Pancreatic cancer (PC) is one of the major causes of cancer-related deaths worldwide [
1,
2]. Although there are many therapeutic approaches, such as chemotherapy and radiofrequency, surgical resection is the only effective treatment. However, the early diagnosis of PC is a key factor for surgery. Hence, understanding the biological processes and molecular mechanisms underlying PC progression might contribute to the effective treatment of PC.
Long non-coding RNAs (lncRNAs) exert an essential role in the occurrence and progression of tumors [
3,
4], mainly in cancer proliferation, metastasis, and other biological functions associated with tumorigenesis [
5,
6]. In PC, abnormal expression and dysfunction of lncRNAs are shown to be associated with rapid progression of cancer and distant metastasis [
7,
8]. A large number of studies have shown that lncRNA can participate in the regulation of various biological functions of tumors such as epigenetics, post-transcriptional regulation, genomic stability, and ceRNA regulation mechanism [
9‐
11]. For example, Wang et al. [
12] reported that UCA1 increased PDL1 expression from the repression of miR-26a/b, miR-193a, and miR-214, contributed to the gastric cancer cell proliferation, migration, and immune escape. Besides, lncRNA NONHSAT101069 was overexpressed in breast cancer tissues and promoted epirubicin resistance, migration, and invasion of breast cancer cells through regulation of NONHSAT101069/miR-129–5p/Twist1 axis in breast cancer [
13]. Moreover, the role of lncRNA in epigenetics was usually reported in various cancers. A previous study showed that lncRNA GLS-AS mediates a feedback loop between Myc and GLS, providing a potential therapeutic target for metabolic reprogramming in pancreatic cancer. PMSB8-AS1, researched in this study, could be a new host factor target for developing antiviral therapy against influenza virus [
14]. The bioinformatic analysis provides new, potential prognostic biomarkers, and therapeutic targets for PDAC that need to be further investigated [
15]. However, the function and molecular mechanism of lncRNA PSMB8-AS1 remain unclear.
It is well known that the competing endogenous RNA (ceRNA) regulation network is the most frequently reported molecular mechanism to elucidate the function in tumor biology progress [
16‐
19]. Therefore, miRNA as the pivotal downstream of lncRNA mediated tumorigenesis via regulation of the target gene. For example, lncRNA GAS5 upregulated the expression of PTEN by functioning as a ceRNA of miR-222–3p, regulating the PC cell migration, invasion, and autophagy [
20]. Based on current research findings, we speculated PSMB8-AS1 probably acted as a sponge regulating miRNAs exerted corresponding biological function.
In this study, we found that PSMB8-AS1 and STAT1 are existing binding sites of miR-382–3p, and demonstrated that PSMB8-AS1 promotes the expression of STAT1/PD-L1, forming a new theoretical basis for pancreatic cancer progression and providing a possible approach for targeted therapy.