It is one of the main characters of malignant tumors that malignant tumor cells invade surrounding tissues and metastasize to distant tissues .Multiple factors are involved in this complicated dynamic process .Metastasis is the major factor influencing recurrence and prognosis .Therefore, it is important to explore the mechanism of invasion and metastasis for reducing recurrence rate and mortality of malignant tumors .Engulfment and cell mobility ( ELMO) family is one kind of conserved protein in evolutional process .It includes 3 members, ELMO1, ELMO2 and ELMO3.The members of ELMO family play an important role in cell phagocytosis and cell migration , and they also have close correlation with ma-lignant tumor cell invasion and metastasis .In this paper , we review the progress of the relationship between ELMO family and malignant tumor invasion and metastasis .

Antibodies, Neutralizing ; Apoptosis ; Hep G2 Cells ; Humans ; Receptors, Tumor Necrosis Factor, Member 6b ; immunology ; metabolism

Adult ; Aged ; Aged, 80 and over ; Apoptosis ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Female ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Receptors, Tumor Necrosis Factor, Member 6b ; metabolism

AIM:To reveal the role and function of engulfment and cell mobility 1 (ELMO1) in the invasion and migration of gastric cancer cells.METHODS:The expression of ELMO1 at protein and mRNA levels was detected in 5 kinds of gastric cancer cells and 1 normal human gastric epithelial cells by Western blot and real-time PCR, and the gastric cancer cells with the highest expression of ELMO1 were screened out.The cell transfection experiment was used to silence ELMO1 expression in the gastric cancer cells, and the effect of ELMO1 silencing on the invasion and migration of the gastric cancer cells was detected by Transwell assay.RESULTS:The expression level of ELMO1 in the gastric cancer cells was significantly higher than that in human normal gastric epithelial cells (P<0.01), and the SGC7901 cells had the highest expression level of ELMO1.ELMO1-siRNA significantly silenced the expression of ELMO1 in the SGC7901 cells (P<0.01).Silencing of ELMO1 expression significantly reduced the invasion and migration abilities of the human gastric can-cer cells (P<0.01).CONCLUSION:ELMO1 is highly expressed in the gastric cancer cells, and promotes the invasion and migration abilities of the gastric cancer cells.ELMO1 may become an effective target for the treatment of invasion and metastasis of gastric cancer.

To investigate the effect of microRNA-221 (miR-221) on cell viability and apoptosis of hepatocellular carcinoma HepG2 cells. MiR-221 inhibitors and mimics were transfected into HepG2 cells. The expression of miR-221 was detected by real time quantitative RT-PCR. CellTiter-blue cell viability kit, Hoechst 33342/propidium iodide (PI) double staining assay, flow cytometry and Apo-ONE homogeneous caspase-3/7 kit were used to measure cell viability and apoptosis. MiR-221 inhibitors significantly inhibited the cell growth and miR-221 mimics increased cell viability 48 hours post-transfection measured by both CellTiter-blue cell viability kit and Hoechst 33342/PI assay (P is less than to 0.05). There was a positive correlation between these two assays (r = 0.993, P is less than to 0.01). With miR-221 mimics, the number of G1 stage cells (47.67%+/-1.53%) was significantly reduced as compared to the blank control (59.00%+/-1.00%) and the negative control (58.00%+/-1.00%, F = 81.77, P is less than to 0.01), and it was significantly raised in S stage (20.33%+/-1.15%) than in blank control (11.00%+/-1.00%) and negative control (12.00%+/-1.00%, F = 70.9, P is less than to 0.01) with flow cytometry analysis. More cell apoptosis and necrosis were significantly induced by miR-221 inhibitors 48 hours post-transfection detected by both Hoechst 33342/PI assay and flow cytometry PE Annexin V kit (P is less than to 0.05). The result from Apo-ONE homogeneous caspase-3/7 kit was consistent with the above two apoptotic assays, which showed that with miR-221 inhibitors, the activity of caspase-3/7 was significantly enhanced (P is less than to 0.05). MiR-221 contributes to the growth of hepatocellular carcinoma cells and miR-221 inhibition can induce cell apoptosis. miR-221 has the potential to become one of the new molecular targets for liver cancer therapy.
Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; Cell Proliferation ; drug effects ; Hep G2 Cells ; Humans ; Liver Neoplasms ; MicroRNAs ; metabolism

