lncRNA FOXP4­AS1 predicts poor prognosis and accelerates the progression of mantle cell lymphoma through the miR­423­5p/NACC1 pathway.

Long non­coding RNA (lncRNA) forkhead box P4 antisense RNA 1 (FOXP4­AS1) has been determined to function as an oncogene in various types of cancer. However, the biological function and the underlying mechanisms of FOXP4­AS1 in mantle cell lymphoma (MCL) remain to be uncovered. The expression and the associated clinicopathological characteristics and prognostic significance of FOXP4­AS1 were explored in MCL clinical samples. The effects of FOXP4­AS1 on MCL cellular behaviors, including proliferation, migration and invasion were analyzed using CCK­8, crystal violet and Transwell assays. The downstream molecules of FOXP4­AS1 were explored using bioinformatics analysis and dual luciferase assay. Our results showed that FOXP4­AS1 expression was upregulated in MCL patients, and that the high expression of FOXP4­AS1 was correlated with the unfavorable prognosis of patients. Functionally, while FOXP4­AS1 downregulation inhibited proliferation, migration and invasion of MCL cells, FOXP4­AS1 overexpression had promotive effects on these cellular processes. Mechanistically, FOXP4­AS1 was found to act as a competing endogenous (ce)RNA for miR­423­5p to regulate the expression of nucleus accumbens­associated 1 (NACC1). The negative regulation of FOXP4­AS1 on miR­423­5p compared to that of miR­423­5p on NACC1 was determined at the mRNA or protein levels in MCL cells. Moreover, an inverse expression correlation between FOXP4­AS1 and miR­423­5p, and that between miR­423­5p and NACC1 was confirmed in MCL clinical samples. In addition, rescue assay showed that miR­423­5p upregulation or NACC1 knockdown abolished the promoting effects of FOXP4­AS1 on MCL cell proliferation, migration and invasion. In conclusion, FOXP4­AS1 promotes MCL progression through the upregulation of NACC1 expression by inhibiting miR­423­5p. FOXP4­AS1 may serve as a novel therapeutic target for patients with MCL.

[Experimental studies of rAd-p53 injection by interventional approach for the treatment of rabbit VX2 liver cancer].

OBJECTIVES: To evaluate the efficacy of recombinant human adenovirus p53 gene therapy (rAd-p53) in the rabbit VX2 liver cancer model using different interventional therapy approach. METHODS: Thirty New Zealand rabbits implanted with VX2 tumor in the liver were randomized into five groups with six of each. The tumor volumes (V1) were measured by MRI and CT scan 11 days after tumors implanted. The interventional therapy scheme performed as below: intraarterial 0.9% saline solution perfusion in group A, transcatheter arterial embolization with 0.5 ml ultrafluid lipiodol in group B, intraarterial rAd-p53 gene perfusion in group C (1 x 10(6)/VP); intraarterial rAd-p53 gene perfusion (1 x 10(6)/VP) in combination with transcatheter arterial embolization (ultrofluid lipiodol, 0.5 ml) in group D and intratumoral rAd-p53 gene (1 x 10(6)/VP) injection in group E. The tumor volumes (V2) were measured by MRI and CT scan, and the tumor growth ratios were calculated 14 days after interventional procedures. Then all animals were sacrificed. RESULTS: The tumor tissues were explanted for immunohistochemistry to observe the expressions of vascular endothelial cell growth factor (VEGF) and factor VIII. Microvessel density (MVD) of the tumor tissues was assessed by factor VIII immunohistochemical analysis. In addition, apoptotic index was assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The tumor volumes before therapy were (79.4+/-8.2), (75.3+/-7.8), (74.6+/-6.6), (78.7+/-9.1), (75.8+/-8.4) mm(3) respectively, without differences found among them (F = 12.248, P = 0.0636). But the tumor volumes after therapy were (564.7+/-96.7), (176.5+/-83.2), (239.6+/-42.8), (159.8+/-58.6), (334.7+/-32.6) mm(3) respectively (F = 24.537, P = 0.0218). The tumor growth ratios were 6.9, 2.6, 3.1, 1.6 and 4.1 respectively. The mean apoptosis index were 12.0%+/-1.1%, 14.5%+/-2.1%, 17.6%+/-2.3%, 18.6%+/-2.3% and 19.6%+/-2.5% respectively. with significant differences in group E in comparison with the other four groups. Mean positive ratio of VEGF was 50.0%, 83.3%, 83.3%, 50.0% and 50.0% respectively, with significant differences observed in group B and group C compared with the other three groups (F = 7.84, P = 0.019). The differences of VIII factor positive expression ratio among each group were significant (F = 0.854, P = 0.018). Statistical analysis showed a positive correlation between the expression of VEGF and MVD (r = 2.400, P = 0.0233). CONCLUSION: The rAd-p53 has effective treatment outcomes in VX2 rabbit liver cancer, and intra-arterial rAd-p53 gene perfusion in combination with transcatheter arterial embolization is the best approach in comparison with intra-arterial rAd-p53 gene perfusion, transcatheter arterial embolization and intratumoral rAd-p53 gene injection alone.

