Department of Thoracic Surgery, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, China.
Department of Scientific Research, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, China.
Thorac Cancer. 2020 Aug;11(8):2137-2145. doi: 10.1111/1759-7714.13506. Epub 2020 Jun 22.
Lung adenocarcinoma (LUAD) is the most predominant histological type of lung cancer with a poor prognosis. In this study, we demonstrate that LBX2 regulates cell proliferation, migration and invasion and the potential molecular mechanism in LUAD.
The Cancer Genome Atlas dataset was accessed to screen for novel genes and immunohistochemistry (IHC) assays were performed to determine the association between LBX2 expression and clinicopathological features of LUAD. 5-ethynyl-2'-deoxyuridine, colony formation and Real Time xCELLigence analysis system were used to evaluate the cell proliferation abilities of LUAD. Wound healing, transwell and Matrigel assays were used to detect cell migration and invasion capacities. Xenograft tumor models were used to assess the oncogenic role of LBX2 in vivo.
We found that LBX2 was hyperexpressed in LUAD and correlated with clinicopathological features and poor prognosis in LUAD patients. Knockdown of LBX2 inhibited cell proliferation, migration and invasion of LUAD, whereas ectopic expression of LBX2 enhanced tumor growth, migration, and invasion. We further found that LBX2 might participate in epithelial-to-mesenchymal transition (EMT) progression and influence EMT-related gene expression.
The current study suggests that LBX2 plays an oncogenic role in LUAD and may participate in tumor proliferation, migration, and invasion through EMT progression.
Significant findings of the study LBX2 might participate in LUAD cell proliferation, migration and invasion via EMT progression. What this study adds LBX2 may represent a potential biomarker and a promising therapeutic target for LUAD.
肺腺癌（LUAD）是最主要的肺癌组织学类型，预后较差。本研究旨在探讨 LBX2 在 LUAD 中的作用及其潜在的分子机制。
我们从癌症基因组图谱数据库中筛选出新型基因，并通过免疫组织化学（IHC）检测来确定 LBX2 表达与 LUAD 临床病理特征之间的关系。采用 5-乙炔基-2'-脱氧尿苷（5-ethynyl-2'-deoxyuridine，EdU）、集落形成实验和实时 xCELLigence 分析系统评估 LUAD 细胞增殖能力。通过划痕愈合实验、Transwell 实验和 Matrigel 侵袭实验检测细胞迁移和侵袭能力。利用异种移植肿瘤模型在体内评估 LBX2 的致癌作用。
我们发现 LBX2 在 LUAD 中高表达，与 LUAD 患者的临床病理特征和预后不良相关。LBX2 敲低抑制 LUAD 细胞增殖、迁移和侵袭，而 LBX2 异位表达则增强肿瘤生长、迁移和侵袭。进一步研究发现，LBX2 可能参与上皮间质转化（epithelial-to-mesenchymal transition，EMT）进展，并影响 EMT 相关基因表达。
本研究表明，LBX2 在 LUAD 中发挥致癌作用，可能通过 EMT 进展参与肿瘤增殖、迁移和侵袭。
LBX2 可能通过 EMT 进展参与 LUAD 细胞增殖、迁移和侵袭。本研究的意义：LBX2 可能成为 LUAD 的潜在生物标志物和有前途的治疗靶点。