Objective To assess mucin gene expression in Barrett's esophagus.Methods Mucin core protein-MUC1,MUC2,MUC3,MUCSAC and MUC6 were detected by immunohistochemistry.The re- lationship between mucin expression and magnification-endoscopic characteristics,pathohistologic epithelial types of Barrett's esophagus was analyzed.Results Mild expression of MUC1 was predominantly found in the superficial epithelium of both gastric and specialised intestinal metaplasia.In a small number of specimens, mild expression of MUC1 was also noted in glands.Strong MUC2 expression was noted only in the goblet cells in Barrett's oesophagus.MUC3 was expressed in the superficial columnar cells of specialized intestinal metaplasia with or without globlet cells but not in gastric metaplasia of the oesophagus.In some specimens MUC3 was expressed in the vacuolus of the globlet cells and the lumen of gland.Strong staining of MUCSAC was noted in the columnar epithelium of both gastric metaplasia and specialized intestinal metaplasia in Barrett's oesophagus,as well as expressed in the cytoplasm and vacuolus of the globlet cells in some speci- mens.Expression of MUC6 protein was detected at the basement of the crypts in gastric metaplasia and spe- cialised Barrett's glands.Expression of MUC2 and MUC3 protein was found much higher in villous or irregu- lar pit pattern than that in dot or rod pit pattern(P

OBJECTIVETo explore the relationship between methylenetetrahydrofolate reductase (MTHFR) gene polymorphism and microsatellite instability (MSI) in patients with gastric cancer.

METHODSMTHFR gene C677T and A1298C polymorphism were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and MSI was examined with PCR.

RESULTSMTHFR gene C677T and A1298C polymorphisms were analyzed on 122 gastric cancers and 110 normal controls The genotype frequencies of MTHFR 677CC, 677CT and 677TT were 47.5%, 39.3% and 13.1% on patients with gastric cancer, and 48.5%, 42.6%, 8.9% in the controls respectively. There was no significant difference of genotype frequency between the two groups (P > 0.05). The individuals with 677CT genotype, 677TT genotype and 677CT + TT genotype exhibited significantly reduced risk (OR = 0.38,95% CI: 0.15-0.98; OR = 0.26,95% CI: 0.03-2.18 and OR = 0.36,95% CI: 0.07-0.98) of developing gastric cardia cancer compared with those harboring the wild-type(677CC). The individuals with 677TT genotype having a 3.03-fold (95% CI: 1.07-8.65) increased risk of developing gastric corpus cancer. The genotype frequency of MTHFR 1298AA, 1298AC and 1298CC were 59.8%, 36.1% and 4.1% in gastric cancer patients, and 57.4%, 7.6%, 5.0% in the controls, respectively. The distribution of MTHFR A1298C genotype was not significantly different between gastric cancer and controls (P > 0.05). The individuals with 1298CC genotype had a reduced risk of developing gastric antrum cancer (OR = 0.41- fold, 95% CI: 0.03-2.18, 0.05-3.72) when comparing with those having 1298AA genotype. Patients with MSI+ gastric cancer had an increased frequency of the MTHFR 677TT genotype when comparing with those suffering from MSI- gastric cancer (P = 0.009) and with controlled subjects (P = 0.008). There was no significant association found between MTHFR A1298C polymorphism and MSI (P>0.05).

CONCLUSIONPolymorphism of MTHFR C677T was associated with increased risk on gastric corpus cancer and reduced risk on gastric cardia cancer. The polymorphism of MTHFR A1298C was associated with reduced risk for gastric antrum cancer while MSI pathway was possibly involved in the development of gastric cancer with MTHFR 677TT genotype.

Adult ; Aged ; Aged, 80 and over ; Case-Control Studies ; Female ; Gene Frequency ; Genotype ; Humans ; Male ; Methylenetetrahydrofolate Reductase (NADPH2) ; genetics ; Microsatellite Instability ; Middle Aged ; Polymorphism, Genetic ; Stomach Neoplasms ; genetics

OBJECTIVETo observe the leg length discrepancy and accompanied knee varus/valgus deformity in matured patients with unilateral dislocation of the hip.

