The link between cancer and inflammation involves dynamic signalling networks between the components inside the tumour, ranging from cytokines to growth factors. The type and grade of inflammatory mediators at the tumour site dictate the range and response of various immune cells. Inflammatory diseases represent a concrete base for the development of certain cancers. The expression of certain systems like endoplasmic reticulum (ER) stress and G protein-coupled receptors (GPCRs) in immune systems reveals their key role in inflammatory processes like immune cell activity, modulation of cancer signalling pathways, and processes like angiogenesis.

G protein-coupled receptors (GCPRs) play a lead role during tumorigenesis, with involvement in numerous tissues and cell types. GPCRs have been noted to orchestrate unfolded protein response (UPR) and ER stress. This linkage exists through pathways such as IRE1α-JNK signalling. GPCRs were reported to be key players not only in cancer but also in inflammation-related diseases such as ulcerative colitis and Crohn’s disease. OGR1, for instance, has been identified as one of the prime GPCR proteins expressed in gut-related inflammatory diseases. GPCR adaptor proteins like Arrestin-1 have also been identified to control UPR and other UPR related pathways which add a strong preface to the interplay between GPCR and ER stress. The epithelial-mesenchymal transition (EMT), on the other hand, has been associated with both ER stress and GPCR. The ER stress response has been demonstrated to regulate EMT in a number of tissues via pathways like Src-dependent pathways in airway epithelial cells (AECs). G-protein-coupled receptor kinase-interacting protein-1 (GIT1) activates the MEK/MAPK/ERK signalling cascade to induce epithelial cell migration. Hence, the trio is widely related and symbiotic, and is said to be partially driven by inflammation. Epigenetic alterations define and influence signalling pathways which in turn modulate cell growth and division, cell death, cell fate, and cell motility, which widely promote cancer progression. Other mechanisms which majorly influence cancer are inflammation or microenvironment. Chronic inflammation can lead to DNA damage. Both extrinsic and intrinsic inflammations can result in immunosuppression, thereby providing a preferred background for tumour development. Cancer treatment can be made successful if these mechanisms are well understood and strategically targeted.

The aim of this Special Issue is to invite articles addressing mechanisms, therapeutics, crucial pathways, and clinical studies of mediators of inflammation in diverse cancers, with a particular focus on three prime aspects: GPCR, ER stress and EMT. We welcome both original research and review articles.

Potential topics include but are not limited to the following:

• Unravelling the super trio of ER stress, GPCR, and EMT
• The interrelating role of ER stress and GPCR in colorectal cancer and the influence of inflammation in priming deleterious effects
• Investigating inflammatory mediators in inflammation-driven diseases like colorectal cancer and IBD
• Dissecting inflammation research via omics approaches
• Deciphering the signalling of ER stress, GPCR, and EMT
• Associating the modulatory roles of inflammation in the initiation of cancer
• Oncogenes related to EMT, ERS, and GPCR signalling
• Small molecule inhibitors and planned metabolites in impeding inflammation and inflammation-mediated cancers
• Translational approaches