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Panminerva Medica 2020 Sep 03

DOI: 10.23736/S0031-0808.20.03978-6

Copyright © 2020 EDIZIONI MINERVA MEDICA

lingua: Inglese

PRDX1 stimulates non-small-cell lung carcinoma to proliferate via the Wnt/β-Catenin signaling

Changshan SONG 1, Gang XIONG 2, Shengli YANG 3, Xiaoqun WEI 4, Xiaowei YE 5, Wei HUANG 6 , Riwen ZHANG 7

1 Department of Thoracic Surgery, Foshan Clinical Medical School of Guangzhou University of Chinese Medicine, Foshan, China; 2 Department of Thoracic Surgery, Southern Medical University Nanfang Hospital, Guangzhou, China; 3 Department of Thoracic Surgery, First People’s Hospital of Foshan, Affiliated Hospital of Sun Yat-sen University in Foshan, Foshan, China; 4 Department of Respiratory Medicine, The First People's Hospital of Foshan, Foshan, China; 5 Department of Oncology, First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China; 6 Department of Oncology, Shunde Hospital of Southern Medical University (The First People's Hospital of Shunde), Foshan, China; 7 Department of Oncology, Guangdong Provincial People's Hospital's Nanhai Hospital, The Second People's Hospital Of Nanhai District, Foshan, China


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BACKGROUND: 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.
PATIENTS AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.


KEY WORDS: PRDX1; Wnt/β-Catenin signaling; NSCLC; Proliferation

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