Objective: To explore the molecular mechanisms of FAM129A in regulating the progression of esophageal cancer and its prognosis.
Patients And Methods: FAM129A levels in esophageal cancer tissues and paracancerous ones were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Its influences on clinical features and prognosis in esophageal cancer patients were analyzed. Changes in proliferation and apoptosis in esophageal cancer cells after knockdown of FAM129A were examined by cell counting kit-8 (CCK-8), 5-Ethynyl-2'- deoxyuridine (EdU) assay and flow cytometry, respectively. The feedback loop FAM129A/CXCL14 was finally assessed.
Results: FAM129A was upregulated in esophageal cancer tissues. High level of FAM129A predicted advanced tumor staging, large tumor size and poor prognosis in esophageal cancer patients. Knockdown of FAM129A inhibited proliferative ability and induced apoptosis in OE19 and OE33 cells. In addition, knockdown of FAM129A upregulated protein level of CXCL14 in esophageal cancer cells. CXCL14 was downregulated in esophageal cancer tissues and negatively correlated to FAM129A level. The negative feedback loop FAM129A/CXCL14 was responsible for aggravating the malignant phenotypes of esophageal cancer cells.
Conclusions: FAM129A is upregulated in esophageal cancer samples, and it is linked to tumor staging, tumor size and poor prognosis. FAM129A aggravates the progression of esophageal cancer by negatively regulating CXCL14 level.
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