Trefoil factor 3 silencing can inhibit the proliferation and apoptosis of lung cancer cells.

Q2 Medicine
Journal of Buon Pub Date : 2021-09-01
Moran Liu, Yin Xiao
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引用次数: 0

Abstract

Purpose: At present, the global incidence of lung cancer is still high. Exploring its effective treatment is still a crucial research direction. Trefoil factor 3 (TFF3) was found to be related to the proliferation and apoptosis of many tumor cells. Therefore, this article focuses on the effect of TFF3 on SPC-A1 lung cancer cells.

Methods: The tissue samples of lung cancer patients were collected, and the expression level of TFF3 was detected by Western blot (WB) and Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) techniques. After transfection technique was used to silence the expression of TFF3 in SPC-A1 cells, the proliferation activity of SPC-A1 cells was detected by CCK-8 assay and EdU staining, and the cell cycle and related factor expression levels were also detected. The apoptosis rate of SPC-A1 cells was detected by Tunel staining and flow cytometry, and the expression levels of apoptosis-related factors were also detected.

Results: TFF3 in lung cancer tissues was obviously higher than that in para-carcinoma tissue. At the same time, similar results were found in SPC-A1 lung cancer cells. CCK-8 assay and EdU staining found that silencing TFF3 gene expression can effectively inhibit the proliferation of SPC-A1 cells. Flow cytometry detection of SPC-A1 cell cycle showed that cells were blocked in G0/G1 phase, and the number of cells in S+G2/M phase was obviously reduced. Cyclin D1 expression was also obviously reduced. At the same time, silencing TFF3 gene expression can promote the increase of Bax expression and inhibit the expression of Bcl-2, thereby increasing the apoptosis rate of SPC-A1 cells. Furthermore, silencing the TFF3 gene can effectively inhibit the excessive activation of the Wnt/β-catenin pathway in SPC-A1 cells.

Conclusions: Our results show that the expression of TFF3 in lung cancer was obviously increased. Silencing TFF3 in SPC-A1 cells can inhibit the cell proliferation and promote cell apoptosis. At the same time, we confirmed that silencing TFF3 gene can inhibit the abnormal activation of Wnt/β-catenin signaling pathway in SPC-A1 cells.

三叶因子3沉默可抑制肺癌细胞的增殖和凋亡。
目的:目前,肺癌在全球的发病率仍然很高。探索其有效治疗方法仍是一个重要的研究方向。三叶因子3 (TFF3)被发现与许多肿瘤细胞的增殖和凋亡有关。因此,本文重点研究TFF3对SPC-A1肺癌细胞的影响。方法:采集肺癌患者组织标本,采用Western blot (WB)和qRT-PCR (qRT-PCR)技术检测TFF3的表达水平。采用转染技术沉默SPC-A1细胞中TFF3的表达后,采用CCK-8法和EdU染色检测SPC-A1细胞的增殖活性,同时检测细胞周期及相关因子的表达水平。采用Tunel染色和流式细胞术检测SPC-A1细胞的凋亡率,并检测凋亡相关因子的表达水平。结果:肺癌组织中TFF3明显高于癌旁组织。同时,在SPC-A1肺癌细胞中也发现了类似的结果。CCK-8实验和EdU染色发现沉默TFF3基因表达可有效抑制SPC-A1细胞的增殖。流式细胞术检测SPC-A1细胞周期显示细胞在G0/G1期被阻断,S+G2/M期细胞数量明显减少。Cyclin D1的表达也明显降低。同时,沉默TFF3基因表达可促进Bax表达增加,抑制Bcl-2的表达,从而提高SPC-A1细胞的凋亡率。此外,沉默TFF3基因可以有效抑制SPC-A1细胞中Wnt/β-catenin通路的过度激活。结论:我们的研究结果表明,TFF3在肺癌中的表达明显升高。沉默SPC-A1细胞中的TFF3可抑制细胞增殖,促进细胞凋亡。同时,我们证实沉默TFF3基因可以抑制SPC-A1细胞中Wnt/β-catenin信号通路的异常激活。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Buon
Journal of Buon 医学-肿瘤学
自引率
0.00%
发文量
0
审稿时长
4-8 weeks
期刊介绍: JBUON aims at the rapid diffusion of scientific knowledge in Oncology. Its character is multidisciplinary, therefore all aspects of oncologic activities are welcome including clinical research (medical oncology, radiation oncology, surgical oncology, nursing oncology, psycho-oncology, supportive care), as well as clinically-oriented basic and laboratory research, cancer epidemiology and social and ethical aspects of cancer. Experts of all these disciplines are included in the Editorial Board. With a rapidly increasing body of new discoveries in clinical therapeutics, the molecular mechanisms that contribute to carcinogenesis, advancements in accurate and early diagnosis etc, JBUON offers a free forum for clinicians and basic researchers to make known promptly their achievements around the world. With this aim JBUON accepts a broad spectrum of articles such as editorials, original articles, reviews, special articles, short communications, commentaries, letters to the editor and correspondence among authors and readers. JBUON keeps the characteristics of its former paper print edition and appears as a bimonthly e-published journal with continuous volume, issue and page numbers.
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