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首页> 外文期刊>Thoracic cancer. >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 enhances the survival and metastasis of non‐small cell lung cancer through the AKT / mTOR and MDM2 /p53 signaling pathway

机译:HAX1通过AKT / MTOR和MDM2 / P53信号通路增强非小细胞肺癌的存活率和转移

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Background: 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. Methods: 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. Results: 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. Conclusions: The present study provided a better understanding of HAX1 mechanism in NSCLC and potential therapeutic target for NSCLC.
机译:背景: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,先前尚未证明NSCLC中HAX1的潜在机制。本研究研究了HAX1在NSCLC中的作用和潜在机制。方法:通过TCGA数据库和QRT-PCR在NSCLC组织中证实HAX1表达。此外,我们进行了QRT-PCR,Western印迹,Transwell测定,Tunel测定等,以评估Hax1在A549和H1299细胞系中的作用。结果:与根据癌症基因组Atlas(TCGA)数据库的相邻正常组织相比,HAX1的mRNA表达在NSCLC组织中过表达。 QRT-PCR测定显示HAX1 mRNA表达在NMSCLC组织中上调。发现高HAX1 mRNA水平与肿瘤大小,TNM阶段和淋巴结转移呈正相关。通过抑制AKT / mTOR和MDM2 / P53信号通路,HAX1的沉默促进凋亡和降低A549和H1299细胞的侵袭。 AKT激动剂SC79可以抑制凋亡,促进用Si-hax1转染A549和H1299细胞的增殖,迁移和侵袭。结论:本研究提供了对NSCLC中的HAX1机制和NSCLC的潜在治疗靶标的更好理解。

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