<p>Long noncoding RNA Linc00460 promotes breast cancer progression by regulating the miR-489-5p/FGF7/AKT axis</p>

Abstract

Purpose: Evidence indicates that long noncoding RNAs (lncRNA) possess important roles in various cellular processes and that dysregulation of lncRNAs promotes tumor progression. However, the expression patterns and biological functions of many specific lncRNAs in breast cancer remain to be determined. Methods: Quantitative real-time polymerase chain reaction was performed to detect Linc00460, miR-489-5p and FGF7 expression. Protein levels were determined using Western blot. MTT and colony formation assay were used to measure cell proliferation. Transwell assays were conducted to determine cell migration and invasion. Luciferase reporter assays were carried out to assess the interaction between miR-489-5p and Linc00460 or FGF7. Biotin pull-down assay was used to detect the direct interaction between miR-489-5p and Linc00460. In vivo experiments were performed to measure tumor formation and lung metastasis. Results: We demonstrated that lncRNA Linc00460 was upregulated in breast cancer, and its expression level was positively associated with lymphatic metastasis and poor overall survival. Forced expression of Linc00460 increased, whereas Linc00460 silencing decreased, breast cancer cell viability, migration and invasion both in vitro and in vivo. Linc00460 was identified as a direct target of miR-489-5p, which further targeted FGF7 and exerted oncogenic functions in breast cancer. Mechanistically, Linc00460 served as a competing endogenous RNA of FGF-7 mRNA by sponging miR-489-5p, resulting in upregulated FGF7 expression and AKT activity. Notably, forced expression of miR-489-5p abrogated Linc00460-mediated oncogenic behavior and activation of the FGF7-AKT pathway in breast cancer cells. Conclusion: We have demonstrated that Linc00460 promotes breast cancer progression partly through the miR-489-5p/FGF7/AKT axis.

Comprehensive analysis of tumor mutation burden and immune microenvironment in gastric cancer

“…FGF7 belongs to fibroblast growth factor (FGF) family and possess mitogenic and cell survival activities. Zhu et al reported that FGF7 could promote breast cancer progression through AKT signaling pathway [ 39 ]. In GC, several studies indicated that FGF7 might play a role in GC cell proliferation and metastasis [ 40 , 41 ].…”

Long non‑coding RNA LINC00460 predicts poor survival and promotes cell viability in pancreatic cancer

“…In glioma, LINC00460 has been demonstrated to be overexpressed in cancer tissues and cell lines, and to promote cancer cell progression by negatively regulating miR-320a (23). Additionally, a recent study reported that LINC00460 could promote breast cancer cell migration, invasion and proliferation by targeting the miR-489-5p/fibroblast growth factor 7/AKT axis (24). Notably, nicotine has been found to facilitate carcinogenesis in the bronchus by activating LINC00460 and the PI3K/AKT signaling pathway (25).…”

A signature related to lung adenocarcinoma prognosis: A study based on TCGA database

“…Via targeting of the miR-302c-5p/FOXA1 axis, LINC00460 can facilitate tumor growth in LUAD [31]. Similarly, LINC00460 has also been confirmed to promote the progression of multiple cancers through different target genes [32][33][34]. The last lncRNA, DGCR5, is slightly different because when it is highly expressed it exerts anticancer activity in various cancers, including gastric cancer, hepatocellular carcinoma, cervical cancer, and bladder cancer, suggesting a good prognosis [35][36][37][38].…”