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Detection of DNA molecules and possible chemotherapy-induced changes in its structure has been the goal of researchers using rapid, sensitive and inexpensive approaches. Therefore, the aim of this study was to fabricate a new electrochemical DNA biosensor using pencil graphite electrodes modified with polypyrrole/Ce doped hexagonal nickel oxide nanodisks or PP/Ce-doped H-NiO-ND composites for determination of Abemaciclib (AMC) and ds-DNA molecules. The DNA biosensor was prepared by immobilizing ds-DNA on the surface of PP/Ce-doped H-NiO-ND/PGE. Differential pulse voltammetry (DPV) was used to electrochemically detect AMC. The results elucidate the extremely high sensitivity of the ds-DNA/PP/Ce-doped H-NiO-ND/PGE biosensor to AMC, with a narrow detection limit of 2.7 nM and a lengthy linear range of 0.01–600.0 μM. The admirable performance of as-fabricated biosensor could be related to the active reaction sites and the unique electrochemical response related to the nanocomposites by enhancing ds-DNA stabilization and accelerating electron transfer on the surface of electrode.

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Cancer is now one of the major causes of death across the globe. The imbalance of cytokine and chemokine secretion has been reported to be involved in cancer development. Meanwhile, CC chemokines have received considerable interest in cancer research. CCR10, as the latest identified CC chemokine receptor (CCR), has been implicated in the recruitment and infiltration of immune cells, especially lymphocytes, into epithelia such as skin via ligation to two ligands, CCL27 and CCL28. Other than homoeostatic function, several mechanisms have been shown to dysregulate CCR10/CCL27–CCL28 expression in the tumour microenvironment. As such, these receptors and ligands mediate T-cell trafficking in the tumour microenvironment. Depending on the types of lymphocytes recruited, CCR10/CCL27–CCL28 interaction has been shown to play conflicting roles in cancer development. If they were T helper and cytotoxic T cells and natural killer cells, the role of this axis would be tumour-suppressive. In contrast, if CCR10/CCL27–CCL28 recruited regulatory T cells, cancer-associated fibroblasts or myeloid-derived suppressor cells, it would lead to tumour progression. In addition to the trafficking of lymphocytes and immune cells, CCR10 also leads to the migration of tumour cells or endothelial cells (called angiogenesis and lymphangiogenesis) to promote tumour metastasis. Furthermore, CCR10 signalling triggers tumour-promoting signalling such as PI3K/AKT and mitogen-activated protein kinase/extracellular signal-regulated kinase, resulting in tumour cell growth. Since CCR10/CCL27–CCL28 is dysregulated in the tumour tissues, it is suggested that analysis and measurement of them might predict tumour development. Finally, it is hoped using therapeutic approaches based on this axis might increase our knowledge to overcome tumour progression.

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