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长链非编码RNA OR3A4通过KLF6通路促进卵巢癌的增殖和转移。

lncRNA OR3A4 Promotes the Proliferation and Metastasis of Ovarian Cancer Through KLF6 Pathway.

作者信息

Guo Fangfang, Du Jianan, Liu Lingling, Gou Yawei, Zhang Mingming, Sun Wei, Yu Hongmei, Fu Xueqi

机构信息

Edmond H. Fischer Signal Transduction Laboratory, College of Life Sciences, Jilin University, Changchun, China.

Department of Gynecology, Xinhua Hospital Affiliated to Dalian University, Dalian, China.

出版信息

Front Pharmacol. 2021 Oct 27;12:727876. doi: 10.3389/fphar.2021.727876. eCollection 2021.

DOI:10.3389/fphar.2021.727876
PMID:34776953
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8578722/
Abstract

Ovarian cancer is a collaborative malignant tumor of the female reproductive system in clinical research. Some clinical studies have shown that OR3A4, which is a cancer-causing lncRNA, plays a major role in promoting the occurrence and development of a variety of tumors. And we also expressed the view that it expressed in ovarian tissue. However, the function of OR3A4 in ovarian cancer remains unclear. To further verify the function of lncRNA OR3A4 in ovarian cancer, we established the xenograft model in the zebra fish. In this study, cells transformed with OR3A4 shRNA plasmids were transplanted into the zebra fish, and the cell proliferation and migration ability were significantly reduced compared to the empty vector. While knocking out OR3A4, we further downregulated its expression by siRNA of KLF6. Our study found that the knocked out OR3A4 resulted in a decrease in cell proliferation and migration level, which can be found in the downregulated expression of KLF6. We also verify the relationship between OR3A4 and circulating tumor cells in the zebra fish xenograft model, the results indicate that lncRNA OR3A4 may be involved in the resistance of ovarian cancer to complain. lncRNA OR3A4 promotes the proliferation and metastasis of ovarian cancer through the KLF6 pathway.

摘要

卵巢癌是临床研究中女性生殖系统的一种协同性恶性肿瘤。一些临床研究表明,致癌长链非编码RNA(lncRNA)OR3A4在多种肿瘤的发生和发展中起主要作用。并且我们也表达过其在卵巢组织中表达的观点。然而,OR3A4在卵巢癌中的功能仍不清楚。为了进一步验证lncRNA OR3A4在卵巢癌中的功能,我们在斑马鱼中建立了异种移植模型。在本研究中,将用OR3A4 shRNA质粒转化的细胞移植到斑马鱼中,与空载体相比,细胞增殖和迁移能力显著降低。在敲除OR3A4的同时,我们通过KLF6的小干扰RNA(siRNA)进一步下调其表达。我们的研究发现,敲除OR3A4导致细胞增殖和迁移水平降低,这可以在KLF6表达下调中发现。我们还在斑马鱼异种移植模型中验证了OR3A4与循环肿瘤细胞之间的关系,结果表明lncRNA OR3A4可能参与卵巢癌的耐药性。lncRNA OR3A4通过KLF6途径促进卵巢癌的增殖和转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/9bce37693642/fphar-12-727876-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/00768f52b552/fphar-12-727876-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/c1384471a98b/fphar-12-727876-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/fe79fabdb104/fphar-12-727876-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/e24704252d69/fphar-12-727876-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/403cff991f7b/fphar-12-727876-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/9bce37693642/fphar-12-727876-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/00768f52b552/fphar-12-727876-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/c1384471a98b/fphar-12-727876-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/fe79fabdb104/fphar-12-727876-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/e24704252d69/fphar-12-727876-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/403cff991f7b/fphar-12-727876-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d989/8578722/9bce37693642/fphar-12-727876-g006.jpg

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