In recent years, malignant breast cancer metastasis has caused a great increase in mortality. Research on the genetic and molecular mechanisms of malignant breast cancer has continued to deepen, and targeted therapy has become the general trend. Among them, competing endogenous RNA (ceRNA)-related molecules have received much attention. Homeobox transcript antisense RNA (HOTAIR) has been reported to function extensively as a ceRNA in breast cancer. Notably, miR-203 and Caveolin 1 (CAV1) have also been found to play a role in breast cancer. However, the relationship between the three remains unclear. In this study, we present a new mechanic through bioinformatics tool and basic experiments: the HOTAIR/miR-203/CAV1 axis, which complemented the role network of HOTAIR as a ceRNA, thus, it will provide a novel potential idea for breast cancer research and therapy.

Cancer, as the second leading cause of death worldwide, is a major public health concern that imposes a heavy social and economic burden. Effective approaches for either diagnosis or therapy of most cancers are still lacking. Dynamic monitoring and personalized therapy are the main directions for cancer research. Cancer-derived extracellular vesicles (EVs) are potential disease biomarkers. Cancer EVs, including small EVs (sEVs), contain unique biomolecules (protein, nucleic acid, and lipids) at various stages of carcinogenesis. In this review, we discuss the biogenesis of sEVs, and their functions in cancer, revealing the potential applications of sEVs as cancer biomarkers.

Background: Fluorocitrate (FC) ranging from 5 μM to 5 mM is often used as a specific metabolic inhibitor of the astrocytes to study astrocytic functions. Whether FC at such concentrations may affect neuronal metabolism and function in vivo remains unclear. Methods: We examined the effects of FC on the ATP levels and Ca²⁺ activity of the astrocytes and neurons in the motor cortices of living mice using two-photon microscopy. Results: We found that 25 μM and 250 μM of FC decreased the intracellular ATP levels and Ca²⁺ activity in the astrocytes in the motor cortex. Equally, 250 μM of FC, but not 25 μM of FC, reduced the intracellular ATP levels in the dendritic processes of the layer 5 pyramidal neurons. However, 25 μM of FC increased the neuronal Ca²⁺ activity, whereas ≥250 μM of FC decreased it. To test whether the differential effects of FC on neuronal Ca²⁺ activity reflect the direct effect of FC on the neurons or its indirect effect on the astrocytes, we used the CNO-hM3Dq chemogenetic approach to block astrocytic Ca²⁺ activity and examined the effect of FC. In the absence of astrocytic Ca²⁺ activity, 25 μM of FC still increased and ≥250 μM of FC reduced the dendritic Ca²⁺ activity of the neurons, respectively, suggesting a direct effect of 250 μM of FC on inhibiting neuronal Ca²⁺ activity. Further, 250 μM, but not 25 μM, of FC increased the size of the dendritic spines over 2 h. Conclusions: Our findings suggest that FC at high concentrations (≥250 μM) is not a specific inhibitor of astrocytic functions, as it directly affects neuronal metabolism and synaptic plasticity in vivo.