LncRNA CYTOR knockdown inhibits tumor development via regulating miR-503-5p/PCSK9 in lung adenocarcinoma.

The intricate biological mechanism underlying lung adenocarcinoma (LUAD), characterized by a deficiency of distinctive biomarkers, remain elusive. The presence of Long non-coding RNAs (lncRNAs) have been established to play a role in carcinogenesis. Nevertheless, the regulatory effects and mechanisms of lncRNA CYTOR in LUAD have yet to be elucidated. In this study, RT-qPCR and Western blot were adopted to examine gene mRNA and protein expression, respectively. Cell proliferation was evaluated by CCK-8 assays. Transwell was performed to assay cell migration and invasion. The function of CYTOR in vivo was investigated through a xenograft animal model. We observed an apparent upregulation of CYTOR in LUAD. Silencing CYTOR significantly reduced proliferation, migration, and invasion capabilities of LUAD cells. Mechanism analysis indicated that CYTOR targeted the miR-503-5p/PCSK9 axis. Additionally, inhibiting of miR-503-5p partially reversed the inhibitory effects of CYTOR silencing on the malignant progression of LUAD cells. Animal experiments revealed that CYTOR/miR-503-5p/PCSK9 curbed tumor formation of nude mice in vivo. These findings demonstrated that lncRNA CYTOR acted as an oncogene in LUAD, regulating tumor malignant progression through the miR-503-5p/PCSK9 axis. This study unveiled a new regulation mechanism of LUAD progression, offering potential therapeutic targets for LUAD.

Zhu Z ，Lu J ，Tong J ，Yin Y ，Zhang K ... -  《-》

lncRNA CYTOR promotes lung adenocarcinoma gemcitabine resistance and epithelial-mesenchymal transition by sponging miR-125a-5p and upregulating ANLN and RRM2.

Cao Q ，Wang H ，Zhu J ，Qi C ，Huang H ，Chu X ... -  《-》

USF1-induced overexpression of long noncoding RNA WDFY3-AS2 promotes lung adenocarcinoma progression via targeting miR-491-5p/ZNF703 axis.

Ren P ，Hong X ，Chang L ，Xing L ，Zhang H ... -  《-》

LINC01572 promotes the malignant progression of lung adenocarcinoma by modulating p53 mediated by miRNA-338-5p/TTK axis.

Liu S ，Liu X ，Yang Q ，Zeng C ，Hu G ，Ren B ... -  《-》

LncRNA SGMS1-AS1 regulates lung adenocarcinoma cell proliferation, migration, invasion, and EMT progression via miR-106a-5p/MYLI9 axis.

Lung cancer mainly includes non-small cell lung cancer (NSCLC). Lung adenocarcinoma (LUAD) is the main subtype of NSCLC. Long non-coding RNAs (LncRNAs) had been found to exert numerous functions on the progressions of cancers. MicroRNAs often exist as the target of LncRNAs to regulate a series of signaling pathways in human. We explored the effects and molecular mechanism of LncRNA SGMS1-AS1 on the procedures of LUAD cells. The ENCORI and GEPIA databases were used to analyze the differences in SGMS1, miR-106a-5p, and MYLIP between LUAD and normal tissue. Their expression levels were examined by RT-PCR. CCK8, colony formation, migration, and invasion assay were conducted in LUAD cells which had silenced SGMS1-AS1. To verify the relationship between SGMS1-AS1, miR-106a-5p, and MYLIP, we overexpressed miR-106a-5p inhibitor or MYLIP in LUAD cells after decreasing SGMS1-AS1 and repeated the above assays. SGMS1-AS1 was downregulated in LUAD tissue as well as cells, which was related to good prognosis of patients with lung adenocarcinoma. Additionally, knockdown of SGMS1-AS1 promoted proliferation, migration, invasion, and epithelial mesenchymal transition (EMT) progression of LUAD cells, which meant that SGMS1-AS1 inhibited the progression of LUAD cells. Furthermore, miR-106a-5p was the direct target of SGMS1-AS1 and transfecting miR-106a-5p inhibitor could reversed the impact induced by knockdown of SGMS1-AS1. Subsequently, we found that MYLIP was the target of miR-106a-5p, which was negatively correlated with miR-106a-5p, but had high positive correlation with SGMS1-AS1. Consistently, overexpression MYLIP partly eliminated the effects on A549 cells induced by silencing of SGMS1-AS1. LncRNA SGMS1-AS1 inhibits the proliferation, invasion, migration and EMT progression of LUAD cells via targeting miR-106a-5p/MYLIP axis.

Liu T ，Yang C ，Wang W ，Liu C ... -  《-》