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下调 LINC00115 通过靶向 miR-212-5p/FZD5/Wnt/β-catenin 轴抑制前列腺癌细胞增殖和侵袭。

Down-regulated LINC00115 inhibits prostate cancer cell proliferation and invasion via targeting miR-212-5p/FZD5/Wnt/β-catenin axis.

机构信息

Department of Urology, Shenzhen Longhua District Central Hospital, The Affiliated Central Hospital of Shenzhen Longhua District, Guangdong Medical University, Shenzhen, China.

Wake Forest University, Winston-Salem, NC, USA.

出版信息

J Cell Mol Med. 2021 Nov;25(22):10627-10637. doi: 10.1111/jcmm.17000. Epub 2021 Oct 26.

DOI:10.1111/jcmm.17000
PMID:34697900
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8581327/
Abstract

Prostate cancer is the second most frequent malignancy in men worldwide, and its incidence is increasing. Therefore, it is urgently required to clarify the underlying mechanisms of prostate cancer. Although the long non-coding RNA LINC00115 was identified as an oncogene in several cancers, the expression and function of LINC00115 in prostate cancer have not been explored. Our results showed that LINC00115 was significantly up-regulated in prostate cancer tissues, which was significantly associated with a poor prognosis for prostate cancer patients. Functional studies showed that knockdown LINC00115 inhibited cell proliferation and invasion. In addition, LINC00115 served as a competing endogenous RNA (ceRNA) through sponging miR-212-5p to release Frizzled Family Receptor 5 (FZD5) expression. The expression of miR-212-5p was noticeably low in tumour tissues, and FZD5 expression level was down-regulated with the knockdown of LINC00115. Knockdown LINC00115 inhibited the Wnt/β-catenin signalling pathway by inhibiting the expression of FZD5. Rescue experiments further showed that LINC00115 inhibits prostate cancer cell proliferation and invasion via targeting miR-212-5p/ FZD5/ Wnt/β-catenin axis. The present study provided clues that LINC00115 may be a promising novel therapeutic target for prostate cancer patients.

摘要

前列腺癌是全世界男性第二大常见恶性肿瘤，其发病率正在上升。因此，迫切需要阐明前列腺癌的潜在机制。虽然长链非编码 RNA LINC00115 已被确定为几种癌症中的致癌基因，但 LINC00115 在前列腺癌中的表达和功能尚未得到探索。我们的研究结果表明，LINC00115 在前列腺癌组织中显著上调，与前列腺癌患者的预后不良显著相关。功能研究表明，敲低 LINC00115 抑制细胞增殖和侵袭。此外，LINC00115 通过海绵吸附 miR-212-5p 作为竞争性内源 RNA (ceRNA) 来释放卷曲家族受体 5 (FZD5) 的表达。肿瘤组织中 miR-212-5p 的表达明显降低，LINC00115 敲低后 FZD5 表达水平下调。LINC00115 通过抑制 FZD5 的表达抑制 Wnt/β-catenin 信号通路。进一步的挽救实验表明，LINC00115 通过靶向 miR-212-5p/FZD5/Wnt/β-catenin 轴抑制前列腺癌细胞的增殖和侵袭。本研究为 LINC00115 可能成为前列腺癌患者有前途的新型治疗靶点提供了线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/4a3d8933f304/JCMM-25-10627-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/dca25e0be931/JCMM-25-10627-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/9da41017949f/JCMM-25-10627-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/cb6d6e42a095/JCMM-25-10627-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/5977c3f72839/JCMM-25-10627-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/9f929d948b84/JCMM-25-10627-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/4a3d8933f304/JCMM-25-10627-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/dca25e0be931/JCMM-25-10627-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/9da41017949f/JCMM-25-10627-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/cb6d6e42a095/JCMM-25-10627-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/5977c3f72839/JCMM-25-10627-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/9f929d948b84/JCMM-25-10627-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd5/8581327/4a3d8933f304/JCMM-25-10627-g001.jpg

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LINC00115 promotes chemoresistant breast cancer stem-like cell stemness and metastasis through SETDB1/PLK3/HIF1α signaling.LINC00115 通过 SETDB1/PLK3/HIF1α 信号促进化疗耐药乳腺癌干细胞样细胞干性和转移。
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Structure of human Frizzled5 by fiducial-assisted cryo-EM supports a heterodimeric mechanism of canonical Wnt signaling.人卷曲蛋白 5 的结构通过基准辅助 cryo-EM 支持经典 Wnt 信号的异二聚体机制。
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