Arthroscopic reduction and fixation for isolated greater tuberosity fractures / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Traditionally, displaced greater tuberosity fractures are treated with open reduction and internal fixation. Arthroscopic treatment and outcome of greater tuberosity fractures is far from comprehensive. The objective of the current study was to assess the surgical procedure and outcome of an arthroscopic method in the treatment of isolated greater tuberosity fractures.</p><p><b>METHODS</b>From January 2006 to December 2009, 23 patients with isolated greater tuberosity fractures were treated with an arthroscopic procedure using three cannulated screws combined with washers. During follow-up, radiographs and the constant shoulder score (CSS) were used to evaluate the outcome.</p><p><b>RESULTS</b>Three cannulated screws with washers were used to fix the fractured fragment of the greater tuberosity under an arthroscope. All incisions healed at primary intention without infection. The mean duration of follow-up was 20 months (range 18 - 36 months). Fracture fixation was excellent, and fractures healed 2 - 6 months (mean 3.8 months) after surgery. At final follow-up, the CSS was 92 (range 86 - 100).</p><p><b>CONCLUSIONS</b>The described arthroscopic procedure provides anatomical reduction and firm fixation for isolated greater tuberosity fractures. It is a successful and minimally invasive procedure with satisfying therapeutic effects as well as excellent functional recovery.</p>

Effects of PTEN gene on invasion and migration of ovarian cancer cell line A2780 and related mechanisms / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To evaluate the effects of PTEN on invasive and migration ability of human ovarian cancer cell line A2780 and related mechanisms.</p><p><b>METHODS</b>The plasmid including WT-PTEN and mutant PTEN were transferred into A2780 cells. The invasive and migration ability were measured before and after transfection by transwell chamber and wound-healing assays. The expression of PTEN protein and related proteins in the cells were detected by Western blot analysis. Empty plasmid-transfected A2780 and normal A2780 cells were used as control (the different four groups were named as WT-PTEN/A2780, C124A-PTEN/A2780, GFP/A2780 and A2780).</p><p><b>RESULTS</b>The number of penetrating cells was significantly less in WT-PTEN/A2780 cells (24.3 ± 2.5) than those in C124A-PTEN/A2780, GFP/A2780 and A2780 cells (43.7 ± 3.8, 44.7 ± 2.1 and 45.0 ± 3.0) (P < 0.05). The migration distance was markedly shorter in WT-PTEN/A2780 cells (54.1 ± 3.7) than those in C124A-PTEN/A2780, GFP/A2780 and A2780 cells (78.7 ± 3.4, 78.1 ± 3.1 and 76.8 ± 3.5) (P < 0. 05).</p><p><b>CONCLUSIONS</b>Transfection with PTEN may suppress the invasive and migration ability of ovarian cancer cell line A2780 depending on its phosphatase activity, and the suppressive effect may be due to the down-regulation of MMP-9 in the cancer cells.</p>

