LncRNA MIR4435-2HG triggers ovarian cancer progression by regulating miR-128-3p/CKD14 axis

Abstract

Background: Accumulating studies showed that long noncoding RNAs (lncRNAs) played vital roles in cancer progression. LncRNA MIR4435-2HG was proved to act as an oncogene in various tumors. However, the underlying function of MIR4435-2HG in ovarian cancer (OC) remains unclear. Methods: The expression levels of MIR4435-2HG, miR-128-3p and cyclin-dependent kinase 14 (CDK14) were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation and apoptosis in OC cells were detected by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and flow cytometric analysis, respectively. Transwell assay was applied to evaluate cell migration and invasion. Wound healing assay was performed to monitor the migration rate. Western blot assay was performed to detect the protein levels of Bcl-2, Cleaved PARP, E-cadherin, Vimentin and CDK14 in OC cells. The binding sites between miR-128-3p and MIR4435-2HG or CDK14 were predicted by online tool starBase and their relationship was confirmed by dual-luciferase reporter assay, RIP assay and pull-down experiment. Results: MIR4435-2HG and CDK14 were over-expressed in OC tissues and cells. Patients with high MIR4435-2HG expression had poorer overall survival (OS) than patients with low MIR4435-2HG expression. MIR4435-2HG knockdown inhibited proliferation, invasion and migration but induced apoptosis of OC cells via miR-128-3p/CDK14 axis. In conclusion, MIR4435-2HG knockdown suppressed the progression of OC cells through downregulating CDK14 expression by the promotion of miR-128-3p.

LncRNA AWPPH as a Prognostic Predictor in Human Cancers: Evidence From Meta-analysis

“…In gastric cancer, Bu et al demonstrated that AWPPH promotes cell proliferation and tumorigenesis by regulating miR-497/NTRK3 axis [22]. Recently, miR-128-3p was found to be a target of AWPPH in ovarian cancer by Zhu et al [13]. In NSCLC, Wu et al also demonstrated that AWPPH could function as an oncogenic lncRNA by regulating miR-204/CDK6 axis [25].…”

“…The characteristics of the included 19 studies were summarized in Table 1. A total of 1699 patients from 19 studies between 2016 and 2020 were included [11][12][13][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30]. All of the included studies were conducted in China.…”

Downregulation of long non‑coding RNA MR4435‑2HG suppresses breast cancer progression via the Wnt/β‑catenin signaling pathway

“…Additionally, a previous study revealed that MIR4435-2HG was upregulated in gastric cancer and promotes tumor growth and metastasis via activating the Wnt/β-catenin signaling pathway (17). Several recent reports (18,19) have revealed that MIR4435-2HG was involved in the regulation of cell apoptosis. Knockdown of MIR4435-2HG in cisplatin-resistant cell line HCT116R significantly promoted cell apoptosis and restored the sensitivity to cisplatin (18).…”

“…Knockdown of MIR4435-2HG in cisplatin-resistant cell line HCT116R significantly promoted cell apoptosis and restored the sensitivity to cisplatin (18). MIR4435-2HG knockdown induced ovarian cancer cell apoptosis via the miR-128-3p/CDK14 axis (19). Therefore, targeting MIR4435-2HG using antisense oligonucleotides to induce apoptosis may be a potential advancement in cancer drug development.…”

Long non‑coding RNA MIR4435‑2HG promotes the progression of head and neck squamous cell carcinoma by regulating the miR‑383‑5p/RBM3 axis

“…The lncRNA MIR4435-2 host gene (MIR4435-2HG) is located on human chromosome 2q13, and it is a proven oncogenic lncRNA that is implicated in various tumors (10). For example, MIR4435-2HG knockdown was shown to suppress the proliferation and invasion of ovarian cancer cells (11). MIR4435-2HG expression is upregulated in glioblastoma tissues and is associated with shorter overall survival in patients with glioblastoma (12).…”