KIAA1429 induces the m6A modification of LINC01106 to enhance the malignancy of lung adenocarcinoma cell via JAK/STAT3 pathway

Background: Sustained expression of LINC01106 in tumors is crucial for malignant phenotype of tumor cells; Nevertheless, LINC01106’s mechanisms and clinical effects in lung adenocarcinoma (LUAD) is confined. This report focus on reveal the effect of vir-like m6A methyltransferase associated (KIAA1429)-mediated N6-methyladenosine (m6A) modification to steady LINC01106 expression on LUAD progression. Methods: qRT-PCR was conducted to clarify the LINC01106 and KIAA1429 levels in LUAD tissues. LINC01106’s and KIAA1429’s functional roles were analyzed utilizing Transwell, EdU as well as CCK-8 assays. Xenograft was cconducted to verify the function of silencing LINC01106 in tumor growth. The regulatory role between LINC01106 was investigated using MeRIP, qRT-PCR as well as Actinomycin D assay. Key proteins of JAK/STAT3 (JAK2, STAT3) pathway were revealed via western blotting. Results: LINC01106 and KIAA1429 were high-expressed in LUAD, and LINC01106 were interconnected with high tumor grade, stage, and poor prognosis. Data revealed LINC01106 inhibition reduced LUAD cell proliferation, invasion as well as migration, and restrained LUAD cell tumorigenicity. Additionally, phosphorylated JAK2, STAT3 levels were reduced by LINC01106 silencing. LINC01106 was mediated by KIAA1429 to enhance its m6A modification and expression in LUAD cells. Moreover, KIAA1429 promotion abolished the malignant phenotypic suppression induced by LINC01106 lowexpression in LUAD cells. Conclusion: This research revealed LINC01106 m6A modification was enhanced by KIAA1429 to play the promotive role in LUAD development. The results may conduce to the comprehending of the act of KIAA1429-m6A-LINC0110