致癌 tRNA 衍生片段 tRF-Leu-CAG 通过靶向 TCEA3 和增加自噬促进肺癌的肿瘤发生

IF 3.2 4区 医学 Q2 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Fan Wu, Binshu Chai, Pengfei Qi, Yaqi Han, Zhitao Gu, Wei Pan, Hui Zhang, Xianyi Wang, Xiaomin Liu, Heng Zou, Chen Liang, YanLi Li, Wentao Fang, Zhongliang Ma
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引用次数: 0

摘要

tRF-Leu-CAG 是最近发现的一种源自转移 RNA 的非编码单链小 RNA,它引发了人们对其在肺癌中的生物学功能和潜在分子机制的兴趣。 方法 通过实时定量聚合酶链反应(qRT-PCR)测定了 96 组临床患者肺癌组织样本中 tRF-Leu-CAG 的丰度。随后,通过体内和体外实验验证了 tRF-Leu-CAG 在肺癌中的生物学功能。此外,研究人员还探讨了 tRF-Leu-CAG 的潜在靶基因及其与肺癌自噬和耐药性的关系。 结果 我们的分析发现,tRF-Leu-CAG 在非小细胞肺癌(NSCLC)组织中明显上调。此外,我们还观察到,tRF-Leu-CAG 的高表达明显增加了 NSCLC 细胞的增殖和迁移,促进了细胞周期的进展,并抑制了细胞凋亡。此外,我们还发现转录延伸因子 A3(TCEA3)是 tRF-Leu-CAG 的直接靶基因。TCEA3抑制NSCLC的增殖和迁移,而tRF-Leu-CAG通过介导TCEA3的沉默促进NSCLC的增殖和迁移。此外,我们还证明了tRF-Leu-CAG对紫杉醇耐药性的增强取决于自噬作用。最后,tRF-Leu-CAG 明显加速了肿瘤的生长,并促进了体内上皮-间质转化(EMT)过程。 结论 tRF-Leu-CAG 通过靶向 TCEA3 促进 NSCLC 肿瘤生长和转移,并通过增强细胞自噬促进紫杉醇抗性。这些结果为临床治疗 NSCLC 提供了潜在的有效靶点和治疗方案。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Oncogenic tRNA-derived fragment tRF-Leu-CAG promotes tumorigenesis of lung cancer via targeting TCEA3 and increasing autophagy

Oncogenic tRNA-derived fragment tRF-Leu-CAG promotes tumorigenesis of lung cancer via targeting TCEA3 and increasing autophagy

Background

Lung cancer is a prevalent and severe form of malignant tumors worldwide. tRF-Leu-CAG, a recently discovered non-coding single-stranded small RNA derived from transfer RNA, has sparked interest in exploring its biological functions and potential molecular mechanisms in lung cancer.

Methods

The abundance of tRF-Leu-CAG was measured via quantitative real-time polymerase chain reaction (qRT-PCR) in 96 sets of lung cancer tissue samples obtained from clinical patients. Subsequently, both in vivo and in vitro experiments were conducted to validate the biological functions of tRF-Leu-CAG in lung cancer. Furthermore, an exploration of the potential target genes of tRF-Leu-CAG and its association with autophagy and drug resistance in lung cancer was undertaken.

Results

Our analysis revealed a significant upregulation of tRF-Leu-CAG in non-small cell lung cancer (NSCLC) tissues. Additionally, we observed that heightened expression of tRF-Leu-CAG significantly augmented the proliferation and migration of NSCLC cells, facilitated cell cycle progression, and suppressed apoptosis. Furthermore, we identified transcription elongation factor A3 (TCEA3) as a direct target gene of tRF-Leu-CAG. TCEA3 inhibited the proliferation and migration of NSCLC, and tRF-Leu-CAG promoted the proliferation and migration of NSCLC by mediating the silencing of TCEA3. Moreover, we demonstrated that the augmentation of paclitaxel resistance by tRF-Leu-CAG was contingent on autophagy. Finally, tRF-Leu-CAG notably accelerated tumor growth and promoted the process of epithelial-mesenchymal transition (EMT) in vivo.

Conclusions

tRF-Leu-CAG promotes NSCLC tumor growth and metastasis by targeting TCEA3 and promotes paclitaxel resistance by enhancing cellular autophagy. These results provide potentially effective targets and therapeutic options for the clinical treatment of NSCLC.

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来源期刊
Journal of Gene Medicine
Journal of Gene Medicine 医学-生物工程与应用微生物
CiteScore
6.40
自引率
0.00%
发文量
80
审稿时长
6-12 weeks
期刊介绍: The aims and scope of The Journal of Gene Medicine include cutting-edge science of gene transfer and its applications in gene and cell therapy, genome editing with precision nucleases, epigenetic modifications of host genome by small molecules, siRNA, microRNA and other noncoding RNAs as therapeutic gene-modulating agents or targets, biomarkers for precision medicine, and gene-based prognostic/diagnostic studies. Key areas of interest are the design of novel synthetic and viral vectors, novel therapeutic nucleic acids such as mRNA, modified microRNAs and siRNAs, antagomirs, aptamers, antisense and exon-skipping agents, refined genome editing tools using nucleic acid /protein combinations, physically or biologically targeted delivery and gene modulation, ex vivo or in vivo pharmacological studies including animal models, and human clinical trials. Papers presenting research into the mechanisms underlying transfer and action of gene medicines, the application of the new technologies for stem cell modification or nucleic acid based vaccines, the identification of new genetic or epigenetic variations as biomarkers to direct precision medicine, and the preclinical/clinical development of gene/expression signatures indicative of diagnosis or predictive of prognosis are also encouraged.
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