LITAF通过调节fox01介导的SIRT1表达抑制结直肠癌的干细胞和转移行为。

IF 4.2 3区 医学 Q2 ONCOLOGY
Jiao Guan, Zheng-Yun Zhang, Jian-Hua Sun, Xin-Ping Wang, Zun-Qiang Zhou, Lei Qin
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引用次数: 1

摘要

脂多糖诱导的肿瘤坏死因子α因子(LITAF)是一种激活TNF-α转录,调节炎症反应的转录因子。LITAF已被发现在几种肿瘤中具有潜在的抗癌作用。然而,LITAF在结直肠癌(CRC)中的作用尚不清楚。通过对癌症基因组图谱(TCGA)的全面泛癌分析,LITAF被确定为CRC中差异下调的基因。我们假设LITAF可能参与了CRC进展的调节。本研究旨在探讨LITAF在结直肠癌中的表达谱及其对转移行为和干细胞性的影响及其潜在的分子机制。利用公共数据库探讨LITAF在结直肠癌中的表达谱及其与结直肠癌预后的关系。采用实时荧光定量PCR (qRT-PCR)、western blot和免疫组织化学检测LITAF的表达。此外,我们还在体外研究了LITAF过表达或低表达对CRC细胞增殖、凋亡、迁移、侵袭和干细胞性的影响。并探讨了LITAF对forkhead Box O1 (fox01)-sirtuin 1 (SIRT1)信号轴的调控作用。此外,采用异种移植小鼠模型来研究LITAF在体内的作用。LITAF在肿瘤组织中表达下调,其表达与预后、病理分期及肝转移有关。体外实验证实,LITAF能抑制肿瘤细胞的增殖、迁移、侵袭和干性,并诱导细胞凋亡。体内实验表明,LITAF对荷瘤小鼠的致瘤性和肝转移有抑制作用。此外,LITAF促进fox01介导的SIRT1抑制,从而调节癌症的干性和恶性表型。LITAF在CRC中被沉默,它通过抑制CRC细胞干性和恶性表型参与CRC的进展。因此,LITAF可能作为结直肠癌预后的一种新的生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

LITAF inhibits colorectal cancer stemness and metastatic behavior by regulating FOXO1-mediated SIRT1 expression.

LITAF inhibits colorectal cancer stemness and metastatic behavior by regulating FOXO1-mediated SIRT1 expression.

Lipopolysaccharide-induced tumor necrosis factor alpha factor (LITAF) is a transcription factor that activates the transcription of TNF-α and regulates the inflammatory response. LITAF has been found to have potential anti-cancer effects of in several tumors. However, the role of LITAF in colorectal cancer (CRC) remains unclear. Through a comprehensive pan-cancer analysis of the Cancer Genome Atlas (TCGA), LITAF was identified as a differentially downregulated gene in CRC. We hypothesized that LITAF may participate in the modulation of CRC progression. The present study was aimed to investigate the expression profile of LITAF in CRC and its effect on metastatic behavior and stemness as well as the underlying molecular mechanism. The expression profile of LITAF in CRC, and its relationship with the prognosis of CRC were explored using public databases. LITAF expression was detected by quantitative real-time PCR (qRT-PCR), western blot, and immunohistochemistry. Furthermore, the effects of overexpression or knockdown of LITAF on cell proliferation, apoptosis, migration, invasion, and stemness of CRC cells were investigated in vitro. The regulatory effect of LITAF on forkhead Box O 1 (FOXO1)-sirtuin 1 (SIRT1) signaling axis was also explored. In addition, a xenograft mouse model was used to investigate the in-vivo role of LITAF. LITAF was downregulated in tumor tissues and its expression was associated with the prognosis, pathological stage and liver metastasis. In-vitro experiments confirmed that LITAF inhibited tumor cell proliferation, migration, invasion and stemness, and induced cell apoptosis. In vivo experiments demonstrated that LITAF inhibited the tumorigenicity and liver metastasis in tumor-bearing mice. Additionally, LITAF promoted FOXO1-mediated SIRT1 inhibition, thus regulating cancer stemness and malignant phenotypes. LITAF was silenced in CRC and it participated in the progression of CRC by inhibiting CRC cell stemness, and malignant phenotypes. Therefore, LITAF may serve as a novel biomarker of CRC prognosis.

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来源期刊
CiteScore
7.80
自引率
5.00%
发文量
55
审稿时长
12 months
期刊介绍: The Journal''s scope encompasses all aspects of metastasis research, whether laboratory-based, experimental or clinical and therapeutic. It covers such areas as molecular biology, pharmacology, tumor biology, and clinical cancer treatment (with all its subdivisions of surgery, chemotherapy and radio-therapy as well as pathology and epidemiology) insofar as these disciplines are concerned with the Journal''s core subject of metastasis formation, prevention and treatment.
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