China Oncology ›› 2016, Vol. 26 ›› Issue (12): 974-980.doi: 10.19401/j.cnki.1007-3639.2016.12.003

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The influence of ACSS2 knockdown on the proliferation, apoptosis and migration of NSCLC cell line A549

LU Xiaoxia1,2, CHANG Shu3, BI Minghong1, WANG Yaping1   

  1. 1. Department of Medical Oncology, the First Affiliated Hospital of Bengbu Medical College, Bengbu 233000, Anhui Province, China; 2. Anhui Key Laboratory of Tissue Transplantation of Bengbu Medical College, Bengbu 233000, Anhui Province, China; 3. Department of Library, the First Affiliated Hospital of Bengbu Medical College, Bengbu 233000, Anhui Province, China
  • Online:2016-12-30 Published:2017-01-23
  • Contact: BI Minghong E-mail: bmh2003@126.com

Abstract: Background and purpose: Metabolism change is one of the main characteristics of the tumor development. Many studies have confirmed that cytosolic acetyl-CoA synthetase 2 (ACSS2) plays a critical role in hydrocarbon metabolism of cancer cells. This study aimed to explore the effect of ACSS2 on cellular proliferation, apoptosis and migration of A549 cells by RNA interference. Methods: The ACSS2 interference fragment ACSS2-siRNA and negative control were designed and synthesized for RNA interference followed by the transient transfection in non-small cell lung cancer (NSCLC) cell line A549. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect ACSS2 mRNA expression. Methyl thiazolyl tetrazolium (MTT), flow cytometry and wound healing assay were used to detect cell proliferation, apoptosis rate and migration. Results: The expression of ACSS2 mRNA was significantly decreased after transfection with the interference fragment ACSS2-siRNA in NSCLC cell line A549. The proliferation and migration activity of ACSS2-siRNA treated cells were decreased significantly compared with the control group. The apoptosis rate, especially the early apoptosis, was increased.. Conclusion: Knockdown of the ACSS2 expression in NSCLC cell line A549 can significantly inhibit the cell proliferation, migration ability and pro- mote the apoptosis rate, especially early apoptosis. This study indicates that ACSS2 may contribute to the progression of human lung adenocarcinoma and may have the potential to serve as a novel therapeutic target.

Key words: Lung neoplasm, Cytosolic acetyl-CoA synthetase 2, RNA interference