[Corrigendum] Induction of microRNA­let­7a inhibits lung adeno-carcinoma cell growth by regulating cyclin D1.

After the publication of the article, an interested reader drew to the authors' attention that, in the western blots shown in Fig. 5C and D, a pair of data panels were inadvertently duplicated comparing between panels (C) and (D); in addition, the cell migration data shown in Fig. 7F on p. 1852 were selected incorrectly. The authors have examined their original data, and realize that these errors arose inadvertently as a consequence of their mishandling of their data. The revised versions of Figs. 5 and 7, featuring the corrected data for the caspase-8 experiment in Fig. 5C and alternative data for the cell migration assay experiments in Fig. 7F, are shown on the next two pages. The revised data shown for these Figures do not affect the overall conclusions reported in the paper. All the authors agree to the publication of this corrigendum, and are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this. Furthermore, the authors apologize to the readership for any inconvenience caused. [Oncology Reports 40: 1843-1854, 2018; DOI: 10.3892/or.2018.6593].

Efficacy and safety of Jiu-Wei-Xi-Feng granules for treating tic disorders in children: study protocol for a randomized controlled equivalence trial.

BACKGROUND: Tic disorders (TD) is a neuropsychiatric disease with twitch as the main manifestation in childhood. Jiu-Wei-Xi-Feng granules has been marketed in China for treating children with TD. As Long Gu (Os Draconis) in the composition of this Chinese patent medicine is a rare and expensive medicinal material protected by the Chinese government, therefore, we consider replacing it with Mu Li (Concha Ostreae) that has the same effect and is cheaper. This study is designed to evaluate the clinical equivalence between Jiu-Wei-Xi-Feng granules (Os Draconis replaced by Concha Ostreae) (JWXFD) and Jiu-Wei-Xi-Feng granules (original formula) (JWXFO) in children with TD (consumption of renal yin and liver wind stirring up internally syndrome). METHODS/DESIGN: This is a multicenter, randomized, double-blind, equivalence trial comparing the efficacy and safety of JWXFD and JWXFO in treating Children with tic disorders (consumption of renal yin and liver wind stirring up internally syndrome). A total of 288 patients will be recruited and randomly assigned to two groups in a 1:1 ratio. The treatment course is 6 weeks, with a 2 weeks follow-up. The primary outcome is the mean change value from baseline to 6th week by the Yale Global Tic Severity Scale total tic score (YGTSS-TTS). Secondary outcomes include total effective rate of tic, Yale Global Tic Severity Scale (YGTSS) scores and its factor scores (the degree of motor tics, phonic tics and social function damage), Clinical Global Impression-Severity scale, and TCM syndrome efficacy. DISCUSSION: The design of this study refers to a large number of similar research design points, and asked for opinions of peer experts, and finally reached a consensus. This trial will provide high-quality evidence on the clinical equivalence between JWXFD and JWXFO and provide a basis for the marketing of JWXFD. TRIAL REGISTRATION: ChiCTR2000032312 Registered on 25 April 2020, http://www.chictr.org.cn/showproj.aspx?proj=52630.

[Application and thinking of cohort study in clinical research of acupuncture and moxibustion].

Cohort study has been greatly considered and widely used in clinical research of traditional Chinese medicine in China, but it is seldom applied in the field of acupuncture and moxibustion. This paper introduces the development background, basic concepts, advantages and limitations of cohort study, analyzes the existing problems in the evaluation of acupuncture and moxibustion curative effect and development status of cohort study in the cycle of acupuncture and moxibustion, explores the feasibility and value of such method in clinical research of acupuncture and moxibustion and proposes the methodological suggestions on rigorous design, control of selective bias, control of cohort migration and reduction of loss to follow-up, aiming at broadening the new ideas andmethods for clinical research of acupuncture and moxibustion.

Induction of microRNA­let­7a inhibits lung adenocarcinoma cell growth by regulating cyclin D1.

