Downregulated LRRK2 gene expression inhibits proliferation and migration while promoting the apoptosis of thyroid cancer cells by inhibiting activation of the JNK signaling pathway.

Emerging studies have indicated that leucine­rich repeat kinase 2 (LRRK2) is associated with thyroid cancer (TC). The present study investigated the effect of LRRK2 on the cell cycle and apoptosis in TC, and examined the underlying mechanisms in vitro. To screen TC­associated differentially expressed genes, gene expression microarray analysis was conducted. Retrieval of pathways associated with TC from the Kyoto Encyclopedia of Genes and Genomes database indicated that the c­Jun N­terminal kinase (JNK) signaling pathway serves an essential role in TC. SW579, IHH­4, TFC­133, TPC­1 and Nthy­ori3­1 cell lines were used to screen cell lines with the highest and lowest LRRK2 expression for subsequent experiments. The two selected cell lines were transfected with pcDNA­LRRK2, or small interfering RNA against LRRK2 or SP600125 (a JNK inhibitor). Subsequently, flow cytometry, terminal deoxynucleotidyl transferase­mediated dUTP­biotin nick end labeling, a 5­ethynyl­2'­deoxyuridine assay and a scratch test was conducted to detect the cell cycle distribution, apoptosis, proliferation and migration, respectively, in each group. The LRRK2 gene was determined to be elevated in TC based on the microarray data of the GSE3678 dataset. The SW579 cell line was identified to exhibit the highest LRRK2 expression, while IHH­4 cells exhibited the lowest LRRK2 expression. LRRK2 silencing, through inhibiting the activation of the JNK signaling pathway, increased the expression levels of genes and proteins associated with cell cycle arrest and apoptosis in TC cells, promoted cell cycle arrest and apoptosis, and inhibited cell migration and proliferation in TC cells, indicating that LRRK2 repression could exert beneficial effects through the JNK signaling pathway on TC cells. These observations demonstrate that LRRK2 silencing promotes TC cell growth inhibition, and facilitates apoptosis and cell cycle arrest. The JNK signaling pathway may serve a crucial role in mediating the anti­carcinogenic activities of downregulated LRRK2 in TC.

[Free deep inferior epigastric artery perforator flap techniques for the immediate post modified radial mastectomy reconstruction].

OBJECTIVE: To discuss the feasibility and method of immediate breast reconstruction right after modified radical mastectomy in early breast carcinoma patients. METHODS: Deep inferior epigastric artery perforation flaps were immediately applied on patients to reconstruct the breast after the skin-sparing mastectomy. The breasts were shaped after the deep inferior epigastric artery and vein were anastomosed to the thoracodorsal artery and vein. RESULTS: In 10 cases of breast reconstruction by DIEP flaps since 2005, there were completely survival in 8 flaps, distal skin necrosis in 1 flap, adiponecrosis in 1 flap. With the follow-up of 9-28 months, the reconstructed breasts were well-shaped and there were no abdominal complication in dnor sites. Ninety percent patients were satisfied with the results from the good to the best level. CONCLUSION: Most patients were satisfied with the results of mastectomy reconstruction.