MicroRNA-30e (miR-30e) is downregulated in various tumor types. However, its mechanism in inhibiting tumor growth of breast cancer remains to be elucidated. In this study, we found that miR-30e was significantly downregulated in tumor tissues of breast cancer (BC) patients and cell lines, and overexpression of miR-30e inhibited cell proliferation, migration and invasion. To understand the potential mechanism of miR-30e in inhibiting tumor growth, we showed that miR-30e blocked the activation of AKT and ERK1/2 pathways, and the expression of HIF-1α and VEGF via directly targeting IRS1. Moreover, miR-30e regulates cell proliferation, migration, invasion and increases chemosensitivity of MDA-MB-231 cells to paclitaxel by inhibiting its target IRS1. MiR-30e also inhibited tumor growth and suppressed expression of IRS1, AKT, ERK1/2 and HIF-1α in mouse xenograft tumors. To test the clinical relevance of these results, we used 40 pairs of BC tissues and adjacent normal tissues, analyzed the levels of miR-30e and IRS1 expression in these tissues, and found that miR-30e levels were significantly inversely correlated with IRS1 levels in these BC tissues, suggesting the important implication of our findings in translational application for BC diagnostics and treatment in the future.

Breast cancer is a kind of malignant tumor that severely threatens women's lives and health worldwide. Tumor‐associated macrophages (TAMs) have been reported to mediate tumor progression, while the mechanism still needs further identification. In this study, we found that M2 macrophages promoted increased cell proliferation and migration as well as reduced expression of interferon regulatory factor 7 (IRF7) and increased the expression of miR‐1587 in breast cancer cells. Overexpression of IRF7 or miR‐1587 knockdown reversed M2 macrophage‐induced cell proliferation and migration as well as tumor growth in vivo. Mechanistically, miR‐1587 targeted the 3ʹ‐untranslated region (3ʹ‐UTR) of IRF7 mRNA to regulate its protein expression leading to tumor progression. Collectively, this study revealed that the miR‐1587/IRF7 axis mediates M2 macrophage‐induced breast cancer progression, and this sheds light on further clinical therapy for breast cancer by targeting TAMs as well as the miR‐1587/IRF7 axis.

MiR-301a is as an oncogene involved in the regulation of gastric cancer (GC) progression, but the underlying mechanism is unclear. This study was to explore the lncRNA PCAT18/miR-301a/TP53INP1 axis in regulating the GC cell proliferation and metastasis. In the present study, GC tissues and cell lines were collected for the detection of PCAT18 expression. Herein, we found that, PCAT18 is significantly decreases in human GC tissues and five GC cell lines. Overexpression of PCAT18 inhibits cell viability, invasion, and migration of GC cells and tumor growth of GC xenograft tumors. PCAT18 negatively regulates the expression level of miR-301a. The interaction between PCAT18 and miR-301a is confirmed by RIP and RNA pull down. MiR-301a mimic increases cell viability and promotes cell migration and invasion and reverses the inhibitory action of PCAT18. TP53INP1 expression is negatively regulated by miR-301a and TP53INP1/miR-301a is involved in GC viability, migration, and invasion. The promoting of PCAT18 on TP53INP1 expression is abolished by miR-301a overexpression. In conclusion, lncRNA PCAT18 acts as a tumor suppressor for GC and lncRNA PCAT18, miR-301a, and TP53INP1 comprise a signal axis in regulating GC cell proliferation, migration, and invasion.

miRNA-34a is a tumor suppressor that is expressed in a variety of different types of cancer. The current study aimed to determine the involvement of miRNA-34a in triple negative breast cancer. miRNA-34a expression was detected using reverse transcription-quantitative PCR in the breast tissue and serum of patients with triple negative breast cancer and of healthy controls. The diagnostic value of miRNA-34a in triple negative breast cancer was analyzed using receiver operating curve analysis. A miRNA-34a inhibitor was transfected into triple negative breast cancer cells and the effects on cell proliferation, glucose uptake and glucose transporter 1 (GLUT1) expression were detected using a cell counting kit-8 assay, glucose uptake assay and western blot analysis, respectively. The results demonstrated that miRNA-34a was downregulated in patients with triple negative breast cancer compared with healthy controls and the downregulation of miRNA-34a effectively distinguished patients with triple negative breast cancer from healthy controls. miRNA-34a inhibition promoted cancer cell proliferation, accelerated glucose uptake and upregulated GLUT1. The current study concluded that the inhibition of miR-34a may promote triple negative cancer cell proliferation by promoting glucose uptake.