Department of Thoracic Surgery, Foshan Clinical Medical College of Guangzhou University of Traditional Chinese Medicine, Foshan, China.
Department of Thoracic Surgery, Southern Medical University Nanfang Hospital, Guangzhou, China.
Panminerva Med. 2023 Mar;65(1):37-42. doi: 10.23736/S0031-0808.20.03978-6. Epub 2020 Sep 3.
Previous studies have shown that PRDX1 is upregulated in some types of malignant tumors. The role of PRDX1 in non-small-cancer lung carcinoma (NSCLC) remains unclear. This study aims to identify the role of PRDX1 in influencing in-vitro biological functions of NSCLC and the molecular mechanism.
We collected 50 cases of fresh NSCLC and adjacent non-tumoral tissues for detecting differential expressions of PRDX1 by quantitative real-time polymerase chain reaction (qRT-PCR). Survival time of NSCLC patients, defined as the period from the operation to the latest follow-up or death due to recurrence or metastasis, was recorded for assessing the relationship between PRDX1 and prognosis in NSCLC. Using lentivirus transfection, PRDX1 level was downregulated in NSCLC cells. Subsequently, proliferative and apoptotic abilities, and expression levels of vital genes in the Wnt/β-Catenin signaling were examined. Finally, the significance of activated Wnt/β-Catenin signaling during PRDX1-regulated NSCLC proliferation was explored.
Using GEPIA database and NSCLC tissues we collected, PRDX1 was detected to be upregulated in NSCLC samples than controls. PRDX1 level was related to tumor staging and prognosis in NSCLC. Knockdown of PRDX1 attenuated proliferative ability and stimulated apoptosis in NSCLC. Protein levels of Wnt5A was downregulated in H1299 and SPC-A1 cells with PRDX1 knockdown. Overexpression of β-Catenin enhanced proliferative ability and inhibited apoptosis in NSCLC cells with PRDX1 knockdown.
PRDX1 is upregulated in NSCLC samples, and linked to tumor staging and prognosis. It stimulates NSCLC to proliferate by activating the Wnt/β-Catenin signaling.
先前的研究表明，PRDX1 在某些类型的恶性肿瘤中上调。PRDX1 在非小细胞肺癌（NSCLC）中的作用尚不清楚。本研究旨在确定 PRDX1 在影响 NSCLC 体外生物学功能中的作用及其分子机制。
我们收集了 50 例新鲜 NSCLC 及相邻非肿瘤组织，通过实时定量聚合酶链反应（qRT-PCR）检测 PRDX1 的差异表达。记录 NSCLC 患者的生存时间，定义为手术至最新随访或因复发或转移导致死亡的时间，以评估 PRDX1 与 NSCLC 预后的关系。通过慢病毒转染下调 NSCLC 细胞中 PRDX1 的水平。随后，检测增殖和凋亡能力以及 Wnt/β-Catenin 信号通路中关键基因的表达水平。最后，探讨 PRDX1 调控 NSCLC 增殖过程中激活的 Wnt/β-Catenin 信号的意义。
使用 GEPIA 数据库和我们收集的 NSCLC 组织，检测到 NSCLC 样本中 PRDX1 上调。PRDX1 水平与 NSCLC 中的肿瘤分期和预后相关。下调 PRDX1 减弱了 NSCLC 的增殖能力并刺激了凋亡。PRDX1 敲低的 H1299 和 SPC-A1 细胞中 Wnt5A 蛋白水平下调。过表达 β-Catenin 增强了 PRDX1 敲低的 NSCLC 细胞的增殖能力并抑制了凋亡。
PRDX1 在 NSCLC 样本中上调，并与肿瘤分期和预后相关。它通过激活 Wnt/β-Catenin 信号刺激 NSCLC 增殖。
