High­risk pathological subtype associated FAM83A­AS1 promotes malignancy and glycolysis of lung adenocarcinoma via miR­202­3p/HK2 axis.

ABSTRACT

According to the diverse cellular morphology, lung adenocarcinoma (LUAD) was classified into five pathological subtypes, referred to as follows High­risk group (micropapillary and solid), intermediate­risk group (acinar and papillary) and low­risk group (epidic). Nevertheless, little is known about the biological function of long non­coding RNA (lncRNA) in the molecular determination of LUAD histologic patterns. Screening the transcriptional expression data from TCGA­LUAD, the differentially expressed lncRNA across the divergent pathological subtypes were explored. Pan­cancer analysis revealed the characteristic of FAM83A­AS1, which was also confirmed in the LUAD tissues. The function of FAM83A­AS1 was uncovered through the in vitro assays. RNA immunoprecipitation and dual­luciferase reporter assays were performed to explore the molecular mechanisms of FAM83A­AS1. In the present study, it was identified that the expression of FAM83A­AS1 was increased from the low­risk group to the high, which was associated with a poorer prognosis and higher risk of recurrence. Pan­cancer analysis revealed that FAM83A­AS1 was positively correlated with high tumor mutational burden. Additionally, FAM83A­AS1 promoted cell migration, invasion and growth of LUAD cancer cells. Mechanistically, FAM83A­AS1 sponged miR­202­3p to regulate the expression of hexokinase II (HK2) in post­transcription, which facilitated the malignancy and glycolysis. The present study uncovered the biological roles of FAM83A­AS1/miR­202­3p/HK2 axis in regulating malignancy and glycolysis of LUAD, which provided novel avenues to addressing the determination of histologic patterns.