Wenwei Mao1, Tingjian Li1. 1. Department of Respiratory Medicine, The First People's Hospital of Wenling City, Wenling City, China.
Abstract
Background: MACC1-AS1 is an oncogenic lncRNA in gastric cancer, which interacts with AMP-activated protein kinase (AMPK) to promote cancer development. AMPK is known to interact with phosphatase and tensin homolog (PTEN). Therefore, MACC1-AS1 may also have associations with PTEN. This study aimed to investigate the interactions between MACC1-AS1 and PTEN in lung adenocarcinoma (LUAD). Materials and Methods: This study recruited 64 LUAD patients admitted to The First People's Hospital of Wenling City. Gene and protein expression levels were determined by qPCR and western blot, respectively. Cell transfections were performed to assess gene interactions. Cell proliferation was evaluated by CCK-8 assay. Results: MACC1-AS1 was upregulated in LUAD and inversely correlated with the expression of PTEN. High expression levels of MACC1-AS1 in LUAD tissues were closely correlated with poor survival rate of LUAD patients. In LUAD cells, overexpression of MACC1-AS1 led to decreased expression of PTEN and increased proliferation rate of LUAD cells, while MACC1-AS1 silencing led to increased expression of PTEN and decreased proliferation rate of LUAD cells. Furthermore, overexpression of PTEN attenuated the effects of overexpressing MACC1-AS1. Conclusions: The authors' results demonstrated that MACC1-AS1 promoted cell proliferation by downregulating PTEN in LUAD cells.
Background: MACC1-AS1 is an oncogenic lncRNA in gastric cancer, which interacts with AMP-activated protein kinase (AMPK) to promote cancer development. AMPK is known to interact with phosphatase and tensin homolog (PTEN). Therefore, MACC1-AS1 may also have associations with PTEN. This study aimed to investigate the interactions between MACC1-AS1 and PTEN in lung adenocarcinoma (LUAD). Materials and Methods: This study recruited 64 LUADpatients admitted to The First People's Hospital of Wenling City. Gene and protein expression levels were determined by qPCR and western blot, respectively. Cell transfections were performed to assess gene interactions. Cell proliferation was evaluated by CCK-8 assay. Results:MACC1-AS1 was upregulated in LUAD and inversely correlated with the expression of PTEN. High expression levels of MACC1-AS1 in LUAD tissues were closely correlated with poor survival rate of LUADpatients. In LUAD cells, overexpression of MACC1-AS1 led to decreased expression of PTEN and increased proliferation rate of LUAD cells, while MACC1-AS1 silencing led to increased expression of PTEN and decreased proliferation rate of LUAD cells. Furthermore, overexpression of PTEN attenuated the effects of overexpressing MACC1-AS1. Conclusions: The authors' results demonstrated that MACC1-AS1 promoted cell proliferation by downregulating PTEN in LUAD cells.