Introduction:
The most typical kind of lung cancer is non-small cell lung cancer (NSCLC). Surgery, targeted therapy, chemotherapy, and immunotherapy are all options for the treatment of NSCLC. LncRNA KTN1-AS1 is significantly increased in NSCLC, and it modulates the expression of microRNAs and downstream genes, promoting NSCLC progression.

Material and methods:
TCGA was employed to predict lncRNA KTN1-AS1 expression in NSCLC. The starBase was utilized to predict downstream microRNAs of KTN1-AS1. The RNA22 database was employed to predict corresponding binding sites. Subcellular localization of KTN1-AS1 was forecasted using the lncLocator database, and the results were validated by FISH. qRT-PCR was used to test KTN1-AS1, microRNA-153-3p, and KLF5 expression. CCK-8, flow cytometry, and Transwell were used to determine cell viability, proliferation, migration, and invasion. Western blot was used to test KLF5 and Ki67 protein levels, and dual-luciferase assay was used to assess bindings of KTN1-AS1 with microRNA-153-3p, and KLF5 with microRNA-153-3p.

Results:
KTN1-AS1 was significantly upregulated in NSCLC cells. Silencing KTN1-AS1 significantly repressed the proliferation, migration, and invasion of NSCLC cells. KTN1-AS1 bound to microRNA-153-3p, and KLF5 was a direct target of microRNA-153-3p. Inhibition of microRNA-153-3p or overexpression of KLF5 restored the stimulatory impact of KTN1-AS1 knockdown on NSCLC cell proliferation and migration.

Conclusions:
KTN1-AS1 drove proliferation, migration, and invasion of NSCLC cells by regulating microRNA-153-3p/KLF5 axis. By studying the role of the KTN1-AS1/microRNA-153-3p/KLF5 axis in NSCLC, the possibility of targeting this axis as a therapeutic target in NSCLC can be explored.