Besides, the expression of TIMP3 was subjected to targeted regulation of miR-17-5p (P < 0.05), and its overexpression could reverse the effects of miR-17-5p on proliferation and metastasis (P < 0.05).
Based on the results obtained in the last decade, some miRNAs are emerging as biomarkers of BC for diagnosis (i.e., miR-9, miR-10b, and miR-17-5p), prognosis (i.e., miR-148a and miR-335), and prediction of therapeutic outcomes (i.e., miR-30c, miR-187, and miR-339-5p) and have important roles in the control of BC hallmark functions such as invasion, metastasis, proliferation, resting death, apoptosis, and genomic instability.
These data demonstrated that miR-17-3p promoted keratinocyte cells proliferation and metastasis via targeting MYOT and activating Notch1/NF-κB signal pathways in cutaneous wound healing.
Two miRNAs, hsa-miR-17-5p and hsa-miR-16-5p, were identified as having the highest associations with targeted mRNAs [such as B-cell lymphoma 2 (BCL2), small body size/mothers against decapentaplegic 3 (SMAD3) and suppressor of cytokine signaling 1 (SOCS1)] and pathways associated with epithelial-mesenchymal transitions and other processes linked with cancer metastasis (including cell cycle, adherence junctions and extracellular matrix-receptor interaction). mRNAs for two genes [HECT, UBA and WWE domain containing 1 (HUWE1) and BCL2] were found to have the highest associations with miRNAs, which were down-regulated in brain metastasis specimens of breast cancer.
Consequently, our study suggests that miRNA 17 family (including miR-17, 20a, 20b) can act as TGFβR2 suppressor for reversing cisplatin-resistant and suppressing metastasis in NSCLC.
Nine dysregulated miRNA pairs fell into three miRNA gene families, namely let-7, mir-8/200 and mir-17, which showed frequent cross-targeting in the metastasis process.
The expression of miR-18a and miR-19a (belonging to miR-17 cluster) increased in HCC cells by CXCL8 simulation and led to the enhancement of HCC cell proliferation and metastasis.
In conclusion, we show a new role for miR-17 in melanoma, facilitating cell motility, by targeting the translation of ETV1 protein, which may support the development of metastasis.
Together, these findings indicate that miR-17 acts as an oncogenic miRNA and may contribute to the progression and metastasis of OS, suggesting miR-17 as a potential novel diagnostic and therapeutic target of OS.
These results provide evidence supporting that EMT activation and IFN pathway inactivation are markers of metastatic progression of basal-like tumors, and members of miR-17, miR-200, and miR-96 families play a role in suppressing EMT and metastasis.
Our results suggest microRNA involvement in malignant pituitary progression, whereby increased miR-20a, miR-106b and miR-17-5p promote metastasis by attenuating PTEN and TIMP2 in pituitary carcinoma.
Moreover, miR17-92 was related to TNM stage (III/IV vs I/II, HR 1.37, 95% CI 1.17-1.570; <i>P</i>=0.012), but there was no relationship between miR17-92 and metastasis (HR 1.64, 95% CI 1.34-1.95; <i>P</i>=0.491) or tumor size (≥5 cm vs <5 cm, HR 1.29, 95% CI 1.09-1.49; <i>P</i>=0.586).
In addition, miR-17-5p upregulation more frequently occurred in osteosarcoma specimens with advanced clinical stage, positive distant metastasis and poor response to neo-adjuvant chemotherapy.
The present study investigated the underlying regulatory network involved in the differential expression of metastasis associated lung adenocarcinoma transcript 1 (MALAT1) long non‑coding (lnc)RNA, microRNA‑17‑5p (miR‑17‑5p) and frizzled class receptor 2 (FZD2) mRNA under the influence of Casiopeina II‑gly (Cas‑II‑gly) via the Wnt signaling pathway in cervical carcinoma (CC).
Here, we demonstrate that the miR-21, miR-17 and miR-19a expressions induced by PRL-3 are involved in the proliferation and metastasis of colon cancer.
Among the significantly differentially expressed miRNAs, we have identified three miRNAs (miR-146a-5p, miR-128a-3p, and miR-17-5p) that were upregulated in primary tumors from patients without metastasis and downregulated in primary tumors from patients with metastasis.