Globally, lung cancer is the most frequently occurring malignant tumor and the number one cause of cancer-related deaths [1]. Based on histological characteristics, lung cancer is predominantly divided into two types: non-small cell lung cancer (NSCLC) and small cell lung cancer. Among them, NSCLC accounts for approximately 85 % of all lung cancer cases [2]. Despite significant advancements in diagnostic and therapeutic technologies, the majority of patients with NSCLC still face inevitable metastasis and recurrence, which are major contributors to the high mortality rates associated with this disease [3,4]. Regrettably, at present, there are no truly effective strategies for treating metastatic lung cancer [4].

Circular RNAs (circRNAs) represent an emerging class of non-coding RNAs. These molecules possess unique single-stranded, covalently closed-loop structures, lacking the conventional 5′ caps and 3′ tails found in linear RNAs. Primarily generated from their precursor mRNAs through a process known as back-splicing, circRNAs are extensively expressed across various eukaryotic organisms [5,6]. Their distinctive closed-loop structure confers greater resistance to degradation by the exonuclease RNase R, compared to their linear mRNA counterparts [7]. Emerging evidence has affirmed that circRNAs participate in the progression of many cancers through acting as microRNA sponges and transcription modulators, interacting with RNA-binding proteins (RBPs), regulating alternative splicing and protein translation [6,8,9].

With the advancement and widespread application of sequencing technologies, the expression patterns, roles, and mechanisms of circRNAs are increasingly elucidated in NSCLC [10,11]. For example, circNDUFB2 was lowly expressed in NSCLC tissues and negatively associated with the malignant features. During NSCLC progression, circNDUFB2 suppressed the growth and metastasis of NSCLC cells via IGF2BPs destabilization and anti-tumor immune activation [12]. In NSCLC tissues, circ_0007432 expression was much higher than in para-carcinoma tissues. It promoted malignant behaviors of NSCLC cells and M2 macrophage polarization via binding to SRSF1, thereby facilitating KLF12 mRNA stability and then promoting IL-8 release [13].

Previous studies have shown that circCOL1A2 (hsa_circ_0081069) exhibited elevated expression and oncogenic activity in several cancers. For instance, in tongue squamous cell carcinoma and gastric cancer cells, circCOL1A2 enhanced the migratory and invasive capacities of tumor cells [14,15]. In colorectal cancer, circCOL1A2 not only promoted cell migration and invasion but also stimulated proliferation and epithelial-mesenchymal transition (EMT) in tumor cells [16]. Another circRNA derived from COL1A2 via back-splicing is hsa_circ_0081111, which is located at chr7:94037494–94058742 and has a length of 3315 nt. Our analysis of the GSE236879 dataset revealed higher hsa_circ_0081111 expression in brain metastasis specimens than in primary tumor specimens from NSCLC patients. However, the precise role of hsa_circ_0081111 in NSCLC progression is not yet clear. Therefore, this research delves deeper into the function and underlying mechanisms of hsa_circ_0081111 in NSCLC.