RESUMO
Although chemotherapy is the first-line treatment strategy for a variety of tumors, its side effects have limited its efficacy. This review summarizes the progress on the use of acupoint stimulation to combat chemotherapy-associated side effects, including chemotherapy-induced peripheral neuropathy (CIPN), cognitive impairment (CICI), and gastrointestinal toxicity (GI), as well as myelosuppression and immunosuppression. It was found that acupoint stimulation attenuated CIPN and GI by modulating the 5-hydroxytryptamine system in dorsal root ganglia, the dorsal horn of the spinal cord, and the duodenum by reducing oxidative stress and neuroinflammation. Acupoint stimulation also alleviated GI by activating vagal activity in the nucleus tractus solitarius and promoting the secretion of gastrointestinal neuropeptide hormones. Acupoint stimulation restored both bone marrow hematopoiesis and immune function to combat cancer. In addition, the combination of acupoint stimulation and chemotherapy could inhibit tumor growth by promoting tumor cell apoptosis and the enrichment of chemotherapeutic agents in tumor tissue and by modulating the tumor immune microenvironment and normalizing the vasculature. Multiple evidence also indicates that neuroimmune regulation may be involved in the effects of acupoint stimulation. In conclusion, the evidence suggests that acupoint stimulation can alleviate the side effects of chemotherapy and can also assist chemotherapeutic agents in inhibiting tumor growth, which expands the clinical application of acupoint stimulation in cancer treatment. However, more high-quality clinical studies are needed to confirm the clinical value of acupoint stimulation.
RESUMO
Breast cancer is the most common cancer in women and is one of the three most common malignancies worldwide. Serum microRNAs (miRNAs/miRs) are ideal biomarkers for tumor diagnosis and prognosis due to their specific biological characteristics. In several different types of cancer, miRNAs are associated with cell migration and invasion. In the present study, miR253p expression levels were detected in tissue and serum samples derived from patients with breast cancer, and the diagnostic and prognostic value of miR253p in breast cancer was evaluated. Cellular function assays were performed to evaluate the role of miR253p in breast cancer. Moreover, dualluciferase reporter assays and western blotting were performed to investigate the target of miR253p. miR253p expression was upregulated in breast cancer tissue and serum samples compared with normal breast tissue and serum samples. Patients with breast cancer with high serum miR253p levels were more likely to have lymph node metastasis compared with those with low serum miR253p levels. The area under the curve for miR253p in the diagnosis of breast cancer was 0.748, with 57.1% sensitivity and 95.0% specificity. Moreover, the KaplanMeier survival curves demonstrated that patients with breast cancer with a low expression of serum miR253p had a higher overall survival rate compared with patients with a high serum miR253p expression. miR253p knockdown suppressed breast cancer cell proliferation and invasion, and transducer of ERBB2, 1 (TOB1) was identified as a potential target gene regulated by miR253p. Therefore, the present study suggested that miR253p regulated cellular functions via TOB1 in breast cancer; therefore, miR253p may serve as a breast cancer biomarker.