[Monobloc distraction osteogenesis and cranial vault remodeling in a pediatric patient with severe Crouzon's syndrome].

OBJECTIVE: To report the treatment of a case of severe Crouzon's syndrome using monobloc distraction osteogenesis and cranial vault remodeling. METHODS: Through intra-and extra-cranial approach, monobloc osteotomy was performed and external distractor was placed. Distraction began on the 7th postoperative day at a rate of 1 mm a day, two times a day. The distractor removed after consolidation for 4 months. RESULTS: The distraction distance attained 20 mm. The exophthalmos and cross bite were corrected completely. The severe obstructive apnea improved markedly. CONCLUSIONS: Monbloc distraction osteogenesis and cranial vault remodeling are effective and safe procedure for Crouzon's syndrome.

[Effects of SODD and survivin on leukemia cell apoptosis induced by chemotherapeutic drugs].

This study was aimed to investigate the changes of silencer of death domains (SODD), survivin, caspase 3, caspase 8 and caspase 9 in the apoptotic process of human leukemia cells induced by chemotherapeutic drugs in order to explore the molecular mechanism of apoptotic modulatory genes and to search for the new target of chemotherapeutic drugs. After Jurkat cells were induced by chemotherapeutic drugs, the translocated phosphatidylserine was labeled with annexin V/PI, and the apoptosis incidence was measured by FCM; The expression changes of SODD, caspase 3, caspase 8 and caspase 9 were determined by Western blot; the changes of survivin mRNA and protein were determined by RT-PCR and immunohistochemistry SABC method respectively. The results indicated that high expressions of SODD and survivin could inhibit apoptotic signaling pathway; VCR down-regulated the function of SODD protein and effectively induced the apoptosis of Jurkat cells in a time-dependent manner and activates caspase 3 through the death receptor-mediated activation of caspase 8, in which caspase 9 and survivin were not degraded. It is concluded that SODD participates in the apoptotic process induced by VCR which induces the Jurkat cell apoptosis by downregulating expression of SODD protein and priming death receptor pathway. In the apoptotic process, the mitochondrion apoptotic pathway is not trigged.

[The regulating effect of antisense-S-Oligo on TYR gene expression and melanin production of melanocytes].

OBJECTIVE: Despite the causes for melanin increase, the increased gene expression of TYR is a common pathological process. Based on this viewpoint, antisense-S-Oligo of TYR was designed and synthesized to regulate synthesis of melanin in order to explore the treatment for skin pigmentation. METHODS: The cultured melanocytes were divided into 3 groups. The group 1 was treated with endothelin, group 2 treated with ultraviolet ray and group 3 was used as the control. In each group, the 5' antisense-S-Oligo, the 3' antisense-S-Oligo, the mixed antisense-S-Oligo of TYR or Dotap only was added. The melanin content and TYR gene expressions were examined. RESULTS: The 5' antisense-S-Oligo, the 3' antisense-S-Oligo and the mixed antisense-S-Oligo significantly inhibited the increase of melanin content and TYR gene expression, which were caused by endothelin or ultraviolet ray treatment. Of the three treatments, the 3' antisense-S-Oligo showed the strongest effect. CONCLUSION: Antisense-S-Oligo has significant regulating effects on TYR gene expression and melanin content. The 3' antisense-S-Oligo is more effective than the 5' antisense-S-Oligo.

[Repair of whole auricular defects with implant-plasty and prosthesis].

OBJECTIVE: To repair the whole auricular defects with implant-plasty and prosthesis technique. The indications, complications and implant sites of this method were discussed. METHODS: In reconstruction of the whole auricular defect, the self-developed pure titanium implants, specialized for plastic surgery, were used for intra-osseous fixation for retaining the artificial ear. 10 cases were treated with this method. RESULTS: Follow-up of three years demonstrated that this implant system, with stable function, could generate osseointegration and be used as an abutment of intra-osseous fixation to retain the auricular prosthesis for a long time. CONCLUSION: The operation is simple and convenient with little trauma and short-term of treatment. The artificial ear has lifelike appearance, proper color and satisfactory effects. This technique has wide indications and is worth popularization.