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Additional file 1: Scheme S1. Syntheses of Compound K derivatives 1-3.Ac2O−C5H5N, 60°C, 24h, 90%;mCPBA,CH2Cl2, rt , 4h, 95%;HIO4, CH3CN−H2O, 0OC, 3h, 85%. Scheme S2. Syntheses of CKN. Reagents and conditions: RNH2, NaBH3, DCM, rt. Figure S1. The NMR spectrum analysis of 1, 2, 3 and CKN. The 1H NMRand 13C NMRof 1, solvent: CDCl3. The 1H NMRof 2, solvent: CDCl3. The 1H NMRand 13C NMRof 3, solvent: CDCl3. The 1H NMRand 13C NMRof CKN, solvent: CDCl3. Figure S2. Effencts of different administration doses of CKN on atherosclerotic plaques in AopE−/− mice. Representative images of thoracic aortic lesionsand quantification of atherosclerotic lesions shown as percentage of thoracic aorta.

Background: Brief behavioral therapy for insomnia (BBT-I) has been proven to be a simple and effective alternative to cognitive behavioral therapy. However, low adherence limits the application in Chinese primary medical institutions, resulting in delayed or irregular treatment for many patients. This study aimed to explore the efficacy of traditional Chinese medicine external treatments on the adherence to behavioral therapy for insomnia in Chinese primary healthcare institutions, with a particular focus on patients who live in regions with weak healthcare systems. Methods: This randomized controlled clinical trial will be conducted in primary medical institutions and will recruit 98 adult participants with insomnia. BBT-I will be used as the base treatment. The participants will be divided into experimental (combined with Wuqinxi and other traditional Chinese medicine [TCM] external treatment n = 49) and control (combined with trazodone treatment, n = 49) groups, and each group will be treated for 4 consecutive weeks. The severity index of insomnia will be used as the main indicator of disease evaluation, with an 8-point reduction in the score considered as effective and a score

Additional file 1. .

Qin Y, Mi W, Huang C, Li J, Zhang Y, Fu Y. Onco TargetsTher. 2020;13:3667–3676. The authors have advised due to an error at the time offigure assembly, Figure 1E on page 3670 is incorrect. Thecorrect Figure 1 is shown below. The authors apologize for this error and advise it does notaffect the results of the paper. Read the original article

Background MicroRNAs (miRNAs) can regulate the post-transcriptional level of gene expression. It has been documented that downregulation of miR-206 is significant in human gastric cancer (GC), whereas its role in GC cell biological behaviors, including proliferation, migration, and invasion, has not been thoroughly investigated. MiR-206 levels have a negative association with lymph node metastasis and tumor invasion, and patients with higher miR-206 expression have better prognoses. Functional studies demonstrated that miR-206 overexpression significantly suppresses GC cell proliferation, migration, and invasion, and induces apoptosis in vitro. Materials and methods MiR-206 and MUC1 were determined by RNA extraction, quantitative real-time polymerase chain reaction, and luciferase reporter gene assays. The viability of GC cells was tested using the Cell Counting Kit 8 assay. Transwell invasion and migration assays detected GC cancer cell proliferation, invasion, and migration. Flow cytometry was applied to analyze apoptotic cells. FACS analysis was applied to detect the mitochondrial membrane potential of cells. Western blotting assay determined protein levels. Results The luciferase reporter gene assay demonstrated that miR-206 might directly bind to the 3′UTR of the MUC1 gene and suppress MUC1 expression. Furthermore, MUCI expression was upregulated and inversely associated with miR-206 levels in GC tissues. More importantly, the miR-206-mediated suppression of proliferation, migration, and invasion, and the induction of apoptosis, were abrogated by MUC1 overexpression. Conclusion Our data demonstrated that miR-206 may exert antitumor activities through inhibiting the expression of MUC1, which may serve as an effective and potential target for GC treatment.

