ArticleInternational journal of molecular medicine2016
Basic helix-loop-helix transcription factor DEC2 functions as an anti-apoptotic factor during paclitaxel-induced apoptosis in human prostate cancer cells.
Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- BHLHE40 as a transcriptional rheostat: decoding microenvironmental signals in context-dependent tumor plasticity.Science China. Life sciences · 2026Review
- Digoxin targets BHLHE40 to inhibit epithelial-mesenchymal transition in cervical cancer cells via downregulation of ANGPTL3.Journal of natural medicines · 2026Article
- BHLHE41, a transcriptional repressor involved in physiological processes and tumor development.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- High expression of DEC2 distinguishes chondroblastic osteosarcoma and promotes tumour growth by activating the VEGFC/VEGFR2 signalling pathway.Journal of cellular and molecular medicine · 2024Article
- Role of differentiated embryo-chondrocyte expressed gene 2 in immunity.Frontiers in immunology · 2024Review
- Co-regulation of circadian clock genes and microRNAs in bone metabolism.Journal of Zhejiang University. Science. B · 2022Review
- Article
- TCF21: a critical transcription factor in health and cancer.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Single cell RNA-sequencing identified Dec2 as a suppressive factor for spermatogonial differentiation by inhibiting Sohlh1 expression.Scientific reports · 2019Article
- Overexpression of BHLHE41, correlated with DNA hypomethylation in 3'UTR region, promotes the growth of human clear cell renal cell carcinoma.Oncology reports · 2019Article
- Loss of the basic helix-loop-helix transcription factor Bhlhe41 induces cell death and impairs neurite outgrowth in Neuro2a cells.Molecular and cellular biochemistry · 2019Article
- BHLHE41 promotes U87 and U251 cell proliferation via ERK/cyclinD1 signaling pathway.Cancer management and research · 2019Article
- Correlation between DEC1/DEC2 and epithelial‑mesenchymal transition in human prostate cancer PC‑3 cells.Molecular medicine reports · 2018Article
- Multiple renal cancer susceptibility polymorphisms modulate the HIF pathway.PLoS genetics · 2017Article
- Genome-wide identification, classification, and functional analysis of the basic helix-loop-helix transcription factors in the cattle, Bos Taurus.Mammalian genome : official journal of the International Mammalian Genome Society · 2017Article
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8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The functions of basic helix-loop-helix (bHLH) transcription factor-differentiated embryonic chondrocyte (DEC)1 (BHLHE40) and 2 (BHLHE41) are involved in various fields such as circadian rhythms, immune responses, cell proliferation, hypoxia reaction as well as malignant tumors. Previous findings showed that DEC served as apoptosis regulators of various cancer cell lines. However, little is known regarding the expression of DEC1 and DEC2 in prostate cancer cells. The present study aimed to examine the roles of DEC1 and DEC2 in human prostate cancer DU145 and PC-3 cells that were treated with paclitaxel. The expression of DEC1 and DEC2 was decreased in DU145 cells but was increased in PC-3 cells when treated with paclitaxel. DU145 cells were more sensitive to paclitaxel than PC-3 cells since the amount of cleaved poly(ADP-ribose) polymerase (PARP) reached its peak at 50 µM of paclitaxel in DU145 cells but at 100 µM in PC-3 cells. In addition, the amount of cleaved PARP was decreased by DEC1 siRNA, while it was increased by DEC2 siRNA in the presence of paclitaxel. Although DEC2 overexpression slightly inhibited cleaved PARP in the two cell lines, the effects of DEC1 overexpression on apoptosis remain to be determined. In conclusion, DEC1, at least partly, exerted a pro-apoptotic effect, whereas DEC2 exerted an anti-apoptotic effect in paclitaxel-induced apoptosis of human prostate cancer cells.
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