Role of interleukins in the pathogenesis of cholangiocarcinoma: A literature review.

This article summarized the role of interleukins (ILs) in the pathogenesis of cholangiocarcinoma (CCA). It discovered a negative feedback mechanism wherein alternative splicing led to the upregulation of the IL 1 receptor antagonist (IL1RN) isoforms IL1RN-201 and IL1RN-203, which play a crucial anti-inflammatory role in -mutant intrahepatic CCA (iCCA). Higher levels of IL-4 receptor were associated with a worse survival rate in patients with CCA. In addition, elevated levels of serum IL-6 have been associated with the start and progression of CCA, a common cancer generated by inflammation. IL-8 was a useful predictor of human hilar CCA. Mechanistically, signal transducer and activator of transcription 3 signaling was used by IL-10 produced from M2-polarized tumor-associated macrophages to enhance the malignant characteristics of iCCA cells. It was suggested that IL-17A and IL-22 have an impact on the development of CCA associated with hepatic fluke infection. The most significant finding was the decreased expression of the IL-23 receptor, a prognostic gene, in iCCA. IL-25 may be a useful prognostic biomarker as aberrant expression of the protein in CCA tissue was linked to tumor spread and a poor prognosis. Tumor cell migration and proliferation were both accelerated by homogenized liver tissue that expressed IL-33 significantly. The correlation between high IL-35 expression and aggressiveness in iCCA highlights it as a useful biomarker for assessing the course and prognosis of iCCA in clinical settings. This article concluded that IL-1, IL-4, IL-6, IL-8, IL-10, IL-17, IL-23, IL-25, IL-33, and IL-35 play significant roles in the pathogenesis of CCA. Further research is required to find the association of other ILs such as IL-2, IL-3, IL-5, IL-7, IL-11, and more in the pathogenesis of CCA.