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新型 lncRNA U731166 的上调与黑色素瘤的迁移、侵袭和vemurafenib 耐药相关。

Upregulation of the novel lncRNA U731166 is associated with migration, invasion and vemurafenib resistance in melanoma.

机构信息

Department of Genetics, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, Brazil.

Center for Cell Based Therapy, Ribeirão Preto Medical School, University of São Paulo (USP), Ribeirão Preto, Brazil.

出版信息

J Cell Mol Med. 2022 Feb;26(3):671-683. doi: 10.1111/jcmm.16987. Epub 2022 Jan 18.

DOI:10.1111/jcmm.16987
PMID:35040264
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8817119/
Abstract

Our previous work using a melanoma progression model composed of melanocytic cells (melanocytes, primary and metastatic melanoma samples) demonstrated various deregulated genes, including a few known lncRNAs. Further analysis was conducted to discover novel lncRNAs associated with melanoma, and candidates were prioritized for their potential association with invasiveness or other metastasis-related processes. In this sense, we found the intergenic lncRNA U73166 (ENSG00000230454) and decided to explore its effects in melanoma. For that, we silenced the lncRNA U73166 expression using shRNAs in a melanoma cell line. Next, we experimentally investigated its functions and found that migration and invasion had significantly decreased in knockdown cells, indicating an essential association of lncRNA U73166 for cancer processes. Additionally, using naïve and vemurafenib-resistant cell lines and data from a patient before and after resistance, we found that vemurafenib-resistant samples had a higher expression of lncRNA U73166. Also, we retrieved data from the literature that indicates lncRNA U73166 may act as a mediator of RNA processing and cell invasion, probably inducing a more aggressive phenotype. Therefore, our results suggest a relevant role of lncRNA U73166 in metastasis development. We also pointed herein the lncRNA U73166 as a new possible biomarker or target to help overcome clinical vemurafenib resistance.

摘要

我们之前使用黑色素瘤进展模型（由黑色素细胞、原发性和转移性黑色素瘤样本组成）进行的研究表明，存在各种失调的基因，包括一些已知的 lncRNA。进一步的分析旨在发现与黑色素瘤相关的新型 lncRNA，并根据它们与侵袭性或其他与转移相关的过程的潜在关联对候选物进行优先级排序。在这个意义上，我们发现了位于基因间的 lncRNA U73166（ENSG00000230454），并决定探索其在黑色素瘤中的作用。为此，我们使用 shRNA 在黑色素瘤细胞系中沉默了 lncRNA U73166 的表达。接下来，我们通过实验研究了其功能，发现敲低细胞中的 lncRNA U73166 表达后，迁移和侵袭能力显著降低，表明 lncRNA U73166 与癌症过程密切相关。此外，我们使用未经过处理的和vemurafenib 耐药的细胞系以及一位患者耐药前后的数据进行研究，发现 vemurafenib 耐药样本中的 lncRNA U73166 表达更高。此外，我们从文献中检索到的数据表明，lncRNA U73166 可能作为 RNA 处理和细胞侵袭的介质，可能诱导更具侵袭性的表型。因此，我们的结果表明 lncRNA U73166 在转移发展中发挥着重要作用。我们还指出，lncRNA U73166 作为一种新的可能的生物标志物或靶点，可以帮助克服临床 vemurafenib 耐药性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/95d0b8b67d00/JCMM-26-671-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/636f21fd2dea/JCMM-26-671-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/18fda9bbdf01/JCMM-26-671-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/ee90b536756a/JCMM-26-671-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/b6386e32494b/JCMM-26-671-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/33f4882bc271/JCMM-26-671-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/a8e0f6205fea/JCMM-26-671-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/95d0b8b67d00/JCMM-26-671-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/636f21fd2dea/JCMM-26-671-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/18fda9bbdf01/JCMM-26-671-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/ee90b536756a/JCMM-26-671-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/b6386e32494b/JCMM-26-671-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/33f4882bc271/JCMM-26-671-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/a8e0f6205fea/JCMM-26-671-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/809a/8817119/95d0b8b67d00/JCMM-26-671-g007.jpg

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