Effect of cancer/testis antigen NY-SAR-35 on the proliferation, migration and invasion of cancer cells

Abstract

NY-SAR-35 is a cancer/testis (CT) antigen that was identified by serological analysis of recombinant complementary DNA expression libraries. The gene encoding NY-SAR-35 is located on the × chromosome and is aberrantly expressed in a number of cancer types and germ cells, such as those in the testes, but not in normal tissue. It has been reported that treatment with a demethylating agent induced the expression of NY-SAR-35 in several types of cancer cells. However, the function of NY-SAR-35 in cancer remains undetermined. In present study, the role of NY-SAR-35 in human lung adenocarcinoma (SK-LC-14) and hepatocellular carcinoma (SNU-449) cells was investigated following stable transfection of the NY-SAR-35 gene. NY-SAR-35 was observed to be expressed in the cytoplasm of the cells. In addition, the bromodeoxyuridine incorporation assay and immunofluorescence staining for proliferating cell nuclear antigen and Ki-67 demonstrated that proliferation was increased in cells transfected with NY-SAR-35. In addition, the trypan blue exclusion assay indicated that NY-SAR-35 increased cancer cell viability. Furthermore, NY-SAR-35 increased the migration and invasion of the cells. These results indicate that NY-SAR-35 increases cancer cell viability, proliferation, migration and invasion.

Cancer/Testis Antigens as Biomarker and Target for the Diagnosis, Prognosis, and Therapy of Lung Cancer

“…ACTL8-knockdown inhibits lung cancer cell proliferation, colony formation, cell cycle progression, migration and invasion, and lung cancer cell A549 tumour growth in vivo , indicating that it exerts an oncogenic role in lung cancer cell tumorigenesis and progression ( 47 ). Overexpression of NY-SAR-35 promotes lung cancer cell proliferation and increases cell viability, migration and invasion ( 48 ). Semenogelins 1 and 2 (SEMG1 and 2) interact with the glycolytic enzymes-pyruvate kinase M2 (PKM2) and lactate dehydrogenase A (LDHA), increase the expression levels of these two partners, and elevate the protein levels of the membrane mitochondrial potential, resulting in increases in glycolysis, respiration and ROS production in several cancer cell lines, implying that SEMG1 and 2 enhance cancer cell energy metabolism and exemplify tumour cell oncogenic features ( 49 ).…”