BACKGROUND:Anterior cruciate ligament (ACL) injury is a commonly sport-induced knee joint injury that does serious harm to the knee stability. ACL reconstruction is a commonly used treatment method, but researches on 1/2 peroneus longus tendon (PLT) graft are rarely reported. OBJECTIVE: To investigate the clinical outcomes of removing the autologous ipsilateral 1/2 PLT under arthroscopy for ACL reconstruction. METHODS:106 patients with complete ACL rupture in the Affiliated Hospital of Traditional Chinese Medicine, Southwest Medical University from December 2010 to December 2014 were enrolled, and autologous ipsilateral 1/2 PLT was removed under arthroscopy for ACL reconstruction. At baseline, 3, 6 and 12 months postoperatively, the knee stability was evaluated manually through the anterior drawer test, Lachman test, and pivot-shift test, and the knee function was evaluated by Tegner activity scale, Lysholm and International Knee Documentation Committee scores. RESULTS AND CONCLUSION: Postoperative anterior drawer test, Lachman test, and pivot-shift test tests were negative in all patients. In terms of Tegner activity scale, Lysholm and International Knee Documentation Committee scores, there were significant differences at baseline and postoperative 3 months as compared with postoperative 6 months (P < 0.05); the scores at baseline and postoperative 3 months showed significant differences compared with 12 months postoperatively (P < 0.05); the scores showed no significant difference between 6 and 12 months postoperatively (P > 0.05). These results indicate that autologous ipsilateral 1/2 PLT is a good choice for ACL reconstruction under arthroscopy, achieving rapid and satisfactory functional recovery of the knee joint, which is not only minimally invasive and easy to operate, but also exhibits good therapeutic efficacy.

N ⁶-methyladenosine (m⁶A) modification is critical for mRNA splicing, nuclear export, stability and translation. Fat mass and obesity-associated protein (FTO), the first identified m⁶A demethylase, is critical for cancer progression. Herein, we developed small-molecule inhibitors of FTO by virtual screening, structural optimization, and bioassay. As a result, two FTO inhibitors namely 18077 and 18097 were identified, which can selectively inhibit demethylase activity of FTO. Specifically, 18097 bound to the active site of FTO and then inhibited cell cycle process and migration of cancer cells. In addition, 18097 reprogrammed the epi-transcriptome of breast cancer cells, particularly for genes related to P53 pathway. 18097 increased the abundance of m⁶A modification of suppressor of cytokine signaling 1 (SOCS1) mRNA, which recruited IGF2BP1 to increase mRNA stability of SOCS1 and subsequently activated the P53 signaling pathway. Further, 18097 suppressed cellular lipogenesis via downregulation of peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), and C/EBPβ. Animal studies confirmed that 18097 can significantly suppress in vivo growth and lung colonization of breast cancer cells. Collectively, we identified that FTO can work as a potential drug target and the small-molecule inhibitor 18097 can serve as a potential agent against breast cancer.