Interleukin(IL)-35 is a new member of the interleukin-12 superfamily. Since its first report in 2007, IL-35 rapidly became a research highlight in the ifeld of immunology. Like other IL-12 superfamily members, IL-35 was a heterodimer which was composed of anαchain P35 and aβchain Epstein-Barr virus induced gene 3 (EBI3). Recent research work revealed two distinct roles of IL-35. Firstly, IL-35 is highly expressed in some kinds of inlfammatory diseases and autoim-mune diseases and plays import roles in the pathogenesis. Secondly, IL-35 is positively expressed in some cancers and plays some roles in the process of tumor progression. Here we demonstrate the structure and the signalling of IL-35. We reviewed the the roles of IL-35 in promoting tumor progression.

Tumor stroma plays key roles in promoting tumor recurrence and treatment resistance. Cancer-associated fibroblasts (CAFs) are one of the most abundant and key components in the stroma of lung cancer. CAFs secrete a variety of inflammatory cytokines and extracellular matrix to form a desmoplastic tumor niche, which play important roles in the occurrence and development of lung cancer. CAFs are mainly derived from normal lung fibroblasts, which are transformed by tumor-derived cytokines. The diverse sources of CAFs lead to great heterogeneity in different CAFs subgroups. Although many studies support that CAFs promote tumor growth, but evolving data also argue for their antitumor actions. The putative bimodal function in oncogenesis of CAFs bring great challenges to the clinical application of CAFs-targeted therapies. This review focuses on the characteristics and functional research of CAFs, and emphasizes the roles and specificity of CAFs in the development of lung cancer.