The role of aldo‐keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer progression. AKR1B1 could participate in a complicated network of signalling pathways, proteins and miRNAs such as mir‐21 mediating mechanisms like inflammatory responses, cell cycle, epithelial to mesenchymal transition, cell survival and apoptosis. AKR1B1 has been shown to be mostly overexpressed in cancer. This overexpression has been associated with inflammatory mediators including nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NFκB), cell cycle mediators such as cyclins and cyclin‐dependent kinases (CDKs), survival proteins and pathways like mammalian target of rapamycin (mTOR) and protein kinase B (PKB) or AKT, and other regulatory factors in response to reactive oxygen species (ROS) and prostaglandin synthesis. In addition, inhibition of AKR1B1 has been shown to mostly have anti‐cancer effects. Several studies have also suggested that AKR1B1 inhibition as an adjuvant therapy could render tumour cells more sensitive to anti‐cancer therapy or alleviate the adverse effects of therapy. AKR1B1 could also be considered as a potential cancer diagnostic biomarker since its promoter has shown high levels of methylation. Although pre‐clinical investigations on the role of AKR1B1 in cancer and the application of its inhibitors have shown promising results, the lack of clinical studies on AKR1B1 inhibitors has hampered the use of these drugs to treat cancer. Thus, there is a need to conduct more clinical studies on the application of AKR1B1 inhibitors as adjuvant therapy on different cancers.

Extracellular concentration of adenosine increases in the hypoxic tumor microenvironment. Adenosine signaling regulates apoptosis, angiogenesis, metastasis, and immune suppression in cancer cells. Adenosine-induced cell responses depend upon different subtypes of adenosine receptors activation and type of cancer. Suppression of adenosine signaling via inhibition of adenosine receptors or adenosine generating enzymes including CD39 and CD73 on ovarian or cervical cancer cells is a potentially novel therapeutic approach for gynecological cancer patients. This review summarizes the role of adenosine in the pathogenesis of gynecological cancer for a better understanding and hence a better management of this disease.

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The concentrations of adenosine may increase under ischemic conditions in the tumor microenvironment, and then it enters the systemic circulation. Adenosine controls cancer progression and responses to therapy by regulating angiogenesis, cell survival, apoptosis, cell proliferation, and metastases in tumors. Hence, adenosine metabolism, adenosine-generating enzymes, and adenosine signaling are potentially novel therapeutic targets in a wide range of pathological conditions, including cerebral and cardiac ischemic diseases, inflammatory disorders, immunomodulatory disorders, and, of special interest in this review, cancer. This review summarizes the role of adenosine in the pathogenesis of head and neck cancer for a better understanding of how this may be applied to treating this type of cancer.

Vitamin D regulates a plethora of physiological processes in the human body and has been proposed to exert several anticancer effects. Epigenetics plays an important role in regulating vitamin D actions. In this review, we highlight the recent advances in the understanding of different epigenetic factors such as lncRNAs, miRNAs, methylation and acetylation influenced by vitamin D and its downstream targets in colorectal cancer to find more potential therapeutic targets. We discuss how vitamin D exerts anticancer properties through interactions between the vitamin D receptor and genes (e.g., SLC30A10), the microenvironment, microbiota and other factors in colorectal cancer. Developing therapeutic approaches targeting the vitamin D signaling system will be aided by a better knowledge of the epigenetic impact of vitamin D.