LADC cell clones.
- In vitro assays assessing cell morphology, proliferation, colony formation, invasion, and migration.
- In vivo metastasis assays.
- RNA-sequencing and pathway analyses to identify Id2-regulated mechanisms.
- Correlation analysis of Id2 expression with target genes and clinical outcomes.
Main Results:
- Id2 overexpression inhibited LADC cell migration, invasion, proliferation, and colony formation.
- Id2 silencing enhanced LADC cell metastatic potential in vivo.
- Bioinformatics analysis suggested Id2 regulates focal adhesion kinase (FAK) signaling and CD44/Twist expression.
- High Id2 and low FAK/Twist expression correlated with superior clinical outcomes in LADC patients.
Conclusions:
- The Id2 gene functions as a metastasis suppressor in lung adenocarcinoma.
- Id2 influences LADC progression through pathways involving FAK and CD44/Twist.
- Id2 represents a promising therapeutic target for improving LADC patient outcomes.
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