ArticleMolecular medicine reports2023
DEPDC1B is involved in the proliferation, metastasis, cell cycle arrest and apoptosis of colon cancer cells by regulating NUP37.
Article in Molecular medicine reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Transcription Activation of DEPDC1B Upon EBF1 Loss Contributes to Cell Cycle Progression and Epithelial-Mesenchymal Transition in Colon Adenocarcinoma.Biochemical genetics · 2026Article
- ASCL1 promotes nuclear shrinkage in transdifferentiation by suppressing NUP37.Stem cell reports · 2026Article
- Anti-tumor efficacy of RAF/MEK inhibitor VS6766 in KRAS-mutated colorectal cancer cells.Cancer chemotherapy and pharmacology · 2025Article
- Targeting colorectal cancer at the level of nuclear pore complex.Journal of advanced research · 2025Review
- Advances in the understanding of nuclear pore complexes in human diseases.Journal of cancer research and clinical oncology · 2024Review
- Genome wide-scale CRISPR-Cas9 knockout screens identify a fitness score for optimized risk stratification in colorectal cancer.Journal of translational medicine · 2024Article
- Fibroblast growth factor 23 regulates hypoxia‑induced osteoblast apoptosis through the autophagy‑signaling pathway.Molecular medicine reports · 2023Article
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3 authors.
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Abstract
It has been reported that DEP domain protein 1B (DEPDC1B) serves several roles in the occurrence and development of various types of cancer. Nevertheless, the effect of DEPDC1B on colorectal cancer (CRC), as well as its particular underlying molecular mechanism remain to be elucidated. In the present study, the mRNA and protein expression levels of DEPDC1B and nucleoporin 37 (NUP37) in CRC cell lines were assessed by reverse transcription‑quantitative PCR and western blotting, respectively. Cell Counting Kit‑8 and 5‑Ethynyl‑2'‑deoxyuridine assays were carried out to determine cell proliferation. In addition, the migration and invasion abilities of cells were evaluated using wound healing and Transwell assays. The changes in cell apoptosis and cell cycle distribution were assessed by flow cytometry and western blotting. Bioinformatics analysis and co‑immunoprecipitation assays were performed to predict and verify, respectively, the binding capacity of DEPDC1B on NUP37. The expression levels of Ki‑67 were detected by immunohistochemical assay. Finally, the activation of phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling was measured using western blotting. The results showed that DEPDC1B and NUP37 were upregulated in CRC cell lines. DEPDC1B and NUP37 silencing both inhibited the proliferation, migration and invasion capabilities of CRC cells and promoted cell apoptosis and cell cycle arrest. Furthermore, NUP37 overexpression reversed the inhibitory effects of DEPDC1B silencing on the behavior of CRC cells. Animal experiments demonstrated that DEPDC1B knockdown inhibited the growth of CRC in vivo by targeting NUP37. In addition, DEPDC1B knockdown inhibited the expression levels of the PI3K/AKT signaling‑related proteins in CRC cells and tissues by also binding to NUP37. Overall, the current study suggested that DEPDC1B silencing could alleviate the progression of CRC via targeting NUP37.
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