miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2

Abstract

The aim of the present study was to investigate the expression and function of microRNA (miR)-371-5p in nasopharyngeal carcinoma (NPC). The levels of miR-371-5p were analyzed in nasopharyngeal epithelium tissues, NPC tissues, human NPC cell lines and NP69 cells using reverse transcription-quantitative polymerase chain reaction analysis. The association between the level of miR-371-5p and clinicopathological variables was also investigated. Cell proliferation was determined using an MTT assay, and the activities of cell metastasis were determined using wound healing and Transwell migration assays. To assess whether miR-371-5p can combine with the targeting sequence of B-cell lymphoma 2 (BCL2) mRNA or not, a luciferase activity assay was performed. An animal experiment was used to examine the effect of miR-371-5p on the development of NPC. The results revealed that the expression of miR-371-5p was reduced in NPC samples and NPC cells. The level of miR-371-5p was associated with clinical stage and distant metastasis in patients with NPC, and was inversely associated with the protein level of BCL-2 in NPC tissues. The upregulation of miR-371-5p reduced cell growth, migration and invasion, and inhibited carcinoma growth through targeting BCL2 mRNA. Taken together, the regulation of miR-371-5p was shown to offer potential as a novel treatment approach for NPC.

Cucurbitacin E Triggers Cellular Senescence in Colon Cancer Cells via Regulating the miR-371b-5p/TFAP4 Signaling Pathway

“…It has been demonstrated that the overexpressed miR-371-5p had considerably accelerated the G1/S phase transformation in hepatoma cells and thereby promoted hepatocellular carcinoma growth . In addition, miR-371-5p significantly suppressed the cell proliferation and migration of human nasopharyngeal carcinoma via inhibiting the expression of the antiapoptotic protein BCL-2 . Several lines of inquiries have evidenced that miR-371-5p was notably downregulated in CRC and repressed the cell proliferation, invasion, metastasis, and self-renewal properties of CRC, , while no data currently exist to describe the role of miR-371-5p in cellular senescence.…”

PPARβ/δ Agonist GW501516 Inhibits Tumorigenesis and Promotes Apoptosis of the Undifferentiated Nasopharyngeal Carcinoma C666-1 Cells by Regulating miR-206

“…In addition, the tumor suppressor miRNAs that previously had been shown to take part in modulating the expression of Bcl-2, including miR-16, miR-29c, miR-15a, and miR-184, were assayed simultaneously in GW501516-treated C666-1 cells. Their expression was usually attenuated in NPC cells, and this led to accelerated tumorigenesis of the NPC cells 8,23 . The cell proliferation, migration, and invasion of the NPC cells could be suppressed by forced expression of these miRNAs, which was found to be achieved majorly through targeting apoptotic-associated proteins 8 .…”

“…Their expression was usually attenuated in NPC cells, and this led to accelerated tumorigenesis of the NPC cells 8,23 . The cell proliferation, migration, and invasion of the NPC cells could be suppressed by forced expression of these miRNAs, which was found to be achieved majorly through targeting apoptotic-associated proteins 8 . As a tumor suppressor in several kinds of human cancers, miR-16 has been identified to inhibit CNE-2 cell proliferation and invasion, and increase apoptosis and chemo- or radiosensitivity by repressing its downstream target Bcl-2 24,25 .…”

“…An increasing body of evidence has demonstrated that miRNAs play an extremely vital role in NPC tumorigenesis 5–7 . Deregulated expression of miRNAs and its deregulation has been demonstrated to be involved in multiple stages of NPC tumorigenesis 8,9 . As either tumor suppressors or oncogenes, miRNAs could suppress or promote the growth, proliferation, invasion, and metastasis of NPC cells (for detailed summary refer to recent reviews 5,6 ).…”

The Role of MicroRNAs in Recurrence and Metastasis of Head and Neck Squamous Cell Carcinoma

“…miRNA-371-5p is seen as a potential stimulant of anoikis since higher levels of the miRNA correlated with lower levels of Bcl-2. [32] Survivin, an anti-apoptotic protein identified in several cancers to inhibit anoikis, may also be regulated by miRNA-34a. It has been hypothesized that miRNA-34a may downregulate cell proliferation in HNSCC through the inhibition of survivin [33].…”