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GEO help: Mouse over screen elements for information. |
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Status |
Public on Feb 14, 2024 |
Title |
Knockdown of NCAPD3 inhibits the tumorigenesis of non-small cell lung cancer by regulation of the PI3K/Akt pathway |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by high throughput sequencing
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Summary |
Background: Accumulating evidence indicates that aberrant non-SMC condensin II complex subunit D3 (NCAPD3) is associated with carcinogenesis of various cancers. Nevertheless, the biological role of NCAPD3 in the pathogenesis of non-small cell lung cancer (NSCLC) remains unclear.Methods: Immunohistochemistry and Western blot were performed to assess NCAPD3 expression in NSCLC tissues and cell lines. The ability of cell proliferation, invasion, and migration was evaluated by CCK-8 assays, EdU assays, Transwell assays, and scratch wound healing assays. Flow cytometry was performed to verify the cell cycle and apoptosis. RNA-sequence and rescue experiment were performed to reveal the underlying mechanisms.Results: The results showed that the expression of NCAPD3 was significantly elevated in NSCLC tissues. In NSCLC patients, high NCAPD3 expression was substantially associated with a worse prognosis. Functionally, knockdown of NCAPD3 resulted in cell apoptosis and cell cycle arrest in NSCLC cells as well as a significant inhibition of proliferation, invasion, and migration. Furthermore, RNA-sequencing analysis suggested that NCAPD3 contributes to NSCLC cancer carcinogenesis by regulating PI3K/Akt/FOXO4 pathway. Insulin-like growth factors-1 (IGF-1), a PI3K/Akt signaling activator, could reverse NCAPD3 silence-mediated proliferation inhibition and apoptosis in NSCLC cells.Conclusion: NCAPD3 suppresses apoptosis and promotes cell proliferation via the PI3K/Akt/FOXO4 signaling pathway, suggesting a potential use for NCAPD3 inhibitors as NSCLC therapeutics.
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Overall design |
To investigate the role of NCAPD3 in regulating the progression of non-small cell lung cancer, we established A549 and SPCA-1 cell lines with target genes knocked down by shRNA
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Contributor(s) |
Yang F, Zheng Y, Luo Q, Zhang S |
Citation(s) |
38566039 |
Submission date |
Dec 06, 2023 |
Last update date |
Apr 17, 2024 |
Contact name |
Xiangqi Chen |
E-mail(s) |
drchxqtg@126.com
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Organization name |
Fujian Medical University Union Hospital
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Street address |
NO.29 of Xinquan Road, Gulou District
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City |
Fuzhou |
ZIP/Postal code |
350000 |
Country |
China |
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Platforms (1) |
GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
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Samples (6)
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Relations |
BioProject |
PRJNA1049503 |
Supplementary file |
Size |
Download |
File type/resource |
GSE249569_Processed_data.txt.gz |
4.7 Mb |
(ftp)(http) |
TXT |
SRA Run Selector |
Raw data are available in SRA |
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