miR-216a-5p inhibits invasion ability in human lung cancer cells by down-regulation of MMP16 expression / 中国癌症杂志

Background and purpose:MicroRNA (miRNA) belongs to a class of 19 to 30 nucleotide-long, endogenous noncoding RNA expressed in eukaryotes and predominantly inhibits gene expression at the post-transcriptional level. The miRNAs play critical roles in cell proliferation and differentiation, apoptosis, metabolism, and immune regulation. This study aimed to detect the expression of miR-216a-5p in lung cancer tissues and lung cancer cell lines, and to discuss the effects of miR-216a-5p on the invasion ability of lung cancer cells and the mechanism.Methods:Quantitative real-time PCR (qRT-PCR) was used to detect the expression of miR-216a-5p in lung cancer tissues of 55 cases and 7 lung cancer cell lines. Three lung cancer cell lines of A549, 95D and H460 were transiently transfected by miR-216a-5p, and Transwell was used to detect the effects of miR-216a-5p on the invasion of lung cancer cell lines. The dual luciferase reporter plasmids containing the miR-216a-5p candidate target gene and the gene of matrix metalloproteinase 16 (MMP16) were predicted and constructed. qRT-PCR and Western blot were used to detect the changes in mRNA and protein levels of target geneMMP16 by miR-216a-5p. The interference of MMP16 by siRNA and up-regulation miR-216a-5p by transfection were compared on the invasion of lung cancer cells.Results:The miR-216a-5p expression levels were all signiifcantly reduced in 90.91% (50 of 55 patients) tumor tissues compared with corresponding adjacent normal lung tissues (P<0.05). The miR-216a-5p expression levels were only 7.00%-32.00%in 7 lung cancer cells compared with the control group (P<0.05). Up-regulation of the expression of miR-216a-5p inhibited the invasion of lung cancer cells; interference of MMP16 by siRNA, as well as up-regulating miR-216a-5p by transfection, inhibited the expression of MMP16 in lung cancer leading to inhibition of the invasion of lung cancer cells. Conclusion:miR-216a-5p can be a candidate marker in clinical diagnosis and it can inhibit the invasion of lung cancer cells by down-regulating the expression of MMP16.

Treating breast cancer radiotherapy-induced moist desquamation with a traditional Chinese medicine formula: a case series pilot study.

UNLABELLED: Abstract Objective: A case series is presented to investigate the efficacy and safety of Erhegao for patients with breast cancer who have radiotherapy-induced moist desquamation. METHODS: Eighteen women with breast cancer who received radiotherapy and developed moist desquamation were enrolled. Erhegao cream, a Traditional Chinese Medicine formula consisting of zinc oxide powder, calamine powder, and lithospermum oil, was applied on areas of moist desquamation. Application was repeated once a day until healing. The primary end point for efficacy was the time to healing of the moist desquamation areas. A numerical rating scale was used to measure wound pain relief daily. Incidence of toxicity was also assessed. RESULTS: The average time to healing of the moist desquamation area was 13.56 days. The mean pain scores on the first, third, and seventh days were 5.22, 2.94, and 0.83, respectively. Eight-three percent of patients reported pain relief after the first 3 days, and 94%, after the first week. The mean daily reduction in the pain score was 0.40. None of the patients developed clinical infections or reported any toxicity. CONCLUSIONS: This formula is effective and safe, especially for pain relief, and may be an alternative treatment for radiotherapy-induced moist desquamation in patients with breast cancer. Future randomized, controlled studies are needed to better evaluate the efficacy of Erhegao cream.

Influence of interference of WIG-1 on the multi-drug resistance in small cell lung cancer / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the role of wild-type p53-induced gene 1 (WIG-1) on the regulation of multi-drug resistance in small cell lung cancer.</p><p><b>METHODS</b>The expressions of WIG-1 protein and gene were detected by Western blot and real-time PCR (RT-PCR) in both the drug-sensitive H69 and drug-resistant H69AR cell lines, respectively. Meanwhile, the differential expression of WIG-1 was also detected in peripheral blood samples of responders and non-responder patients. Furthermore, the WIG-1 expression was inhibited by siRNA in H69AR cells, then the drug-sensitivities of H69AR cells to chemotherapy agents such as ADM, DDP, VP-16 were detected by CCK8 assay, and apoptosis rate was detected by flow cytometry. The possible association of WIG-1 with clinical parameters was evaluated.</p><p><b>RESULTS</b>The expression of WIG-1 was significantly increased in H69AR cells (5.965 ± 0.890) than that in the H69 cells (1.023 ± 0.127) (P = 0.007). The expression of WIG-1 was significantly increased in the non-responder patients (4.169 ± 0. 970) than in the H69 cells and responders (1.673 ± 0.127) (P < 0.001). The drug-sensitivities of H69AR cells to chemotherapeutic drugs were increased when the expression of the WIG-1 was down-regulated. The apoptosis rate was significantly decreased in the H69AR cells (1.037 ± 0.049)% compared with that in the H69 cells [(7.963 ± 0.097)%, (P < 0.01)]. The apoptosis rate was increased in the H69AR-Si-WIG-1 cells (20.915 ± 0.890)% than that of (1.037 ± 0.049)% in the H69AR and H69AR-NC group (2.025 ± 0.097)% (P < 0.01). The expression of WIG-1 was not significantly associated with gender, and age (P > 0.05), but significantly correlated with chemosensitivity, overall survival and clinical stage (P < 0.001 for all).</p><p><b>CONCLUSIONS</b>Our results suggest that WIG-1 is involved in the regulation of the multidrug resistance mechanism in small cell lung cancer. Selective silencing of the WIG-1 gene may reverse the multidrug resistance of SCLC via increasing cell apoptosis.</p>