According to the diverse cellular morphology, lung adenocarcinoma (LUAD) was classified into five pathological subtypes, referred to as follows: High‑risk group (micropapillary and solid), intermediate‑risk group (acinar and papillary) and low‑risk group (epidic). Nevertheless, little is known about the biological function of long non‑coding RNA (lncRNA) in the molecular determination of LUAD histologic patterns. Screening the transcriptional expression data from TCGA‑LUAD, the differentially expressed lncRNA across the divergent pathological subtypes were explored. Pan‑cancer analysis revealed the characteristic of FAM83A‑AS1, which was also confirmed in the LUAD tissues. The function of FAM83A‑AS1 was uncovered through the in vitro assays. RNA immunoprecipitation and dual‑luciferase reporter assays were performed to explore the molecular mechanisms of FAM83A‑AS1. In the present study, it was identified that the expression of FAM83A‑AS1 was increased from the low‑risk group to the high, which was associated with a poorer prognosis and higher risk of recurrence. Pan‑cancer analysis revealed that FAM83A‑AS1 was positively correlated with high tumor mutational burden. Additionally, FAM83A‑AS1 promoted cell migration, invasion and growth of LUAD cancer cells. Mechanistically, FAM83A‑AS1 sponged miR‑202‑3p to regulate the expression of hexokinase II (HK2) in post‑transcription, which facilitated the malignancy and glycolysis. The present study uncovered the biological roles of FAM83A‑AS1/miR‑202‑3p/HK2 axis in regulating malignancy and glycolysis of LUAD, which provided novel avenues to addressing the determination of histologic patterns.
Keywords: FAM83A‑AS1; glycolysis; hexokinase II; histological pathology subtype; lung adenocarcinoma.