Esophageal squamous cell carcinoma (ESCC) is the predominant histologic subtype of esophageal cancer and is characterized by a high mortality rate and geographic differences in incidence. microRNAs (miRNAs) are small, non-coding RNAs that play important roles in the regulation of genes associated with cancer development and progression. In the present study, we demonstrated that microRNA-100 (miR‑100) demonstrated markedly lower expression in the ESCC tissues as validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Furthermore, we found that the downregulation of miR-100 was significantly correlated with the status of lymph node metastasis in the 34 ESCC patients. Next, we investigated the role and mechanism of miR-100 in ESCC cells and found that miR-100 modulated the migration and invasion but not the apoptosis and proliferation of ESCC cells in vitro. We further demonstrated that miR-100 directly targeted the mTOR 3'UTR and repressed the expression of mTOR, a tumor-related gene. Similarly, miR-100 has been reported as a tumor suppressor by controlling cell migration and invasion, as it can target mTOR genes. These results provide insight into the potential mechanisms of miR-100 in the pathogenesis of ESCC.

Lung cancer is the most deadly malignancy in the last decade, accounting for about 1.6 million deaths every year globally. Tanshinone is the constituent of Salvia miltiorrhiza; it has been found that they influence tumorigenesis. However, the role of tanshinones on lung cancer is still not clear. Let-7a-5p, a short non-coding RNA, is regarded as a suppressor gene in tumorigenesis. Herein, we verified that let-7a-5p is significantly downregulated in non-small-cell lung cancer (NSCLC) tissues and cell lines. Tanshinone suppressed the expression of aurora kinase A (AURKA), inhibited cell proliferation, and arrested cell cycle progression. Our results showed that tanshinones suppressed NSCLC by upregulating the expressions of let-7a-5p via directly targeting AURKA. Besides, the data reveal that the knockdown of AURKA can also inhibit cell proliferation, arrest cell cycle, and promote cell apoptosis. Furthermore, this study demonstrates that AURKA was negatively correlated with let-7a-5p in NSCLC patient tissues. Taken together, our findings suggest that tanshinone inhibits NSCLC by downregulating AURKA through let-7a-5p. Tanshinones and let-7a-5p have the potential to be candidates for drug development of NSCLC. In conclusion, this study revealed that tanshinones with miRNA linking lead to partial mechanism in NSCLC.

Lung cancer is acknowledged as a common cancer with high morbidity and mortality. MicroRNAs (miRNAs), kind of non-coding single-stranded RNA molecules, can be used in cancer clinical treatments. In this research, miR-199a-5p was seen lowly expressed in NSCLC sera samples. miR-199a-5p suppressed the cell proliferation, migration and arrested cell cycle in NSCLC cell lines. The results showed that SLC2A1 (glucose transporter 1, GLUT1) was a direct target of miR-199a-5p. Downregulation of SLC2A1 could not only inhibit cell proliferation, migration and cell cycle, but also promote cell apoptosis. The data suggests that miR-199a-5p can inhibit glucose metabolism in NSCLC by targeting SLC2A1.This study proves that miR-199a-5p / SLC2A1 can play an essential role in the development of NSCLC by targeting SLC2A1. It puts forward a new approach for clinical treatments of NSCLC.