Anti-silencing function 1B knockdown suppresses the malignant phenotype of colorectal cancer by inactivating the phosphatidylinositol 3-kinase/AKT pathway.

BACKGROUND: Mounting studies have highlighted the pivotal influence of anti-silencing function 1B (ASF1B) on the malignancy of cancers. AIM: To explore the influence and mechanism of ASF1B in colorectal cancer (CRC). METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect mRNA expression of ASF1B. Immunohistochemical staining was performed to detect protein expression of ASF1B and Ki67 in tumor tissues. Western blot analysis was used to determine levels of ASF1B and proliferation/epithelial mesenchymal transition (EMT)/stemness-related proteins. In addition, the proliferation of CRC cells was assessed using Cell Counting Kit-8 and 5-Ethynyl-2'-Deoxyuridine assays. The migration and invasion of CRC cells were evaluated using transwell assays. Stemness of CRC cells was tested using the sphere formation assay. To construct a xenograft tumor model, HCT116 cells were introduced into mouse flanks via subcutaneous injection. RESULTS: ASF1B expression was markedly increased in CRC tissues and cells, and it was inversely correlated with overall survival of CRC patients and was positively associated with the tumor node metastasis (TNM) stage of CRC patients. Silencing of ASF1B suppressed proliferation, migration, invasion, stemness and EMT of CRC cells as well as tumorigenesis of xenograft mice. Furthermore, protein levels of P-phosphatidylinositol 3-kinase (p-PI3K) and p-AKT were decreased after silencing of ASF1B in CRC cells. The inhibitory effects of ASF1B knockdown on cell proliferation, stemness and EMT were partly abolished by PI3K activator in CRC cells. CONCLUSION: Silencing of ASF1B inactivated the PI3K/AKT pathway to suppress CRC malignancy in vitro.

Lower limb gangrene postcardiac surgery.

A 67-year-old gentleman presented with a 1-day history of left foot pain. He had recently been discharged following a coronary artery bypass graft; during the admission, he had received an intravenous heparin infusion. Examination revealed black-purple discolouration of the first and second digits of the left foot with pitting oedema to the level of the knee. The posterior tibial and dorsalis pedis pulses were both shown to be patent. A new thrombocytopenia was noted. Ultrasound imaging revealed multiple deep vein thrombosis. The history of recent heparin exposure coupled with venous gangrene secondary to deep vein thrombosis was consistent with heparin-induced thrombocytopenia. He was treated acutely with intravenous danaparoid and later with warfarin. There was complete resolution of the venous gangrene at 1 month follow-up.