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

IF 0.8 4区医学 Q4 IMMUNOLOGY

Critical Reviews in Immunology Pub Date : 2024-02-01 DOI:10.1615/critrevimmunol.2024052728

Di Xu, Ziming Wang, Fajiu Li

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引用次数: 0

Abstract

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

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KIAA1429 诱导 LINC01106 的 m6A 修饰，通过 JAK/STAT3 通路增强肺腺癌细胞的恶性程度

背景：LINC01106在肿瘤中的持续表达对肿瘤细胞的恶性表型至关重要；然而，LINC01106在肺腺癌（LUAD）中的作用机制和临床效果尚不明确。方法：采用 qRT-PCR 方法明确 LINC01106 和 KIAA1429 在 LUAD 组织中的水平。利用 Transwell、EdU 和 CCK-8 试验分析了 LINC01106 和 KIAA1429 的功能作用。通过异种移植验证了沉默 LINC01106 在肿瘤生长中的作用。利用 MeRIP、qRT-PCR 和放线菌素 D 试验研究了 LINC01106 之间的调控作用。结果发现，LINC01106与KAK2和STAT3之间存在密切的联系：结果：LINC01106和KIAA1429在LUAD中高表达，LINC01106与肿瘤分级、分期和预后不良有关。数据显示，抑制 LINC01106 可减少 LUAD 细胞的增殖、侵袭和迁移，抑制 LUAD 细胞的致瘤性。此外，LINC01106抑制还降低了磷酸化JAK2和STAT3的水平。LINC01106在KIAA1429的介导下增强了其在LUAD细胞中的m6A修饰和表达。此外，KIAA1429的促进还可消除LINC01106低表达对LUAD细胞恶性表型的抑制作用：结论：该研究发现，KIAA1429可增强LINC01106 m6A修饰，从而在LUAD的发展中发挥促进作用。这些结果可能有助于理解 KIAA1429-m6A-LINC0110 在 LUAD 细胞中的作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Critical Reviews in Immunology 医学-免疫学

CiteScore

2.60

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Immunology covers a broad spectrum of investigations at the genes, molecular, cellular, organ and system levels to reveal defense mechanisms against pathogens as well as protection against tumors and autoimmune diseases. The great advances in immunology in recent years make this field one of the most dynamic and rapidly growing in medical sciences. Critical ReviewsTM in Immunology (CRI) seeks to present a balanced overview of contemporary adaptive and innate immune responses related to autoimmunity, tumor, microbe, transplantation, neuroimmunology, immune regulation and immunotherapy from basic to translational aspects in health and disease. The articles that appear in CRI are mostly obtained by invitations to active investigators. But the journal will also consider proposals from the scientific community. Interested investigators should send their inquiries to the editor before submitting a manuscript.