Zfpm2-antisense RNA 1 (ZFPM2-AS1), a long non-coding RNA, has emerged as a significant player in various biological processes, particularly in cancer-related mechanisms. LncRNAs are known to be involved in regulating dosage compensation, epigenetics, and cell differentiation, and ZFPM2-AS1 is no exception [2]. It is located on the 8q23 chromosome and has been associated with multiple signaling pathways, although the exact core pathways are still under research. Its dysregulation can impact a range of cellular functions such as proliferation, migration, invasion, and apoptosis, making it a gene of high interest in cancer research [2,5].

In multiple cancers, studies have shown that ZFPM2-AS1 acts as an oncogene. In breast phyllodes tumor (PT), its overexpression is linked to high tumor grade and adverse prognosis, promoting proliferation, migration, and invasion. Mechanistically, it competitively binds to CDC42, inhibiting ACK1 and STAT1 activation, and launching the transcription of TNFRSF19 [1]. In cutaneous malignant melanoma, deletion of ZFPM2-AS1 restrained cell proliferation, migration, and elevated apoptosis, as it regulated NOTCH1 to activate the NOTCH pathway via sponging miR-650 [3]. Similar oncogenic roles were observed in lung adenocarcinoma, retinoblastoma, esophageal squamous cell carcinoma, renal cell carcinoma, and thyroid cancer through various miRNA-mediated axes [4,6,7,8,9,10].

In conclusion, ZFPM2-AS1 is a crucial lncRNA involved in cancer-related cellular functions such as proliferation, migration, invasion, and apoptosis. Its role as an oncogene in multiple cancer types, including breast PT, melanoma, lung adenocarcinoma, and others, is well-documented. Understanding ZFPM2-AS1 through model-based research, although no KO/CKO mouse models were directly mentioned in the references, provides valuable insights into cancer pathogenesis, potentially leading to new diagnostic, prognostic, and therapeutic strategies for these diseases.