Spondyloarthritis (SpA) is a group of diseases consisting of psoriatic arthritis (PsA), reactive arthritis, arthritis related to inflammatory bowel disease (a subgroup of juvenile idiopathic arthritis), and ankylosing spondylitis (the prototype of SpA). Axial bone formation and the combination of concurrent erosion and new bone formation are specific characteristics of SpA disease. The use of anti-proinflammatory cytokines, such as inhibitors of tumor necrosis factor α (TNF-α), appears to be the greatest advance in the treatment of SpA over the past 20 years. However, TNF-α blockers do not halt new bone formation. Recent clinical observations and animal studies demonstrate that Wnt signaling proteins and natural Wnt inhibitors, such as DKK1 and sclerostin, are likely to play important roles in the process of ankylosis in SpA, and could potentially serve as therapeutic targets for the treatment of SpA.

Background and Aim Colorectal cancer (CRC) is one of the most deadly cancers in the world, with few treatments and a poor prognosis. In recent years, many circular RNAs have been studied in CRC, but the role of circ_0014130 in CRC has not been investigated. Therefore, this research is designed to investigate the impact of circ_0014130 on the resistance of 5‐fluorouracil (5‐FU) in CRC. Methods Quantitative real‐time polymerase chain reaction was conducted to assess the expression of circ_0014130, microRNA‐197‐3p (miR‐197‐3p), and 6‐phosphofructo‐2‐kinase/fructose‐2, 6‐bisphosphatase 3 (PFKFB3). The expression of PFKFB3 protein was detected by Western blot. The effect of cric_0014130 on drug resistance in CRC was verified by Cell Counting Kit‐8 assay, clone formation assay, Transwell, and flow cytometry. The effect of circ_0014130 on tumor growth was evaluated by xenograft tumor model in vivo. Results Circ_0014130 and PFKFB3 were increased, while miR‐197‐3p was reversed in CRC tissues and cells. Knocking down circ_0014130 can promote cell apoptosis, inhibit the proliferation of CRC cells, and reduced the IC50 of 5‐FU. In addition, miR‐197‐3p inhibitors reversed the effect of si‐circ_0014130 on CRC cells. Similarly, overexpression of PFKFB3 can regulate CRC cell behavior and 5‐FU resistance caused by miR‐197‐3p. Finally, decrease of circ_0014130 was demonstrated to enhance the resistance of 5‐FU in CRC tissues in vivo. Conclusion Circ_0014130 modulates 5‐FU resistance in CRC by modulating the miR‐197‐3p/PFKFB3 axis, which is helpful for drug chemotherapy in CRC.

No abstract