Original Article
Functional role of lncRNA DB327252 in lung cancer
Abstract
Background: Lung cancer becomes a concerning health issue and is considered one of the most deadly cancers in the worldwide. Most recently, long non-coding RNAs (lncRNAs) are newfound non-coding RNAs that are thought as one of the major players in a range of biological processes of human diseases. Although lncRNAs are involved in numerous cancer types, the precise understandings of lncRNAs’ functional roles and mechanisms in lung cancer are limited. In this study, we looked for lung cancer related lncRNAs.
Methods: The quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) technique was utilized to investigate the lncRNA DB327252 expression in 91 paired clinical lung cancer tissues and related cell lines. Moreover, its biological functions were also evaluated in the development of lung cancer.
Results: The results indicated that the expression of DB327252 was up-regulated in lung cancer tissues compared to the cancer-adjacent normal tissues (P<0.05); and the up-regulated expression is likely to relate to those with bigger tumor size, adenocarcinoma and advanced TNM stage (P<0.05). In addition, the knockdown of DB327252 inhibited the growth and proliferation of tumor cell in vitro and in vivo. According to the observation from our study, we found that the knockdown of the DB327252 expression, led to G0/G1 phase cell-cycle arrested, colony formation suppressed in vitro, and tumor growth inhibited in a nude mouse xenograft model. Our experimental results also suggest that lncRNA DB327252 may be a lncRNA related to lung cancer and acts an important role in A549 and 16HBE-T cancer cells, which provides evidence that DB327252 has an oncogene-like function in lung cancer.
Conclusions: The lncRNA DB327252 is up-regulated in lung cancer, and its expression implies that it was probable related to biologic functions of lung cancer.
Methods: The quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) technique was utilized to investigate the lncRNA DB327252 expression in 91 paired clinical lung cancer tissues and related cell lines. Moreover, its biological functions were also evaluated in the development of lung cancer.
Results: The results indicated that the expression of DB327252 was up-regulated in lung cancer tissues compared to the cancer-adjacent normal tissues (P<0.05); and the up-regulated expression is likely to relate to those with bigger tumor size, adenocarcinoma and advanced TNM stage (P<0.05). In addition, the knockdown of DB327252 inhibited the growth and proliferation of tumor cell in vitro and in vivo. According to the observation from our study, we found that the knockdown of the DB327252 expression, led to G0/G1 phase cell-cycle arrested, colony formation suppressed in vitro, and tumor growth inhibited in a nude mouse xenograft model. Our experimental results also suggest that lncRNA DB327252 may be a lncRNA related to lung cancer and acts an important role in A549 and 16HBE-T cancer cells, which provides evidence that DB327252 has an oncogene-like function in lung cancer.
Conclusions: The lncRNA DB327252 is up-regulated in lung cancer, and its expression implies that it was probable related to biologic functions of lung cancer.
