ADAM17 promotes colorectal cancer migration and invasion by regulating the TGF-β/Smad signaling pathway.

Objective: Investigate ADAM17 expression in colorectal cancer (CRC) at molecular and cellular levels and its potential mechanism in promoting tumorigenesis by regulating CRC cell migration and invasion.

Materials And Methods: The study measured ADAM17 mRNA and protein levels in colorectal cancer cells and tissues using qPCR and immunohistochemical staining, and assessed the cells' proliferation, migration, and invasion abilities.

Results: ADAM17 expression was significantly higher in CRC tissues than in non-cancerous tissues and was linked to metastasis and poor prognosis in CRC patients.

FOXM1 promotes the progression of non-small cell lung cancer by inhibiting miR-509-5p expression via binding to the miR-509-5p promoter region.

Background: Forkhead box M1 (FOXM1) functions as a transcription factor and is consistently overexpressed in various cancers, including non-small-cell lung-, breast-, cervical-, and colorectal cancer. Its overexpression is associated with poor prognosis in patients with non-small-cell lung cancer, although the detailed mechanisms by which FOXM1 promotes the development of non-small-cell lung cancer remain unclear.

Objective: The mechanism of FOXM1 in migration, invasion, apoptosis, and viability of lung cancer cells was investigated.

Association between P2Y1 and P2Y12 polymorphisms and acute myocardial infarction and ADP-induced platelet aggregation.

Background: The objective of this study was to investigate the relationship between P2Y1 and P2Y12 genotypes and the risk of acute myocardial infarction (AMI) in the Quanzhou population and to determine associations between P2Y1 and P2Y12 genotypes and ADP-induced platelet aggregation in this population.

Methods: All subjects were screened for P2Y1 (c.1622A > G) and P2Y12 (H1/H2, c.

[Phenotypic and mutational analysis of a pedigree affected with hereditary coagulation factor Ⅴ deficiency].

Objective: To explore the molecular pathogenesis for a pedigree affected with coagulation factor Ⅴ (FⅤ) deficiency.

Methods: Prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FIB), coagulation factor Ⅱ activity (FⅡ: C), FⅤ activity (FⅤ: C), coagulation factor Ⅶ activity (FⅦ: C), and coagulation factor Ⅹ activity (FⅩ: C) were determined with a STAGO automatic coagulometer. FⅤ antigen (FⅤ: Ag) was detected with enzyme linked immunosorbent assay (ELISA).