The reciprocal interplay between TNFα and the circadian clock impacts on cell proliferation and migration in Hodgkin lymphoma cells.
Mónica AbreuAlireza BastiNikolai GenovGianluigi MazzoccoliAngela RelógioPublished in: Scientific reports (2018)
A bidirectional interaction between the circadian network and effector mechanisms of immunity brings on a proper working of both systems. In the present study, we used Hodgkin lymphoma (HL) as an experimental model for a type of cancer involving cells of the immune system. We identified this cancer type among haematological malignancies has having a strong differential expression of core-clock elements. Taking advantage of bioinformatics analyses and experimental procedures carried out in III- and IV-stage HL cells, and lymphoblastoid B cells, we explored this interplay and bear out diverse interacting partners of both systems. In particular, we assembled a wide-ranging network of clock-immune-related genes and pinpointed TNF as a crucial intermediary player. A robust circadian clock hallmarked III-stage lymphoma cells, differently from IV-stage HL cells, which do not harbour a properly functioning clockwork. TNF and circadian gene modulation impacted on clock genes expression and triggered phenotypic changes in lymphoma cells, suggesting a crucial involvement of core-clock elements and TNF in the physiopathological mechanisms hastening malignancy. Our results move forward our understanding of the putative role of the core-clock and TNF in the pathobiology of Hodgkin lymphoma, and highlight their influence in cellular proliferation and migration in lymphatic cancers.
Keyphrases
- induced apoptosis
- hodgkin lymphoma
- cell cycle arrest
- rheumatoid arthritis
- endoplasmic reticulum stress
- cell death
- oxidative stress
- stem cells
- signaling pathway
- papillary thyroid
- dna methylation
- transcription factor
- lymph node
- genome wide
- poor prognosis
- diffuse large b cell lymphoma
- cell proliferation
- bone marrow
- binding protein
- hiv infected