Effect of acupoint catgut embedding combined with western medicine on patients with stable COPD: Acupoint catgut embedding treating stable COPD meta-analysis.

BACKGROUND: Although bronchodilators and glucocorticoids can reduce the symptoms of cough and asthma to a certain extent, the adverse drug reactions and recurrence after recovery still trouble clinicians. Acupoint catgut embedding is effective in preventing and treating acute recurrence and deterioration of COPD, but its clinical efficacy remains controversial. Therefore, this study evaluated the clinical efficacy and safety of acupoint catgut embedding combined with conventional Western medicine for COPD through meta-analysis. METHODS: Pubmed, the Cochrane Library, Web of Science, Sinomed, China Knowledge Network, VIP, and Wanfang databases were searched, with a time frame from database creation to November 2022. Meta-analysis was performed with Revman 5.3. Publication bias was assessed by Stata 15.0. RESULTS: Seventeen studies were listed, with a total sample size of 1516 cases. Meta-analysis showed that compared with conventional western medicine, acupoint catgut embedding combined with conventional western medicine could effectively improve the total effective rate of clinical symptoms of stable COPD [RR = 1.21, 95%CI (1.13, 1.29), P < .00001], forced expiratory volume in 1 second (FEV1) [mean difference (MD) = 0.04, 95%CI (0.00, 0.09), P = .04],the percentage of forced expiratory volume in 1 second predicted value [MD = 1.13, 95%CI (0.38,1.88), P = .003], acute exacerbation of chronic obstructive pulmonary disease [MD = -0.73, 95%CI (-1.04, -0.42), P < .00001], COPD assessment test score [MD = -2.39, 95%CI (-3.65, -1.13), P = .0002], the improved medical research council respiratory questionnaire score (mMRC score) [MD = -0.15, 95%CI (-0.29, -0.02),P = .03], 6-minute walk distance [MD = 28.16, 95%CI (17.31, 39.00), P < .00001], the production of inflammatory factor interleukin-8 [MD = -9.65, 95%CI (-10.44, -8.86), P < .00001], but the adverse event rate was comparable[RR = 1.39, 95%CI (0.28,6.91), P = .69]. However, there was no significant difference in forced expiratory volume in 1 second/forced vital capacity and TNF-α between the acupoint catgut embedding combined group and the conventional western medication group. Harbord test showed no significant publication bias. CONCLUSION: The clinical efficacy of acupoint catgut embedding combined with conventional western medicine for stable COPD is better than that of conventional western medicine, and the safety may be equivalent to that of conventional western medicine, which has the value of further research exploration.

Long Intergenic Non-Coding RNA 01121 Promotes Breast Cancer Cell Proliferation, Migration, and Invasion via the miR-150-5p/HMGA2 Axis.

PURPOSE: Long intergenic noncoding RNA 01121 (LINC01121) has been reported to be aberrantly expressed and acts as an oncogene in pancreatic cancer. However, the detailed molecular mechanism of LINC01121 in breast cancer remains largely unclear. In this study, we aimed to investigate the expression and biological function of LINC01121 in breast cancer. METHODS: LINC01121 and miR-150-5p expression were measured in breast cancer cell lines using quantitative reverse transcription PCR. MTS and flow cytometry assays were performed to determine cell proliferation, the cell cycle, and apoptosis. Cell migration and invasion were assessed by transwell assay. The protein expression of HMGA2 in breast cancer cell lines was measured by Western blotting. A luciferase reporter assay was used to assess the binding of LINC01121 and miR-150-5p. RESULTS: We found that LINC01121 was markedly up-regulated in breast cancer cell lines compared with normal breast epithelial cells. LINC01121 down-regulation markedly suppressed cell proliferation, cell cycle progression, migration, and invasion and promoted apoptosis in breast cancer cells. Further investigation showed that LINC01121 could serve as a molecular sponge for miR-150-5p and indirectly modulate the expression of its target, HMGA2. Moreover, miR-150-5p knockdown rescued the effects of LINC01121 down-regulation on HMGA2 protein expression, cell proliferation, cell cycle progression, apoptosis, migration, and invasion in breast cancer cells. CONCLUSION: Knockdown LINC01121 inhibited breast cancer cell proliferation, migration, and invasion via the miR-150-5p/HMGA2 axis.

Forward and reverse mutations in stages of cancer development.

BACKGROUND: Massive occurrences of interstitial loss of heterozygosity (LOH) likely resulting from gene conversions were found by us in different cancers as a type of single-nucleotide variations (SNVs), comparable in abundance to the commonly investigated gain of heterozygosity (GOH) type of SNVs, raising the question of the relationships between these two opposing types of cancer mutations. METHODS: In the present study, SNVs in 12 tetra sample and 17 trio sample sets from four cancer types along with copy number variations (CNVs) were analyzed by AluScan sequencing, comparing tumor with white blood cells as well as tissues vicinal to the tumor. Four published "nontumor"-tumor metastasis trios and 246 pan-cancer pairs analyzed by whole-genome sequencing (WGS) and 67 trios by whole-exome sequencing (WES) were also examined. RESULTS: Widespread GOHs enriched with CG-to-TG changes and associated with nearby CNVs and LOHs enriched with TG-to-CG changes were observed. Occurrences of GOH were 1.9-fold higher than LOH in "nontumor" tissues more than 2 cm away from the tumors, and a majority of these GOHs and LOHs were reversed in "paratumor" tissues within 2 cm of the tumors, forming forward-reverse mutation cycles where the revertant LOHs displayed strong lineage effects that pointed to a sequential instead of parallel development from "nontumor" to "paratumor" and onto tumor cells, which was also supported by the relative frequencies of 26 distinct classes of CNVs between these three types of cell populations. CONCLUSIONS: These findings suggest that developing cancer cells undergo sequential changes that enable the "nontumor" cells to acquire a wide range of forward mutations including ones that are essential for oncogenicity, followed by revertant mutations in the "paratumor" cells to avoid growth retardation by excessive mutation load. Such utilization of forward-reverse mutation cycles as an adaptive mechanism was also observed in cultured HeLa cells upon successive replatings. An understanding of forward-reverse mutation cycles in cancer development could provide a genomic basis for improved early diagnosis, staging, and treatment of cancers.