Min Deng,1 Yiyu Qin,2 Xiaodong Chen,3 Qizhi Wang,1 Jianchao Wang1 1Department of Gastroenterology, The First Affiliated Hospital, Bengbu Medical College, Bengbu, Anhui 233004, People’s Republic of China; 2Clinical Medical College, Research Centre of Biomedical Technology, Yancheng Institute of Health Sciences, Yancheng, Jiangsu 224005, People’s Republic of China; 3Department of Orthopedics, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, People’s Republic of China Background: MicroRNAs (miRNAs) can regulate the post-transcriptional level of gene expression. It has been documented that downregulation of miR-206 is significant in human gastric cancer (GC), whereas its role in GC cell biological behaviors, including proliferation, migration, and invasion, has not been thoroughly investigated. MiR-206 levels have a negative association with lymph node metastasis and tumor invasion, and patients with higher miR-206 expression have better prognoses. Functional studies demonstrated that miR-206 overexpression significantly suppresses GC cell proliferation, migration, and invasion, and induces apoptosis in vitro. Materials and methods: MiR-206 and MUC1 were determined by RNA extraction, quantitative real-time polymerase chain reaction, and luciferase reporter gene assays. The viability of GC cells was tested using the Cell Counting Kit 8 assay. Transwell invasion and migration assays detected GC cancer cell proliferation, invasion, and migration. Flow cytometry was applied to analyze apoptotic cells. FACS analysis was applied to detect the mitochondrial membrane potential of cells. Western blotting assay determined protein levels. Results: The luciferase reporter gene assay demonstrated that miR-206 might directly bind to the 3'UTR of the MUC1 gene and suppress MUC1 expression. Furthermore, MUCI expression was upregulated and inversely associated with miR-206 levels in GC tissues. More importantly, the miR-206-mediated suppression of proliferation, migration, and invasion, and the induction of apoptosis, were abrogated by MUC1 overexpression. Conclusion: Our data demonstrated that miR-206 may exert antitumor activities through inhibiting the expression of MUC1, which may serve as an effective and potential target for GC treatment. Keywords: miR-206, MUC1, gastric cancer, metastasis

Gallbladder cancer is the most common biliary tract malignancy and the fifth most common gastrointestinal malignancy. Chemo-resistance is the most remarkable characteristic of gallbladder cancer. The relatively dense extracellular space in tumor is the main barrier to nanotherapeutics' anticancer efficacy. Hyaluronan (HA) was shown in our previous study to significantly improve the myxoma virus distribution via promoting the MMP-9 production, which degrades collagen IV. We demonstrated that HA increased the chemo-sensitivity of gallbladder cancer cells both in vitro and in vivo. The in vivo chemo-sensitization effect of HA could partially be due to the penetration-promoting effect of HA via degrading collagen IV.

As one of the mostly aggressive and fatal malignancy, gallbladder carcinoma has been known to be resistant to many anticancer drugs. Although it is under active investigation, it is still difficult to achieve satisfactory effect for most chemo-drugs on this tumor. It has previously reported that somatostatin could increase the chemosensitivity of gallbladder carcinoma cells (GBC-SD) and reduce the therapeutic dose of Doxorubicin in killing GBC-SD cells. SST could enhance the chemosensitivity of gallbladder carcinoma to Doxorubincin (DOX) by transient arresting cell cycle to S phase. We tried to clarify the mechanism by which SST utilized to enhance the chemosensitivity of GBC-SD cells to DOX. We further investigated whether the enhanced chemosensitivity of GBC-SD cells to DOX in the presence of SST is via apoptosis or cell cycle regulation. In addition, we also looked into related factors involved in cell cycle regulation and apoptosis.Twenty-four hours after somatostatin treatment, doxorubicin was gradually added and the growth curve of GBC-SD cells was determined according to MTT test. Cell apoptosis was measured by flow cytometry (FCM) using Annexin V/ Propidium Iodide Binding. Cell cycle was also examined by FCM. The somatostatin receptor (SSTR) subtypes in GBC-SD cells were identified using immunocytochemistry and RT-PCR assay. The expressions of p53, Bax and phosphorylated RB (pRB) protein were examined using western blotting assay.When GBC-SD cells were treated with SST alone, no significant cell growth inhibition and cell apoptosis were observed. SST could induce a transient S phase arrest in GBC-SD cells. The mRNA expression of SSTR1, 2, 3, 4, 5 were all detected in GBC-SD cells, whereas only SSTR1, 2, 3 were detected in GBC-SD cells using immunocytochemistry assay. After GBC-SD cells were treated with SST for 24h, the expression level of p53 and Bax protein in GBC-SD cells was similar to that of the control group, however up-regulated pRB protein expression was observed (p0.05).Our results suggested that the synergistic inhibitory effect of somatostatin and doxorubicin co-treatment on GBC-SD cells was not due to SST induced apoptosis concerning the expression of p53 and Bax protein. Our data clearly showed all 5 SST receptor subtypes expressed in GBC-SD cells by RT-PCR and 3 SST receptors by immunocytochemistry. Accumulated evidence has been proved the relationship between cell cycle regulation and RB protein phosphorylation. In the chemosensitized GBC-SD cell line treated with SST, phosphorylated RB and cell cycle arrest were simultaneously manifested. We reasoned that somatostatin might enhance the chemosensitivity of GBC-SD cells to doxorubin through arresting the cell cycle at S phase, but not P53 and Bax protein induced cell apoptosis.