HAX1 enhances the survival and metastasis of non-small cell lung cancer through the AKT/mTOR and MDM2/p53 signaling pathway.
HAX1 enhances the survival and metastasis of non-small cell lung cancer through the AKT/mTOR and MDM2/p53 signaling pathway.
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HAX1通过AKT/mTOR和MDM2/p53信号通路增强非小细胞肺癌的生存和转移
DOI：
10.1111/1759-7714.13634
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发表时间：
2020-11
期刊：
影响因子：
2.9
通讯作者：
Wang M
中科院分区：
文献类型：
--
作者：
Liang Z;Zhong Y;Meng L;Chen Y;Liu Y;Wu A;Li X;Wang M
据报道，HS-1相关蛋白-1（HAX1）在非小细胞肺癌（NSCLC）组织中过表达。然而，HAX1在NSCLC中的潜在机制以前尚未得到证实。本研究探讨HAX1在NSCLC中的作用及其机制。通过TCGA数据库和qRT-PCR证实HAX1在NSCLC组织中的表达。此外，我们还进行了qRT-PCR、Western blotting、Transwell试验、TUNEL试验等，以评估HAX1在A549和H1299细胞系中的作用。根据癌症基因组图谱（TCGA）数据库，与邻近正常组织相比，HAX1 mRNA在NSCLC组织中过表达。QRT-PCR分析显示HAX1 mRNA在NSCLC组织中表达上调。HAX1 mRNA的高表达与肿瘤大小、TNM分期和淋巴结转移有关。HAX1基因沉默可通过抑制AKT/mTOR和MDM2/P53信号通路促进A549和H1299细胞凋亡并降低侵袭力。AKT激动剂SC79可抑制si-HAX1转染的A549和H1299细胞的凋亡，并促进其增殖、迁移和侵袭。本研究为进一步了解HAX1在NSCLC中的作用机制和NSCLC的潜在治疗靶点提供了新的思路。HAX1通过AKT/mTOR信号通路增强NSCLC细胞的存活、侵袭和上皮-间质转化。HAX1在NSCLC中发挥重要作用，应予以考虑。
HS‐1‐associated protein‐1 (HAX1) has been reported to be overexpressed in non‐small cell lung cancer (NSCLC) tissues. However, the underlying mechanism of HAX1 in NSCLC has not previously been demonstrated. The present study investigated the role and underlying mechanism of HAX1 in NSCLC. The HAX1 expression were confirmed in NSCLC tissues through TCGA database and qRT‐PCR. Moreover, we performed qRT‐PCR, Western blotting, Transwell assays, TUNEL assays and so on to evaluate the role of HAX1 in A549 and H1299 cell lines. mRNA expression of HAX1 was overexpressed in NSCLC tissues compared to adjacent normal tissues according to The Cancer Genome Atlas (TCGA) database. QRT‐PCR assays showed that HAX1 mRNA expression was upregulated in NSCLC tissues. The high HAX1 mRNA levels were found to be positively associated with tumor size, TNM stage and lymphatic metastasis. Silencing of HAX1 promoted apoptosis and reduced invasion of A549 and H1299 cells by inhibiting the AKT/mTOR and MDM2/P53 signal pathway. AKT agonist SC79 could inhibit apoptosis and promote proliferation, migration and invasion of A549 and H1299 cells transfected with si‐HAX1. The present study provided a better understanding of HAX1 mechanism in NSCLC and potential therapeutic target for NSCLC. HAX1 enhances the survival, invasion and epithelial–mesenchymal transition of NSCLC cells through the AKT/mTOR signaling pathway. HAX1 play an important role in NSCLC and should be taken into consideration.
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