The long non-coding RNA (lncRNA) RUSC1-AS1 has been reported to be dysregulated in the progression of many cancers. Also, RUSC1-AS1 had been detected to be highly expressed in laryngeal squamous cell carcinoma and breast cancer cells, suggesting that RUSC1-AS1 may be a biomarker for cancers. However, the biological role and regulatory mechanism of RUSC1-AS1 in hepatocellular carcinoma (HCC) remain unknown. In this study, we found that RUSC1-AS1 was upregulated in HCC tissues and cells, and predicted unfavorable prognosis of HCC patients. The function assays including colony formation, EdU, TUNEL assay revealed that RUSC1-AS1 facilitated HCC cell proliferation and inhibited HCC cell apoptosis. Furthermore, mechanism assays including luciferase reporter assay and RIP assay demonstrated that RUSC1-AS1 could directly bind to hsa-miR-7-5p. Besides, hsa-miR-7-5p targeted and negatively regulated NOTCH3 expression. Moreover, RUSC1-AS1 sponged hsa-miR-7-5p to upregulate NOTCH3 and to trigger the NOTCH signaling pathway. The rescue assays depicted that RUSC1-AS1 regulated HCC cell proliferation and apoptosis through modulating NOTCH signaling. In conclusion, lncRNA RUSC1-AS1 promoted the proliferation and reduced the apoptosis of HCC cells through activation of NOTCH signaling via hsa-miR-7-5p/NOTCH3 axis.

Breast cancer is one of the most common malignancies worldwide and is responsible for a high mortality rate. However, the underlying pathological mechanism of breast cancer remains unclear. MicroRNAs (miRNAs/miRs) play critical roles in the progression of breast cancer. Recent studies have reported that miR-124/CD151 participates in the development of breast cancer. However, the exact molecular mechanism of miR-124/CD151 action in 17β-estradiol (E2)-treated breast cancer cells remains unknown. Thus, the present study aimed to investigate miR-124 and CD151 expression levels in MCF-7 cells treated with E2 via reverse transcription-quantitative PCR and western blot analyses. Bioinformatic analysis was performed to predict and identify whether CD151 is a potential target of miR-124. The Cell Counting Kit-8 and colony formation assays were performed to detect proliferation of MCF-7 cells. In addition, the invasive and migratory abilities of MCF-7 cells were assessed via the Transwell and wound healing assays, respectively. The results demonstrated that E2 downregulated miR-124 expression, while upregulating G protein -coupled estrogen receptor (GPER) expression in MCF-7 cells. Following treatment with the GPER antagonist, G15, miR-124 expression was significantly enhanced and E2-induced proliferation, invasion and migration of MCF-7 cells were notably inhibited. In addition, CD151 was confirmed as a direct target of miR-124. CD151 silencing remarkably suppressed the proliferation, invasion and migration of E2-induced MCF-7 cells. Taken together, these results suggest that upregulation of GPER expression induced by E2 promotes proliferation, invasion and migration of breast cancer cells by regulating the miR-124/CD151 pathway. Thus, the results of the present study provide a potential novel method for the treatment and prognosis of breast cancer.

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