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高风险病理亚型相关 FAM83A-AS1 通过 miR-202-3p/HK2 轴促进肺腺癌的恶性转化和糖酵解。

High‑risk pathological subtype associated FAM83A‑AS1 promotes malignancy and glycolysis of lung adenocarcinoma via miR‑202‑3p/HK2 axis.

机构信息

Department of Thoracic Surgery, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaiyin, Huaian, Jiangsu 223001, P.R. China.

Department of Medical Oncology, Xuzhou Central Hospital, Quanshan, Xuzhou 221000, P.R. China.

出版信息

Oncol Rep. 2023 May;49(5). doi: 10.3892/or.2023.8532. Epub 2023 Mar 24.

DOI:10.3892/or.2023.8532
PMID:36960858
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10086562/
Abstract

According to the diverse cellular morphology, lung adenocarcinoma (LUAD) was classified into five pathological subtypes, referred to as follows: High‑risk group (micropapillary and solid), intermediate‑risk group (acinar and papillary) and low‑risk group (epidic). Nevertheless, little is known about the biological function of long non‑coding RNA (lncRNA) in the molecular determination of LUAD histologic patterns. Screening the transcriptional expression data from TCGA‑LUAD, the differentially expressed lncRNA across the divergent pathological subtypes were explored. Pan‑cancer analysis revealed the characteristic of FAM83A‑AS1, which was also confirmed in the LUAD tissues. The function of FAM83A‑AS1 was uncovered through the assays. RNA immunoprecipitation and dual‑luciferase reporter assays were performed to explore the molecular mechanisms of FAM83A‑AS1. In the present study, it was identified that the expression of FAM83A‑AS1 was increased from the low‑risk group to the high, which was associated with a poorer prognosis and higher risk of recurrence. Pan‑cancer analysis revealed that FAM83A‑AS1 was positively correlated with high tumor mutational burden. Additionally, FAM83A‑AS1 promoted cell migration, invasion and growth of LUAD cancer cells. Mechanistically, FAM83A‑AS1 sponged miR‑202‑3p to regulate the expression of hexokinase II (HK2) in post‑transcription, which facilitated the malignancy and glycolysis. The present study uncovered the biological roles of FAM83A‑AS1/miR‑202‑3p/HK2 axis in regulating malignancy and glycolysis of LUAD, which provided novel avenues to addressing the determination of histologic patterns.

摘要

根据不同的细胞形态，肺腺癌 (LUAD) 被分为五种病理亚型，分别为：高危组（微乳头和实体）、中危组（腺泡和乳头）和低危组（贴壁型）。然而，关于长链非编码 RNA（lncRNA）在 LUAD 组织学模式的分子确定中的生物学功能知之甚少。通过 TCGA-LUAD 的转录表达数据筛选，探讨了不同病理亚型之间差异表达的 lncRNA。泛癌分析揭示了 FAM83A-AS1 的特征，在 LUAD 组织中也得到了证实。通过功能研究揭示了 FAM83A-AS1 的功能。通过 RNA 免疫沉淀和双荧光素酶报告基因实验进行了 FAM83A-AS1 的分子机制研究。在本研究中，确定 FAM83A-AS1 的表达从低危组到高危组增加，与预后较差和复发风险较高相关。泛癌分析表明 FAM83A-AS1 与高肿瘤突变负荷呈正相关。此外，FAM83A-AS1 促进 LUAD 癌细胞的迁移、侵袭和生长。机制上，FAM83A-AS1 海绵吸附 miR-202-3p 调控 hexokinase II (HK2) 的转录后表达，促进恶性肿瘤和糖酵解。本研究揭示了 FAM83A-AS1/miR-202-3p/HK2 轴在调节 LUAD 恶性肿瘤和糖酵解中的生物学作用，为解决组织学模式的确定提供了新的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/6b45b36cea92/or-49-05-08532-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/e8452a01b061/or-49-05-08532-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/05fea45a2b92/or-49-05-08532-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/68a0d2b7847c/or-49-05-08532-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/dfd082eac9e8/or-49-05-08532-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/891ecd43476c/or-49-05-08532-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/0c10967970eb/or-49-05-08532-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/6b45b36cea92/or-49-05-08532-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/e8452a01b061/or-49-05-08532-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/05fea45a2b92/or-49-05-08532-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/68a0d2b7847c/or-49-05-08532-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/dfd082eac9e8/or-49-05-08532-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/891ecd43476c/or-49-05-08532-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/0c10967970eb/or-49-05-08532-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498e/10086562/6b45b36cea92/or-49-05-08532-g06.jpg

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