Pression of human lung adenocarcinoma cells through G1/S cell cycle phase arrest and apoptosis pathways in vitroYI-FAN ZHANG1, RUI JIANG2, JIN-DONG LI1, XING-YI ZHANG1, PENG ZHAO3, MIAO HE3, HOU-ZHONG ZHANG3, LI-PING SUN3, DONG-LEI SHI1, GUANG-XIN ZHANG1 and MEI SUN4 Division of Thoracic Surgery, The Second Hospital of Jilin University, Changchun 130041; Department of Orthopedics, China-Japan Union Hospital of Jilin University, Changchun 130033; Departments of 3Anesthesia and 4Pathology, The Second Hospital of Jilin University, Changchun 130041, P.R. China2Received September two, 2012; Accepted November 27, 2012 DOI: 10.3892/ol.2013.1116 Abstract. SMC1A (structural maintenance of chromosomes 1A), which encodes a structural subunit of the cohesin protein complex, is necessary for the method of sister chromatid cohesion during the cell cycle. Mutation and deregulation of SMC1A are extremely relevant to diverse human illnesses, which includes Cornelia de Lange syndrome and malignant carcinomas. So as to further investigate the function of SMC1A within the oncogenesis of lung cancer, SMC1A-specific brief hairpin RNA (shRNA)-expressing lentivirus (Lv-shSMC1A) was constructed and applied to infect A549 and H1299 cells. SMC1A mRNA and protein expression levels were downregulated in A549 and H1299 cells as demonstrated by real-time PCR and western blot assays. We found that SMC1A inhibition resulted in substantially impaired proliferation and colony formation too as reduced invasiveness of tumor cells. Notably, Lv-shSMC1A-infected cancer cells exhibited a greater proportion of cells inside the G0/G1 phase, but a decrease proportion of S phase cells, in comparison with the parent or Lv-shCon infected cancer cells. Furthermore, a greater proportion of sub-G1 apoptotic cells was observed in Lv-shSMC1A-infected cells. These outcomes suggest that SMC1A is really a novel proliferation regulator that promotes the TAI-1 manufacturer growth of lung cancer cells, and that downregulation of SMC1A expression induces growth suppression of A549 and H1299 cells by way of G1/S cell cycle phase arrest and apoptosis pathways. For that reason, SMC1A may serve as a new molecular target for lung cancer therapy. Introduction Lung cancer may be the most common malignancy and also the leading lead to of cancer-related mortality worldwide (1). Despite important progress in surgical approaches as well as other conventional therapeutic modalities, for example chemotherapy and radiotherapy, most individuals diagnosed with lung cancer succumb to the disease inside a short period (2-4). Consequently, understanding the molecule mechanisms underlying the oncogenesis of lung cancer is crucially essential for the development of more powerful therapy of lung cancer (5-7). The current discovery of the cohesin complicated in yeast has aided the additional understanding on the molecular basis underlying genome instability, which has been recognized as a hallmark of human carcinomas (eight). The cohesin complex, evolutionarily conserved from yeast to humans, comprises 4 subunits: a pair of SMC (structural maintenance of chromosomes) proteins, namely SMC1A and SMC3, and two non-SMC proteins, RAD21/SCC1 and STAG/SCC3/SA. SMC1A and SMC3 are composed of two coiled domains and interact with each other via their hinge domain to type an antiparallel heterodimer. Their head domains interact with RAD21, producing a ring-like structure (9). By trapping DNA inside the ring-like structure, cohesin is connected with chromosomes, holding pairs of sister chromatids in the time of replication in S.