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ANKRD49 通过 P38/ATF-2 信号通路促进肺腺癌的侵袭和转移。

ANKRD49 promotes the invasion and metastasis of lung adenocarcinoma via a P38/ATF-2 signalling pathway.

机构信息

School of Basic Medicine, Basic Medical Science Center, Shanxi Medical University, Jinzhong, China.

Xi'an Jiaotong University-Affiliated Honghui Hospital, Xi'an, China.

出版信息

J Cell Mol Med. 2022 Aug;26(16):4401-4415. doi: 10.1111/jcmm.17464. Epub 2022 Jun 30.

DOI:10.1111/jcmm.17464
PMID:35775112
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9357638/
Abstract

Lung adenocarcinoma (LUAD) is the most challenging neoplasm to treat in clinical practice. Ankyrin repeat domain 49 protein (ANKRD49) is highly expressed in several carcinomas; however, its pattern of expression and role in LUAD are not known. Tissue microarrays, immunohistochemistry, χ test, Spearman correlation analysis, Kaplan-Meier, log-rank test, and Cox's proportional hazard model were used to analyse the clinical cases. The effect of ANKRD49 on the LUAD was investigated using CCK-8, clonal formation, would healing, transwell assays, and nude mice experiment. Expressions of ANKRD49 and its associated downstream protein molecules were verified by real-time PCR, Western blot, immunohistochemistry, and/or immunofluorescence analyses. ANKRD49 expression was highly elevated in LUAD. The survival rate and Cox's modelling analysis indicated that there may be an independent prognostic indicator for LUAD patients. We also found that ANKRD49 promoted the invasion and migration in both in in vitro and in vivo assays, through upregulating matrix metalloproteinase (MMP)-2 and MMP-9 activities via the P38/ATF-2 signalling pathway Our findings suggest that ANKRD49 is a latent biomarker for evaluating LUAD prognosis and promotes the metastasis of A549 cells via upregulation of MMP-2 and MMP-9 in a P38/ATF-2 pathway-dependent manner.

摘要

肺腺癌（LUAD）是临床实践中最具挑战性的肿瘤。锚蛋白重复域 49 蛋白（ANKRD49）在几种癌中高表达；然而，其在 LUAD 中的表达模式和作用尚不清楚。使用组织微阵列、免疫组织化学、χ 检验、Spearman 相关分析、Kaplan-Meier、log-rank 检验和 Cox 比例风险模型对临床病例进行分析。使用 CCK-8、克隆形成、伤口愈合、Transwell 测定和裸鼠实验研究了 ANKRD49 对 LUAD 的影响。通过实时 PCR、Western blot、免疫组织化学和/或免疫荧光分析验证 ANKRD49 及其相关下游蛋白分子的表达。ANKRD49 在 LUAD 中高度表达。生存率和 Cox 模型分析表明，LUAD 患者可能存在独立的预后指标。我们还发现，ANKRD49 通过上调基质金属蛋白酶（MMP）-2 和 MMP-9 活性，通过 P38/ATF-2 信号通路促进体外和体内侵袭和迁移。我们的研究结果表明，ANKRD49 是评估 LUAD 预后的潜在生物标志物，通过上调 MMP-2 和 MMP-9，以 P38/ATF-2 通路依赖性方式促进 A549 细胞的转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae3b/9357638/f58820733b62/JCMM-26-4401-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae3b/9357638/6b340383461b/JCMM-26-4401-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae3b/9357638/7cf0b046ef63/JCMM-26-4401-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae3b/9357638/f58820733b62/JCMM-26-4401-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae3b/9357638/6b340383461b/JCMM-26-4401-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae3b/9357638/7cf0b046ef63/JCMM-26-4401-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae3b/9357638/f58820733b62/JCMM-26-4401-g001.jpg

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