Open AccessH19/let‑7/Lin28 ceRNA network mediates autophagy inhibiting epithelial‑mesenchymal transition in breast cancer
Author(s) -
Hanchu Xiong,
Jianguo Shen,
Zihan Chen,
Jingjing Yang,
Bin Xie,
Yunlu Jia,
Ushani Jayasinghe,
Ji Wang,
Wenqiang Zhao,
Shuduo Xie,
Linbo Wang,
Jichun Zhou
Publication year - 2020
Publication title -
international journal of oncology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.405
H-Index - 122
ISSN - 1019-6439
DOI - 10.3892/ijo.2020.4967
Subject(s) - competing endogenous rna , lin28 , autophagy , microrna , epithelial–mesenchymal transition , biology , cancer research , downregulation and upregulation , cancer , microbiology and biotechnology , transcription factor , long non coding rna , metastasis , apoptosis , gene , genetics , sox2
Long non‑coding RNA (lncRNA) H19 and Lin28 protein have been shown to participate in various pathophysiological processes, including cellular proliferation, autophagy and epithelial‑mesenchymal transition (EMT). A number of studies have investigated lncRNAs, microRNAs and mRNAs, and their roles in the initiation and progression of cancer, in doing so identifying competitive endogenous RNA (ceRNA) networks, including the H19/let‑7/Lin28 network. However, whether the H19/let‑7/Lin28 ceRNA network is involved in autophagy and EMT in breast cancer (BC) remains unclear. The present study demonstrated that the H19/let‑7/Lin28 loop was required for the downregulation of autophagy in BC cells via western blot analysis, reverse transcription‑quantitative PCR and autophagy flux monitoring. Using wound healing, migration and invasion assays, and morphological assays, the H19/let‑7/Lin28 loop was revealed to promote EMT in BC cells. Moreover, the H19/let‑7/Lin28 network was found to contribute to autophagy by inhibiting EMT in BC cells. To the best of our knowledge, the present study is the first to suggest the important roles of the H19/let‑7/Lin28 ceRNA network in BC autophagy and EMT, thus providing insight for the use of these molecules as prognostic biomarkers and therapeutic targets in BC metastasis.