C/EBPβ expression is an independent predictor of overall survival in breast cancer patients by MHCII/CD4-dependent mechanism of metastasis formation

Kurzejamska, Ewa; Johansson, Joel; Jirström, Karin; Prakash, Vineet; Ananthaseshan, Sharan; Boon, Louis; Fuxe, Jonas; Religa, Piotr

doi:10.1038/oncsis.2014.38

Cited by 18 publications

(23 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In support of this, reduced staining of CEBPB was observed in samples of ductal breast carcinomas shown in the Human Protein Atlas database [55]. Furthermore, thte expression of CEBPB was reported to be an indicator of metastasis and overall survival in breast cancer patients [56].…”

Section: Discussionmentioning

confidence: 71%

Tumor cell-secreted angiogenin induces angiogenic activity of endothelial cells by suppressing miR-542-3p

He¹,

Qi²,

Jia³

et al. 2015

Cancer Letters

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 71%

Tumor cell-secreted angiogenin induces angiogenic activity of endothelial cells by suppressing miR-542-3p

He¹,

Qi²,

Jia³

et al. 2015

Cancer Letters

View full text Add to dashboard Cite

“…CEBPB is closely related with lipid metabolism in HepG2 cells and liver cancer cells . CEBPB expression is associated with overall survival in breast cancer and gastric cancer patients . In Ewing sarcoma and ovarian cancer, CEBPB could promote tumor cell resistance to chemotherapy .…”

Section: Discussionmentioning

confidence: 99%

“…57,58 CEBPB expression is associated with overall survival in breast cancer and gastric cancer patients. 59,60 In Ewing sarcoma and ovarian cancer, CEBPB could promote tumor cell resistance to chemotherapy. 61,62 In this study, we found that CEBPB promotes the transcription of CPT1A and activates FAO.…”

Section: Discussionmentioning

confidence: 99%

PGC1α/CEBPB/CPT1A axis promotes radiation resistance of nasopharyngeal carcinoma through activating fatty acid oxidation

Tan

Shi

et al. 2019

Cancer Science

View full text Add to dashboard Cite

The PPAR coactivator‐1α (PGC1α) is an important transcriptional co‐activator in control of fatty acid metabolism. Mitochondrial fatty acid oxidation (FAO) is the primary pathway for the degradation of fatty acids and promotes NADPH and ATP production. Our previous study demonstrated that upregulation of carnitine palmitoyl transferase 1 A (CPT1A), the key regulator of FAO, promotes radiation resistance of nasopharyngeal carcinoma (NPC). In this study, we found that high expression of PGC1α is associated with poor overall survival in NPC patients after radiation treatment. Targeting PGC1α could sensitize NPC cells to radiotherapy. Mechanically, PGC1α binds to CCAAT/enhancer binding protein β (CEBPB), a member of the transcription factor family of CEBP, to promote CPT1A transcription, resulting in activation of FAO. Our results revealed that the PGC1α/CEBPB/CPT1A/FAO signaling axis promotes radiation resistance of NPC. These findings indicate that the expression of PGC1α could be a prognostic indicator of NPC, and targeting FAO in NPC with high expression of PGC1α might improve the therapeutic efficacy of radiotherapy.

show abstract

“…While the overexpression of LAP isoforms determines cell cycle arrest or differentiation, as shown in hepatocytes, hematopoietic cells and adipocytes, LIP induces proliferation and contributes to tumor cells survival. Increased LIP expression antagonizes LAP activity and the high LIP:LAP ratio favors c-myc activation and inactivation of cell cycle inhibitor genes [131,135]. LIP isoform contributes to cell survival and tumor progression, as demonstrated in hepatoma cells.…”

Section: Ccaat-enhancer Binding Protein β (C/ebpβ)mentioning

confidence: 97%

Transcription Factors in Cancer: When Alternative Splicing Determines Opposite Cell Fates

Belluti

Rigillo

Imbriano

2020

Cells

View full text Add to dashboard Cite

Alternative splicing (AS) is a finely regulated mechanism for transcriptome and proteome diversification in eukaryotic cells. Correct balance between AS isoforms takes part in molecular mechanisms that properly define spatiotemporal and tissue specific transcriptional programs in physiological conditions. However, several diseases are associated to or even caused by AS alterations. In particular, multiple AS changes occur in cancer cells and sustain the oncogenic transcriptional program. Transcription factors (TFs) represent a key class of proteins that control gene expression by direct binding to DNA regulatory elements. AS events can generate cancer-associated TF isoforms with altered activity, leading to sustained proliferative signaling, differentiation block and apoptosis resistance, all well-known hallmarks of cancer. In this review, we focus on how AS can produce TFs isoforms with opposite transcriptional activities or antagonistic functions that severely impact on cancer biology. This summary points the attention to the relevance of the analysis of TFs splice variants in cancer, which can allow patients stratification despite the presence of interindividual genetic heterogeneity. Recurrent TFs variants that give advantage to specific cancer types not only open the opportunity to use AS transcripts as clinical biomarkers but also guide the development of new anti-cancer strategies in personalized medicine.

show abstract

C/EBPβ expression is an independent predictor of overall survival in breast cancer patients by MHCII/CD4-dependent mechanism of metastasis formation

Cited by 18 publications

References 32 publications

Tumor cell-secreted angiogenin induces angiogenic activity of endothelial cells by suppressing miR-542-3p

Tumor cell-secreted angiogenin induces angiogenic activity of endothelial cells by suppressing miR-542-3p

PGC1α/CEBPB/CPT1A axis promotes radiation resistance of nasopharyngeal carcinoma through activating fatty acid oxidation

Transcription Factors in Cancer: When Alternative Splicing Determines Opposite Cell Fates

Contact Info

Product

Resources

About