Postoperative early kinesitherapy has been advocated as an optimal method for treating Achilles tendon rupture. However, an insight into the rationale of how early kinesitherapy contributes to healing of Achilles tendon remains to be achieved, and research in the area of proteomic analysis of Achilles tendon has so far been lacking. Forty-two rabbits were randomized into control group, immobilization group, and early motion group, and received postoperative cast immobilization and early motion treatments. Achilles tendon samples were prepared 21 days following microsurgery, and the proteins were separated with two-dimensional polyacrylamide gel electrophoresis. Differentially expressed proteins were first recognized by PDQuest software, and then identified using peptide mass fingerprinting, tandem mass spectrometry, and database searching. A total of 463  ±  12, 511  ±  39, and 513  ±  80 protein spots were successfully detected in the two-dimensional polyacrylamide gels for the Achilles tendon samples of rabbits in the control group, immobilization group, and early motion group, respectively. There were 15, 8, and 9 unique proteins in these three groups, respectively, and some differentially expressed proteins were also identified in each group. It was indicated that some of the differentially expressed proteins were involved in various metabolism pathways and may play an important role in healing of Achilles tendon rupture. Postoperative early kinesitherapy resulted in differentially expressed proteins in ruptured Achilles tendon compared with those treated with postoperative cast immobilization. These differentially expressed proteins may contribute to healing of Achilles tendon rupture through a mechanobiological mechanism due to the application of postoperative early kinesitherapy.

Reports on the correlation between the expression of Survivin/phosphatase and tensin homolog (PTEN) proteins and clinical factors in gastric cancer (GC) are varied, and the sample sizes were also not sufficient. The present study aimed to detect the expression of Survivin and PTEN proteins in GC patients on the basis of a greater number of specimens and to analyze the correlation with clinical features and survival. The results revealed that the Survivin expression rates in GC, normal tissues and metastatic lymph nodes were 72% (232/322), 5% (6/120) and 80% (36/45), respectively, while the PTEN expression rates were 34% (109/322), 92.5% (111/120) and 24.4% (11/45), respectively, and the differences between cancer and normal tissue or metastatic lymph nodes were significant for both proteins (P<0.05). The expression of Survivin was significantly associated with gross type, depth of invasion, distant metastasis, tumor, necrosis and metastasis (TNM) stage and vascular invasion, while PTEN expression was predominantly associated with age, tumor size, invasion depth, TNM stage and lymphatic invasion in GC patients (P<0.05). The expression of both was associated with postoperative metastasis and metastatic site (P= 0.007 and P= 0.011 for Survivin, and P= 0.002 and P= 0.005 for PTEN). There was a negative association between the expression levels of Survivin and PTEN (P= 0.001, r=-0.524). The expression levels of both were also associated with prognosis. The expression of Survivin and PTEN protein exhibit opposing trends in GC, which may indicate adverse biological effects in the occurrence of GC. The Survivin and PTEN expression levels are likely to be an important molecular event in gastric tumorigenesis and may be considered as molecular markers of GC progression and reliable prognostic indicators of GC.

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Colon cancer is a malignant tumor that seriously affects human health. Recently, studies revealed that the expression of MTBP enhanced the proliferation and metastasis of many types of cancer cells. And the data also showed that MTBP has the potential to regulate the expression of ZEB2. However, it is unclear whether MTBP can affect the proliferation, migration and invasion of colon cancer cells by modulating the expression of ZEB2. In this study, we established the MTBP overexpression and knockdown colon cancer cells with the transfection. Next, CCK-8 and transwell assays were carried out to determine the changes of the proliferation and invasion of colon cancer cells, respectively. After that, we overexpressed the ZEB2 in these MTBP knockdown colon cancer cells. Finally, the invasion and migration of these cells were detected with the same methods. We revealed that overexpression of MTBP enhanced the proliferation and invasion of colon cancer cells. Moreover, suppression of MTBP repressed the proliferation, migration and invasion of colon cancer cells. Furthermore, MTBP promoted the expression of ZEB2. The overexpression of ZEB2 abolished the MTBP knockdown induced inhibition of the migration and invasion of colon cancer cells. These results implied that MTBP enhanced the proliferation, migration and invasion of colon cancer cells by activating the expression of ZEB2.

Dysregulated microRNAs (miRNAs) have been implicated in the pathogenic processes of colon cancer. Epithelial mesenchymal transition (EMT) promotes metastatic progression and cancer stem cells are closely involved in colon cancer proliferation and metastasis. Functional effects of miR-377 on colon cancer stem cell phenotypes and EMT were then determined in the present study. Firstly, reduced miR-377 was found in colon cancer tissues and cell lines. Results from flow cytometry, sphere formation and western blot assays showed that miR-377 knockdown increased number of ALDH+ cells and promoted sphere formation ability. Moreover, cell migration/invasion and EMT of colon cancer cells were suppressed by miR-377 over-expression. On the contrary, miR-377 mimics caused the reversed results. ZEB2 (zinc finger E box-binding homeobox 2) was then validated as a binding target of miR-377. ZEB2 over-expression reversed the inhibitory abilities of miR-377 on cancer stem cell phenotypes, EMT, migration and invasion. In conclusion, miR-377 regulates cancer stem cell phenotypes and EMT in colon cancer cells via regulation of ZEB2, suggesting a new therapeutic strategy for colon cancer treatment.

Background: The RAD51 recombinase is involved in homologous recombination and DNA repair. However, the association of RAD51 with the prognosis of adenocarcinoma at the gastroesophageal junction (ACGEJ) is not clear. We aimed to investigate the association of RAD51with ACGEJ prognosis. Methods: The difference in the expression level of RAD51 between ACGEJ tumors and control tissues in the microarray datasets (GSE159721, GSE74553, and GSE96669) were compared. The online Kaplan-Meier plotter survival analysis and meta-analysis were used to analyze the association of RAD51 with overall survival in pan-cancers. MiRNAs targeting RAD51 were identified and their expression profiles in ACGEJ tumors were analyzed. Functional enrichment analysis was performed for miRNAs of RAD51. Results: RAD51 was upregulated in ACGEJ tumors compared with control tissues (P < 0.05). High RAD51 level was correlated with a poor prognosis in stomach adenocarcinoma and esophageal cancer. The meta-analysis showed that high RAD51 level was correlated with a poor prognosis in TCGA pan-cancers (P = 0.03). Six regulatory miRNAs of RAD51, including hsa-miR-182, hsa-miR-221, and hsa-miR-34a, were downregulated in ACGEJ tumor tissues and were associated with pathways including “fatty acid biosynthesis” and “viral carcinogenesis”. Conclusions: RAD51 is a potent prognostic biomarker in ACGEJ. MiRNAs including hsa-miR-182, hsa-miR-221, and hsa-miR-34a might play crucial roles in ACGEJ by regulating the RAD51 gene.

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The original article was inadvertently published with incorrect affiliation of Dr. Jialili. The correct affiliation is shown here.