KEY TAKEAWAYS
- The study aimed to investigate the involvement of NCAPD3 in the pathogenesis of NSCLC and its potential role as a carcinogenic factor.
- Researchers noticed that targeting NCAPD3 could offer a promising therapeutic strategy for NSCLC by inhibiting apoptosis suppression and cell proliferation through the PI3K/Akt/FOXO4 signaling pathway.
Accumulating evidence suggests non-SMC condensin II complex subunit D3 (NCAPD3) involvement in various cancers, yet its role in non-small cell lung cancer (NSCLC) remains unclear.
Fan Yang and the team aimed to assess NCAPD3’s biological significance in NSCLC pathogenesis.
Researchers performed an inclusive analysis utilizing immunohistochemistry and Western blot to assess NCAPD3 expression in NSCLC tissues and cell lines. Cell proliferation, invasion, and migration abilities were evaluated through CCK-8 assays, EdU assays, Transwell assays, and scratch wound healing assays. Flow cytometry was utilized to verify the cell cycle and apoptosis. RNA-sequence and rescue experiments were conducted to reveal the underlying mechanisms.
About the results, the expression of NCAPD3 was notably elevated in NSCLC tissues, with high expression correlating significantly with poorer prognosis. Knockdown of NCAPD3 induced cell apoptosis and cell cycle arrest in NSCLC cells, along with a marked reduction in proliferation, invasion, and migration.
RNA-sequencing analysis indicated that NCAPD3 contributes to NSCLC carcinogenesis by regulating the PI3K/Akt/FOXO4 pathway. Furthermore, insulin-like growth factors-1 (IGF-1), an PI3K/Akt signaling pathway activator, reversed the proliferation inhibition and apoptosis induced by NCAPD3 silence in NSCLC cells.
The study concluded that NCAPD3 exerts its effects by suppressing apoptosis and promoting cell proliferation through the PI3K/Akt/FOXO4 signaling pathway, indicating the potential utility of NCAPD3 inhibitors as therapeutics for NSCLC.
The study was sponsored by the Fujian Provincial Health Technology Project, the Science Technology Innovation Joint Project Foundation of Fujian Province, and the Natural Science Foundation of Fujian Province.
Source: https://pubmed.ncbi.nlm.nih.gov/38566039/
Yang F, Zheng Y, Luo Q, et al. (2024). “Knockdown of NCAPD3 inhibits the tumorigenesis of non-small cell lung cancer by regulation of the PI3K/Akt pathway.” BMC Cancer. 2024 Apr 2;24(1):408. doi: 10.1186/s12885-024-12131-x. PMID: 38566039; PMCID: PMC10986035.
