Lung cancer is one of the most malignant tumors, and its morbidity is second only to that of female breast cancers (Sung et al., 2021). Non-small cell lung cancer (NSCLC) is the most common pathological type of lung cancer, accounting for approximately 85% (Zheng, 2016, Rodriguez-Canales et al., 2016). NSCLC is often diagnosed at an advanced stage owing to the lack of effective diagnostic markers and typical clinical symptoms in the early stages. A late diagnosis contributes to a higher mortality rate. In recent years, the survival rates of patients with NSCLC have improved with the promotion and development of low-dose spiral computed tomography (Jones and Baldwin, 2018), targeted therapy (Shroff et al., 2018) and immunotherapy (Duma et al., 2019). Studies have illustrated that the current 5-year survival rate for NSCLC remains poor at only 23% (Siegel et al., 2019, Nasim et al., 2019). Therefore, exploring novel molecular mechanisms and developing individualized therapies are crucial for improving the survival rate of patients with NSCLC.

Up to 90% of the mammalian genome contains non-coding RNAs (ncRNAs), most of which are not translated into proteins. A portion of ncRNAs that cannot encode proteins and are longer than 200 nucleotides are classified as long noncoding RNAs (lncRNAs) (Jathar et al., 2017). Extensive research has demonstrated that lncRNAs are associated with several biological processes (BPs). They can function as oncogenes or tumor suppressors involved in tumorigenesis and development (Dykes and Emanueli, 2017, Kondo et al., 2017). An increasing number of studies have demonstrated that lncRNAs serve not only as diagnostic or prognostic markers, but also as promising therapeutic targets (Chao and Zhou, 2019, Ma et al., 2017, Chandra Gupta and Nandan Tripathi, 2017). The development of gene chips and RNA sequencing has led to the discovery of an increasing number of lncRNAs. However, only a small portion of them have been functionally characterized, and the majority remain poorly understood in terms of their cellular roles and functions.

LINC011322 is a long intergenic non-coding RNA located on the long arm of chromosome 3. Its function has not been adequately annotated. Previous studies have suggested the involvement of LINC01322 in the construction of prognostic signatures for bladder cancer (Qing et al., 2020) and lung squamous cell carcinoma (Sun et al., 2021). LINC01322 is also involved in neurodevelopment and acts upstream gene of Slitrk3 (Schneider et al., 2022). LINC01322 attracted our attention because it was significantly overexpressed in lung adenocarcinoma (LUAD) and positively correlated with poor prognosis. Although LINC01322 is highly expressed in tumor tissues, it is not expressed in nontumor tissues or expressed at very low levels, suggesting that it can act as a therapeutic target.

Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) is a crucial pathway that transduces signals in cells (Mengie Ayele et al., 2022). The JAK2/STAT3 pathway is involved in cell proliferation, apoptosis, transcription, and other BPs. Extensive studies have demonstrated that the JAK2/STAT3 pathway is dysregulated and abnormally activated during cancer development and progression (Zhou et al., 2022, Noori et al., 2022). Thus, molecules that aberrantly activate the JAK2/STAT3 signaling pathway may be crucial in regulating cancer development. In our study, LINC01322 was screened through a differential expression analysis and was identified to be associated with the JAK2/STAT3 pathway. Therefore, we further analyzed LINC01322 using bioinformatics and verified its function and molecular mechanisms. Our findings confirm that LINC01322 promotes LUAD progression and is a promising new therapeutic target.