Stauprimide is known to prime Embryonic Stem Cells (ESC) by targeting the c-Myc-activating transcription factor NME2. Its mechanism of action is linked to the inhibition of the nuclear localization of NME2 leading to the downregulation of the transcription of the c-myc oncogene.

In a recent study, Bouvard C. et al. evidenced that Stauprimide’s mechanism of action could also be used to pharmacologically targetc-myc transcription in cancers.

The role of the interactions between tumor cells and their microenvironment (TME) is now well-established in various stages of cancer development. Cytokines, produced by both the cancer and the immune cells, actively contribute to these critical connections (see the previous posts related to the crosstalk between cancer and immune cells in relation to tumor escape, immunoediting and immunosurveillance).

In a recent review published in BBA, RayBiotech‘s team highlights the “cytokine signatures and dynamics” seen during cancer development. They also demonstrate the necessity of designing relevant multiplex immunoassays for the profiling and the quantification of cytokines in biomarker and anti-cancer drug discovery programs.

Source:
Valerie Sloane Jones, Ren-Yu Huang, Li-Pai Chen, Zhe-Sheng Chen, Liwu Fu, Ruo-Pan Huang “Cytokines in cancer drug resistance: Cues to new therapeutic strategies” (2016) Biochimica et Biophysica Acta, Volume 1865, Issue 2, 255–265. DOI:10.1016/j.bbcan.2016.03.005.

Download the publication written by RayBiotech, the leader in planar Antibody Arrays.

Following our series of posts on tumour immunity, I’d like to mention an article published by researchers from the Ben-Gurion University of the Negev (Israel). The authors investigated the negative correlation between caffeine consumption and incidence of tumours. Or to say it more simply, intake of caffeine favours the immune system fighting tumours. (1)

The anti-cancer property of the Vitamin K3 (Vitk3) was again recently studied by Dr Meng-Er Huang’s team (Curie Institute, CNRS UMR3348, Paris).
By using in vitro pro-oxydative cellular models, Dr Huang and collaborators observed a cancer-selective cytotoxicity of vitk3 in Peroxyredoxin 1 (PRDX1 aka PRX1)-deficient cancer cell lines.
To further investigate the underlying molecular mechanisms, the authors used a stably PRX1-depleted HeLa cell line (PRX1-) (vs. Control (PRX1+)) under various experimental conditions. They notably treated PRX1- and PRX1+ cell lines by vitk3 and 6 other known anticancer molecules targeting different cellular events (microtubule (vinblastine & taxol); DNA (doxorubicin & daunorubicin); DNA transcription (actinomycin D) and cell cycle (5-FU)).