In fibro blasts, the trend of percentages was instead opposite. The two lists of selected probes were analysed by the In genuity Pathway Analysis software. Results obtained towards on melanoma cells are reported in Additional file 1 B and 1 C. IPA results obtained for BJ fibroblasts are reported in Additional file 2 B and 2 C. D6 treatment Inhibitors,Modulators,Libraries affects cell death and proliferation bio functions The top bio functional categories identified by IPA among the genes modulated in treated melanoma cells are listed in Table 2, where the p values range and number of mole cules involved are reported for each category. The lowest p values were found for the Cell Death cat egory with 194 molecules involved. Cell death is indeed the primary effect detected on melanoma cells after D6 treatment.

Moreover, Inhibitors,Modulators,Libraries a variable number FC value of 368. 61. HSPA6 codifies for the Hsp70B, a highly Inhibitors,Modulators,Libraries stress inducible protein. Additional pathways such as 4 Cell cycle G2/M DNA damage checkpoint regulation, 5 p53 Inhibitors,Modulators,Libraries signalling, 10 Her editary breast cancer signalling, 11 ATM signalling, 26 Role of BRCA1 in DNA damage response, and 27 Role of of molecules differentially modulated by D6 involved func tional categories strictly correlated with cell proliferation processes such as cellular function and maintenance, cell cycle and cell growth and proliferation. D6 induces stress response pathways and down regulates cell proliferation pathways Table 3 lists the most significant pathways that IPA found to be enriched with the input genes in melan oma cells. For each pathway, the respective nominal p value, along with all the input molecules are reported.

A general trend of up regulation for pathways involving Inhibitors,Modulators,Libraries cell stress response was evident . con versely, pathways that control cell proliferation appeared inhibitor purchase down regulated. The first three most significant pathways, 1 Aldosterone signalling, 2 Protein ubiquitination, and 3 NRF2 mediated oxidative stress response as well as the 21 Endoplasmic reticulum stress pathway appear to be up regulated, depicting a strong activation of stress induced molecular responses that involves over expression of heat shock proteins and activation of protein degradation processes. Among up regulated HSPs, HSPA6 is the most over expressed transcript in melanoma treated cells with a CHK proteins in cell cycle checkpoint control are all related to DNA repair mechanisms and cell death triggering, evidencing a DNA damage as cell response to D6 treatment. The up regulation of pathway 5 p53 signalling, which acts in response to cell injury or DNA damage by controlling cell proliferation and driving cells to apoptosis, is noteworthy and points out a central role of this regulatory protein in the D6 anticancer effect on melanoma cells.