Lung cancer is the most common cause of cancer­associated mortality. MicroRNAs (miRNAs), as oncogenes or tumor suppressor genes, serve crucial roles not only in tumorigenesis, but also in tumor invasion and metastasis. Although miRNA­let­7a (let­7a) has been reported to suppress cell growth in multiple cancer types, the biological mechanisms of let­7a in lung adenocarcinoma are yet to be fully elucidated. In the present study, the molecular roles of let­7a in lung adenocarcinoma were investigated by detecting its expression in lung adenocarcinoma tissues and exploring its roles in the regulation of lung cancer cell proliferation. Let­7a expression was identified to be downregulated in lung adenocarcinoma tissues compared with normal tissues. Overexpression of let­7a effectively suppressed cancer cell proliferation, migration and invasion in H1299 and A549 cells. Let­7a also induced cell apoptosis and cell cycle arrest. Furthermore, let­7a significantly inhibited cell growth by directly regulating cyclin D1 signals. This novel regulatory mechanism of let­7a in lung adenocarcinoma provides possible avenues for future targeted therapies of lung cancer.

miR-33a-5p enhances the sensitivity of lung adenocarcinoma cells to celastrol by regulating mTOR signaling.

MicroRNAs (miRNAs or miRs) have recently become a popular focus of cancer research due to their ability to act as oncogenes or tumor suppressors. In the present study, miR­33a­5p expression was identified to be downregulated in lung adenocarcinoma samples compared with normal, which suggested that miR­33a­5p may serve as a tumor suppressor gene. Transfection with miR­33a­5p mimics inhibited the proliferation and migration of A549 and LTEP­a­2 cells and increased cellular apoptosis. A luciferase reporter assay confirmed that miR­33a­5p targets the 3'­untranslated region of the mechanistic target of rapamycin (mTOR) gene. mTOR expression was decreased in A549 and LTEP­a­2 cells treated with miR­33a­5p mimics, as well as the expression of its downstream effectors phosphorylated (p)­p70 ribosomal protein S6 kinase (p70S6K) and p­eukaryotic translation initiation factor 4E binding protein 1 (4EBP1). Following treatment with celastrol, miR­33a­5p expression was upregulated, and miR­33a­5p could enhance cellular sensitivity to celastrol. Western blot analysis revealed that the expression of mTOR, p­p70S6K and p­4EBP1 decreased following celastrol treatment. These results suggested that mTOR was involved in the mechanism by which miR­33a­5p enhanced the sensitivity of lung adenocarcinoma cells to celastrol. Furthermore, LTEP­a­2 cells were xenografted subcutaneously into nude mice, to examine the effect of celastrol and miR­33a­5p on the growth of LTEP­a­2 cells in vivo. The results demonstrated that tumor growth in the celastrol­treated or miR­33a­5p­treated group was attenuated compared with the control group. Notably, tumor growth in the combination treatment group was almost arrested after 2 weeks. In addition, celastrol upregulated the expression of miR­33a­5p, and high expression of miR­33a­5p inhibited mTOR and its downstream effectors. In summary, miR­33a­5p inhibited the proliferation of lung adenocarcinoma cells, enhanced the antitumor effect of celastrol, and improved sensitivity to celastrol by targeting mTOR in lung adenocarcinoma in vitro and in vivo.

Single nucleotide polymorphisms rs701848 and rs2735343 in PTEN increases cancer risks in an Asian population.

We performed this meta-analysis to analyze the cancer risk to individuals carrying the rs701848 and rs2735343 single nucleotide polymorphisms (SNPs) in the phosphatase and tensin homolog (PTEN) gene. We searched the PubMed, EMBASE, Cochrane library and the national knowledge infrastructure of China (CNKI) databases and identified 18 eligible case-control studies with 5458 cases and 6003 controls for rs701848 as well as 5490 cases and 6209 controls for rs2735343. Our analyses demonstrated that cancer risk was associated with rs701848 in the recessive model (CC vs. CT+TT, OR=1.169, 95% CI: 1.061-1.288) and with rs2735343 in the dominant model (GC+CC vs. GG, OR=0.758, 95% CI: 0.590-0.972). Subgroup analysis showed that in Asian subjects, carrying the C allele of rs701848 or GG genotype of rs2735343 was associated with increased cancer risk. Moreover, Asian subjects carrying the TC/CC genotype or C allele of rs701848 were associated with increased risk of esophageal squamous cell cancer. This meta-analysis indicates that the PTEN rs701848 (CC) and rs2735343 (GG) polymorphisms are associated with increased cancer risk in Asian subjects.