Effect of semaphorin4D gene silencing on malignant behavior of human ovarian cancer SKOV3 cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To observe the effect of DNA Sema4D gene silencing by RNA interfering on the proliferation, migration and invasion of human ovarian cancer SKOV3 cells, and to study the effect of pshRNASema4D on the growth of SKOV3 cells in transplanted tumor in nude mice.</p><p><b>METHODS</b>Recombinant plasmid pshRNASema4D-A, B and C were respectively transfected into SKOV3 cells by lipofetamine 2000, while cells transfected by plasmid vector pcDNA3.1 and cells untreated as control groups. RT-PCR was adopted to select the recombinant plasmid which showed the most optimal inhibition effect. RT-PCR and Western blot were used to detected the mRNA and protein expression of Sema4D in SKOV3 cells tranfected for 24, 48 and 72 hours. MTT assay was used to investigate the proliferation of the SKOV3 cells after trasnsfection. Transwell cell migration and invasion assays were used to investigate the migration and invasion abilities of the SKOV3 cells after trasnsfection. Human ovarian cancer model was established in nude mice, and the nude mice were treated with pshRNASema4D-B once every 3 days for 3 weeks. The bulk of the transplanted tumor was measured.</p><p><b>RESULTS</b>Three Sema4D-targeted short hairpin RNA (shRNA) A, B and C were successfully inserted into the plasmid vector pshRNA, and the coding sequences of the obtained shRNA were consistent with the designed fragment. The results indicated that both recombinant plasmid pshRNASema4D-A and B could effectively knock down the expression of Sema4D gene in human ovarian cancer cells, of which pshRNASema4D-B was the better choice, while no effect of pshRNASema4D-C was seen. RT-PCR results showed that the relative mRNA expression of Sema4D gene in SKOV3 cells transfected with pshRNA-Sema4D for 24, 48 and 72 hours were 0.401 ± 0.051, 0.120 ± 0.035 and 0.014 ± 0.015, respectively, which were significantly lower than that in SKOV3 cells transfected by empty vector and non-transfected cells at 72 hours after transfection. (0.521 ± 0.019, 0.536 ± 0.040,respectively, P < 0.05). The Westen blot analysis manifested that the relative expression of Sema4D protein of SKOV3 cells transfected by pshRNASema4D for 24, 48 and 72 hours were 0.196 ± 0.023, 0.074 ± 0.015 and 0.040 ± 0.014, respectively, which were significantly lower than that in SKOV3 cells transfected by empty vector and non-transfected cells at 72 hours after transfection. (0.275 ± 0.009, 0.282 ± 0.015, respectively, P < 0.05). Comparing with the empty vector-transfected and non-transfected cells, the proliferation, invasion and migration ability of SKOV3 cells transfected with pshRNA-Sema4D were obviously weakened. The pshRNASema4D-B significantly suppressed the growth of the SKOV3 cells-transplanted tumors in nude mice, and the IR (inhibitory rate) of pshRNASema 4D-B group was (61.0 ± 3.3)% (P < 0.05).</p><p><b>CONCLUSIONS</b>Sema4D can be successfully silenced by RNA interfering in human ovarian cancer SKOV3 cells. Downregulation of Sema4D can inhibit the proliferation, migration and invasion of ovarian cancer cells. The pshRNASema4D can significantly suppress the growth in transplanted tumor of human ovary cancer in nude mice. Sema4D may become a candidate gene of gene therapy of human ovarian cancer.</p>

Screening, cloning and identification of the human endometrial carcinoma-related genes / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To screen, clone and identify the cDNA fragments of human endometrial carcinoma-related genes,and explore the molecular mechanism of endometrial carcinogenesis.</p><p><b>METHODS</b>Pure endometrial glandular epithelial cells and endometrial carcinoma cells were obtained by laser capture microdissection (LCM). RNA from these cells was isolated, and differentially expressed gene fragments that were specialy relevant to endometrial carcingenesis were identified by using fluorescence differential display reverse transcription polymerase chain reaction (FDD-PCR). The selected fragments were cloned, sequenced and verified by reverse Northern blot analysis, and positive fragments were BLAST analysed and compared with those in Genbank.</p><p><b>RESULTS</b>38 differential fragments were isolated, 3 of which were expressed more abundantly in normal endometrium and 35 were highly expressed in endometrial carcinoma. 10 fragments were recoverd, cloned and sequenced, confirmed by reverse Northern blot analysis, among which 6 fragments were positive. BLAST analysis showed that T1.1 was homologous to cyclin-dependent protein kinase 7 (CDK7, 99%); L1.9 was homologous to protein phosphatase 1 regulatory (inhibitor) subunit 12A (PPP1R12A, 99%); L1.21 and L1.22 were homologous to cellular repressor of E1A-stimulated genes 1 (CREG, 100%); L1.25 and L1.26 were homologous to solute carrier family 39 (zinc transporter) member 10 (SLC39A10, >98%).</p><p><b>CONCLUSION</b>Gene fragments related to endometrial carcinoma have been obtained by applying LCM and FDD-PCR. To our knowledge it is the first time that the correlation between CDK7, PPP1R12A, CREG, SLC39A10 and endometrial carcinoma is discovered at mRNA level, and their role in molecular mechanism of cancinogenesis is discussed. CDK7, CREG, SLC39A10 as new candidate oncogene and PPP1R12A as new candidate anti-oncogene are worthy of being further investigated in the future.</p>