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长链非编码RNA P4713通过激活JAK/STAT3信号通路促进口腔鳞状细胞癌的恶性表型。

Long non-coding RNA P4713 contributes to the malignant phenotypes of oral squamous cell carcinoma by activating the JAK/STAT3 pathway.

作者信息

Zhang Xiaojie, Li Yuanyuan, Li Xiaoxu, Ren Xianyue, Xia Juan, Wang Zhi, Cheng Bin, Wang Yun

机构信息

Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat-sen University Guangzhou, Guangdong, China.

出版信息

Int J Clin Exp Pathol. 2017 Nov 1;10(11):10947-10958. eCollection 2017.

PMID:31966439
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6965841/
Abstract

Oral squamous cell carcinoma (OSCC) is a common and aggressively malignant tumor of the head and neck region. Long non-coding RNAs (lncRNAs) are important regulatory molecules in many types of cancer. However, there are limited studies on the role of lncRNAs in OSCC. In this study, we identified that lncRNA P4713 was one of the most up-regulated lncRNAs in OSCC by exploring the expression profile of lncRNAs/mRNAs in four pairs of OSCC samples and adjacent non-cancer tissues. In addition, silencing of P4713 inhibited OSCC proliferation, migration, and invasion . Furthermore, through bioinformatics analysis and functional experiments, we found that decreased P4713 expression affected the expression and phosphorylation of Janus Kinase (JAK) 2 and signal transducer and activator of transcription (STAT) 3. Taken together, the results suggest that P4713 contributes to OSCC cell proliferation, migration, and invasion by activating the JAK/STAT3 pathway. Accordingly, this molecule could be a potential biomarker and therapeutic target in the treatment of OSCC.

摘要

口腔鳞状细胞癌(OSCC)是头颈部常见的侵袭性恶性肿瘤。长链非编码RNA(lncRNA)是多种癌症中的重要调控分子。然而,关于lncRNA在OSCC中的作用的研究有限。在本研究中,我们通过探索四对OSCC样本和相邻非癌组织中lncRNAs/mRNAs的表达谱,确定lncRNA P4713是OSCC中上调最为明显的lncRNA之一。此外,沉默P4713可抑制OSCC的增殖、迁移和侵袭。此外,通过生物信息学分析和功能实验,我们发现P4713表达降低会影响Janus激酶(JAK)2和信号转导及转录激活因子(STAT)3的表达和磷酸化。综上所述,结果表明P4713通过激活JAK/STAT3通路促进OSCC细胞的增殖、迁移和侵袭。因此,该分子可能是OSCC治疗中的潜在生物标志物和治疗靶点。

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本文引用的文献

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Activation of tumor suppressor LKB1 by honokiol abrogates cancer stem-like phenotype in breast cancer via inhibition of oncogenic Stat3.厚朴酚激活肿瘤抑制因子LKB1可通过抑制致癌性Stat3消除乳腺癌中的癌症干细胞样表型。
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HOTAIR is a promising novel biomarker in patients with thyroid cancer.HOTAIR是甲状腺癌患者中一种很有前景的新型生物标志物。
Exp Ther Med. 2017 May;13(5):2274-2278. doi: 10.3892/etm.2017.4231. Epub 2017 Mar 17.
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MiR-93-5p inhibits the EMT of breast cancer cells via targeting MKL-1 and STAT3.微小RNA-93-5p通过靶向肌动蛋白结合蛋白1和信号转导与转录激活因子3抑制乳腺癌细胞的上皮-间质转化。
Exp Cell Res. 2017 Aug 1;357(1):135-144. doi: 10.1016/j.yexcr.2017.05.007. Epub 2017 May 9.
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