Despite great progress has been made in treatment strategies, colorectal cancer (CRC) remains the predominant life-threatening malignancy with the feature of high morbidity and mortality. It has been widely acknowledged that the dysfunction of immune system, including aberrantly expressed cytokines, is strongly correlated with the pathogenesis and progression of colorectal cancer. As one of the most well-known cytokines that were discovered centuries ago, interleukins are now uncovering new insights into colorectal cancer therapy. Herein, we divide currently known interleukins into 6 families, including IL-1 family, IL-2 family, IL-6 family, IL-8 family, IL-10 family and IL-17 family. In addition, we comprehensively reviewed the oncogenic or antitumour function of each interleukin involved in CRC pathogenesis and progression by elucidating the underlying mechanisms. Furthermore, by providing interleukins-associated clinical trials, we have further driven the profound prospect of interleukins in the treatment of colorectal cancer.

Methionine-and choline-deficient diet-induced nonalcoholic steatohepatitis mice models using wild-type caspase-11deficient mice were established. Caspase-11-mediated hepatocytic pyroptosis promotes the progression of nonalcoholic steatohepatitis.BACKGROUND: Nonalcoholic steatohepatitis (NASH) is an inflammatory disease with severe outcomes. Hepatocyte death, including apoptosis, necrosis, and pyroptosis, has been implicated in pathophysiology of NASH. Pyroptosis is mediated by inflammasome activation pathways including caspase-1-mediated canonical signaling pathway and caspase-11-mediated noncanonical signaling pathway. Until now, the precise role of caspase-11 in NASH remains unknown. In the present study, the potential roles of caspase-11 in NASH were explored. METHODS:We established methionine-and choline-deficient diet (MCD)-induced NASH mice model using wild-type caspase-11-deficient mice. The expression of caspase-11, liver injury, fibrosis, inflammation, and activation of gasdermin D and interleukin-1b were evaluated.RESULTS: Upregulated caspase-11 was detected in liver of mice with NASH. MCD-treated caspase-11-deficient mice had significantly decreased liver injury, fibrosis, and inflammation.The activation of gasdermin D and interleukin-1b was inhibited in caspase-11-deficient mice after MCD treatment. Overexpression of caspase-11 promoted steatohepatitis.CONCLUSIONS: Caspase-11-mediated hepatocytic pyroptosis promotes the progression of NASH.

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