PIWI-interacting RNA-YBX1 inhibits proliferation and metastasis by the MAPK signaling pathway via YBX1 in triple-negative breast cancer.
PIWI-interacting RNA-YBX1 inhibits proliferation and metastasis by the MAPK signaling pathway via YBX1 in triple-negative breast cancer.
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在三阴性乳腺癌中，PIWI相互作用RNA - YBX1通过YBX1经MAPK信号通路抑制增殖和转移。
DOI：
10.1038/s41420-023-01771-w
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发表时间：
2024-01-05
影响因子：
7
通讯作者：
Xie, Xinhua
中科院分区：
文献类型：
--
作者：
Wu, Linyu;Huang, Shanshan;Tian, Wenwen;Liu, Peng;Xie, Yi;Qiu, Yu;Li, Xing;Tang, Yuhui;Zheng, Shaoquan;Sun, Yuying;Tang, Hailin;Du, Wei;Tan, Weige;Xie, Xinhua
乳腺癌是全球女性死亡的第二大原因，三阴性乳腺癌（TNBC）预后最差。虽然有许多关于TNBC的研究，但没有有效的治疗方法，它仍然是今天的一个主要问题。对PIWI相互作用RNA（piRNA）的研究正在增加，并且研究piRNA在TNBC增殖和转移中的机制可能导致新的潜在治疗靶点。在这里，我们鉴定了一种新的皮尔纳，piR-YBX 1，与匹配的正常乳腺组织相比，它在TNBC中下调。过表达piR-YBX 1可显著抑制TNBC细胞的增殖、迁移和侵袭能力。机制上，piR-YBX 1可直接与Y-box结合蛋白1（YBX 1）的mRNA结合，过表达piR-YBX 1可在mRNA和蛋白水平下调YBX 1的表达，而过表达YBX 1可部分挽救piR-YBX 1的功能。此外，YBX 1可与MAPK信号通路中的关键分子RAF 1结合，过表达piR-YBX 1可抑制p-MEK和p-ERK 1/2的表达，而p-MEK和p-ERK 1/2可被YBX 1逆转。总之，我们的研究发现piR-YBX 1/YBX 1/MAPK轴抑制TNBC的增殖和转移，因此piR-YBX 1具有成为乳腺癌有效治疗剂的潜力。
Breast cancer is the second leading cause of death in women worldwide, with triple-negative breast cancer (TNBC) having the worst prognosis. Although there are numerous studies on TNBC, there is no effective treatment for it, and it is still a major problem today. Studies on PIWI-interacting RNAs (piRNAs) are increasing and investigating the mechanism of piRNAs in the proliferation and metastasis of TNBC may lead to new potential treatment targets. Here, we identified a novel piRNA, piR-YBX1, which was downregulated in TNBC compared to matched normal breast tissue. Overexpression of piR-YBX1 significantly inhibited the proliferation, migration, invasion ability of TNBC cells both in vivo and in vitro. Mechanistically, piR-YBX1 could bind directly to mRNA of Y-box binding protein 1 (YBX1) and overexpression of piR-YBX1 downregulated YBX1 in both mRNA and protein levels, while the function of piR-YBX1 could be partly rescued by overexpression of YBX1. In addition, YBX1 could bind to RAF1 which is the key molecule in the MAPK signaling pathway, and overexpression of piR-YBX1 inhibited the p-MEK and p-ERK1/2, which can be reverted by YBX1. In conclusion, our findings discovered that the piR-YBX1/YBX1/MAPK axis suppresses the proliferation and metastasis of TNBC and therefore piR-YBX1 has the potential to be an effective therapeutic agent for breast cancer.
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