<p>Long Non-Coding RNA H19 Promotes Proliferation, Migration and Invasion and Inhibits Apoptosis of Breast Cancer Cells by Targeting miR-491-5p/ZNF703 Axis</p>

Abstract

Background: Breast cancer is one of the most common cancers worldwide. Long noncoding RNAs and microRNAs act as important regulators in human cancers. This study aims to explore the molecular mechanism among H19, miR-491-5p and zinc finger 703 (ZNF703) in breast cancer. Materials and Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to detect the expression of H19, miR-491-5p and ZNF703. Cell Counting Kit 8 (CCK-8) assay was performed to evaluate cell proliferation. Cell apoptosis was assessed by flow cytometry assay. The number of migrated and invaded cells was counted by transwell assay. Dual luciferase reporter assay was carried out to test luciferase activity. Protein level of ZNF703 was measured by Western blot assay. Results: H19 was highly expressed in breast tissues and cells. H19 knockdown inhibited proliferation, induced apoptosis and blocked migration and invasion. Moreover, H19 bound to miR-491-5p and negatively regulated miR-491-5p expression. MiR-491-5p inhibition abrogated the activities of proliferation, apoptosis, migration and invasion affected by H19 knockdown. Furthermore, miR-491-5p directly targeted ZNF703 and inversely modulated ZNF703 expression. ZNF703 up-regulation rescued the effects of miR-491-5p overexpression on proliferation, apoptosis, migration and invasion. In addition, H19 knockdown reduced ZNF703 expression by targeting miR-491-5p/ZNF703 axis. Conclusion: H19 promoted proliferation, migration and invasion and retarded apoptosis of breast cancer cells via sponging miR-491-5p to down-regulate ZNF703 expression.

Identification of the Novel Tumor Suppressor Role of FOCAD/miR-491-5p to Inhibit Cancer Stemness, Drug Resistance and Metastasis via Regulating RABIF/MMP Signaling in Triple Negative Breast Cancer

“…Various directly targeted proteins by miR-491-5p in many cancers have been recognized such as hTERT and JMJD2A in cervical cancer [13,14], BCL-XL and EGFR in ovarian cancer [15], Wnt3a and Notch3 in gastric cancer [16,63], TP53 and Bcl-XL in pancreatic cancer [17], G-protein-coupled receptor kinase-interacting protein 1 (GIT1) in OSCC [19] and FOXP4 in osteosarcoma [20]. Although miR-491-5p was also found to target JMJD2B and ZNF-703 to act as a tumor suppressor in breast cancer as mentioned previously [9,10,12], no investigations to pinpoint that RABIF is a direct target of miR-491-5p in breast cancer especially in TNBC in the past. RABIF was once to be identified as a new biomarker candidate of breast cancer development by a bioinformatics tool named PINCAGE (probabilistic integration of cancer genomics data for perturbed gene) [64].…”

lncRNA H19 promotes glioblastoma multiforme development by activating autophagy by sponging miR-491-5p

“…The downstream signaling pathway of H19 in the progression of GBM was further investigated. The Encyclopedia of RNA Interactomes (ENCORI) database ( http://starbase.sysu.edu.cn/ ) was used to search the possible miRNA candidates of H19, followed by literature mining to identify candidate miRNAs with known oncogenic effects in human cancers [ 31–33 ]. Subsequently, human miR-491-5p was identified as a possible downstream competing candidate for H19.…”

Circ_0009910 sponges miR‐491‐5p to promote acute myeloid leukemia progression through modulating B4GALT5 expression and PI3K/AKT signaling pathway

“…Through a series of analyses, miR-491-5p was selected as a target of circ_0009910 in AML cells, and the interaction was validated through RIP, RNA pulldown, and dual-luciferase reporter assays. Previous studies have given evidence of the regulatory role of miR-491-5p in multifarious malignancies, including breast cancer, 33 glioma, 34 and lung cancer. 35 Similarly, miR-491-5p was certified to participate in leukemia progression and it was low expressed in ALL cells.…”