We also analyzed the mRNA levels of target genes that candidate miRNAs might regulate in patient tissues. miR-214-3p was highly expressed in tissues and exosomes derived from EOC with high malignancy and also found to regulate the expression of LIM homeobox domain 6 (LHX6) mRNA.
MicroRNAs (miRNAs/miRs) are identified to serve key functions in the progression of various tumors. miR-214 is aberrantly expressed in various types of cancer.
We provided evidence of DB as a potential therapeutic agent for overcoming 5-FU resistance induced by IGF1, and suppressing cancer stem-like properties in association with miR-214 regulation.
Compared to normal cervical epithelium, cancer tissues had lower expression of miR-214 and higher mTOR, both of which were correlated with TNM stage and tissue pathology grade.
Mitochondrial transcription factor A (TFAM) and miR-214 expression in tumor samples from colorectal cancer patients and cancer cell lines were examined by reverse transcription and real-Time PCR (qPCR) or Western Blotting.
Correction to: MicroRNA-214-3p inhibits proliferation and cell cycle progression by targeting MELK in hepatocellular carcinoma and correlates cancer prognosis.
Results showed 12 miRNAs (miR-7, miR-17, miR-20a, miR-21, miR-92a, miR-96, miR-106a, miR-134, miR-183, miR-196a, miR-199a-3p, and miR214) to have an increased expression in stool of CC patients, and that later TNM stages exhibited more increased expressions than adenomas, while 8 miRNAs (miR-9, miR-29b, miR-127-5p, miR-138, miR-143, miR-146a, miR-222, and miR-938) showed decreased expressions in stool of CC patients, which becomes more pronounced as the cancer progresses from early to late TNM stages (0-IV).
CD164 identifies CD4<sup>+</sup> T cells highly expressing genes associated with malignancy in Sézary syndrome: the Sézary signature genes, FCRL3, Tox, and miR-214.
The level of miR‑214 was determined using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis in osteosarcoma and matched paracancerous tissues, and in human osteosarcoma cancer cell lines.
MicroRNAs (miRNAs) are critical endogenous small noncoding RNAs that negatively modulate gene expression by regulating its translation. miRNAs are implicated in most physiological processes of the heart and in the pathological progression of cardiovascular diseases. miR-214 is a deregulated miRNA in many pathological conditions, and it contributes to the pathogenesis of multiple human disorders, including cancer and cardiovascular diseases. miR-214 has dual functions in different cardiac pathological circumstances.
Sulforaphane inhibits cancer stem-like cell properties and cisplatin resistance through miR-214-mediated downregulation of c-MYC in non-small cell lung cancer.
Using miR expression profiling analysis, we found that miR-214-3p is one of the most markedly downregulated miRs in two esophageal squamous cancer cell lines compared with esophageal epithelial cells.
Forced expression of miR-214 in breast cancer cells diminished cancer cell survival possibly through inhibiting WNT signaling by direct repression of β-catenin.
This article describes known targets and signaling pathways that impact tumorigenesis and tumor suppression and summarizes all information available on circulating levels of miR-214 to address whether miR-214 may function as a potential biomarker and therapy for cancer patients in the future.
Targeting the Wnt-Regulatory Protein CTNNBIP1 by microRNA-214 Enhances the Stemness and Self-Renewal of Cancer Stem-Like Cells in Lung Adenocarcinomas.
An increasing number of studies has confirmed that microRNAs (miRNAs or miRs) play an important role in the development and progression of BC. microRNA-214 (miR-214), a member of the miRNA family, has been demonstrated to function as both a tumor suppressor and oncogene in various types of human cancer.
The sum of current literature reports suggests that miR-214 is a molecular hub involved in the control of cancer networks and, as such, could be a potential diagnostic/prognostic biomarker and target for therapeutic intervention.