The role of Necl-5 in the invasive activity of lung adenocarcinoma

Necl-5在肺腺癌侵袭活性中的作用

• 批准号: 23592060
• 负责人: MANIWA YOSHIMASA
• 金额: $ 3.24万
• 依托单位: Kobe University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592060/
• 关键词: 原発性肺癌; 肺腺癌; 細胞接着分子; Necl5; 浸潤能; 上皮間葉移行; 分子標的; バイオマーカー; Necl-5; 肺癌; 癌宿主相互作用; 癌浸潤

In this study,we used a bronchioloalveolar carcinoma (BAC) cell line and fibroblasts to assess the expression of Necl-5 in the development of cancer–stroma communication by using an easy-to-prepare double-layered collagen gel hemisphere (DL-CGH) systemthat enables visualization of cellmigration during invasion. The expression of Necl-5 was higher in BAC cells than in fibroblasts. This tendency didn't change even when the BAC cells were mixed with fibroblasts. To assess the role of Necl-5 in the invasive activity of the BAC cells, we knocked down its expression using RNA interference (RNAi). The invasion assay with DL-CGH revealed that inhibition of Necl-5 expression in the BAC cells was associated with suppressed invasiveness. Necl-5 expression in lung cancer cells is crucial for their invasiveness in the cancer–stromal interaction, suggesting that Necl-5 could be a favorable molecular target for the suppression of invasiveness in lung adenocarcinoma.

在这项研究中，我们使用细支气管肺泡癌（BAC）细胞系和成纤维细胞来评估NECL-5通过使用易于预备的双层胶原蛋白凝胶半球（DL-CGH）系统的癌症 - 质质通信发展中的表达。在BAC细胞中，NECL-5的表达高于成纤维细胞。即使BAC细胞与成纤维细胞混合在一起，这种趋势也不会改变。为了评估NECL-5在BAC细胞的侵入性活性中的作用，我们使用RNA干扰（RNAI）击倒了其表达。使用DL-CGH的侵袭测定表明，BAC细胞中NECL-5表达的抑制与抑制作用有关。肺癌细胞中的NECL-5表达对于它们在癌症 - 基质相互作用中的侵入性至关重要，这表明NECL-5可能是抑制肺腺癌侵入性的有利分子靶标。