METHODSFrom March 2011 to December 2012, 28 patients who had unilateral dislocation of hip (Hartofilakidis classification II 17 cases and III 11 cases) were involved in this study.There were 6 male patients and 22 female patients, the age of the patients were 13.4-66.2 years, with mean age of 29.8 years. The standing anteroposterior full leg length X-ray films were obtained. Leg length discrepancy, the length of the femur, the length of the tibia and identified the varus/valgus knee deformities were measured. Statistical analysis was performed. A student's t test for paired samples was done for comparison of the parameters in the same patient between dislocated and undislocated leg, and the χ(2) test were used to assess valgus and varus knees, leg length discrepancy in high dislocation and low dislocation groups.

RESULTSSeventeen (60.7%) cases had longer femur length on the dislocated side than that on the undislocated side (t = 1.328, P = 0.197), with the maximum lengthening of 32.7 mm and a mean lengthening of 9.5 mm. Twenty-one (75.0%) cases had longer tibia length on the dislocated side (t = 3.039, P = 0.006), with a maximum lengthening of 10.9 mm and a mean lengthening of 4.5 mm. Twenty (71.4%) cases had longer relative leg length on the dislocated side (t = 2.451, P = 0.022), with a maximum lengthening of 25.0 mm and a mean lengthening of 9.4 mm. On the dislocated side of the leg, the degree of valgus angle was 3° ± 4°,while on the undislocated side, that was -3° ± 4°(t = 5.642, P = 0.000). On the dislocated side, 12 cases (42.9%) were of valgus deformities and 1 case was of varus deformity. On the contralateral side, 15 cases of varus deformities (53.6%) and 1 case of valgus deformity were observed(χ(2) = 18.139,P = 0.000).

CONCLUSIONSMost dislocated legs are longer in length than the contralateral side, both femur and tibia have also lengthened accordingly. Many knees on the dislocated side present valgus deformity, half of the knees on the contralateral side present varus deformity.

Adolescent ; Adult ; Aged ; Female ; Femur ; abnormalities ; diagnostic imaging ; Hip Dislocation, Congenital ; complications ; radiotherapy ; Humans ; Knee Joint ; abnormalities ; diagnostic imaging ; Leg Length Inequality ; diagnostic imaging ; etiology ; Male ; Middle Aged ; Radiography ; Tibia ; abnormalities ; diagnostic imaging ; Young Adult

OBJECTIVETo evaluate the relationship between mitochondrial DNA instability (mtMSI) and interleukin-8 (IL-8) activity in gastric mucosa of various lesions.

METHODSIL-8 level in gastric mucosa was assayed using ELISA method. The mtMSI was detected by PCR-SSCP techniques.

RESULTSmtMSI was observed in 11 out of 30 (36.7%) gastric cancers, 2 of 15 (13.3%) intestinal metaplasia, 2 of 10 dysplasia and 1 of 10 chronic atrophic gastritis. IL-8 level in mtMSI+ group [(76.8 +/- 3.8) pg/mg] was significantly higher than that in mtMSI- group [(48.3 +/- 3.6) pg/mg, P < 0.05].

CONCLUSIONmtMSI closely correlates with IL-8 level in gastric mucosa and is involved in gastric carcinogenesis.

DNA, Mitochondrial ; genetics ; Enzyme-Linked Immunosorbent Assay ; Gastric Mucosa ; metabolism ; pathology ; Gastritis, Atrophic ; genetics ; metabolism ; Genomic Instability ; Humans ; Interleukin-8 ; metabolism ; Metaplasia ; genetics ; metabolism ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Precancerous Conditions ; genetics ; metabolism ; Stomach Neoplasms ; genetics ; metabolism

AIMTo explore whether the anti-tumor action of 17beta-estradiol is enhanced by re-expression of the homeodomain transcription factor Nkx3.1 in PC3 human prostate cancer cells.

METHODSPC3 cells were stably transfected with pcDNA3.1-Nkx3.1-His vector, which carries a full-length cDNA of human Nkx3.1. The PC3 cells stably transfected with vector pcDNA3.1 were set as a control. The expression of Nkx3.1 protein in the cells was confirmed by Western blot analysis. The effect of Nkx3.1 on cell proliferation of PC3 cells was examined with MTT assay. The antiproliferative and apoptotic effects of 17beta-estradiol alone or in combination with Nkx3.1 were estimated on PC3 cells by using MTT growth tests and flow cytometric analyses. The expression of apoptosis-related proteins was analyzed using Western blotting.

RESULTSThe plasmid carrying Nkx3.1 gene induced high expression of Nkx3.1 protein in PC3 cells. The re-expression of exogenous Nkx3.1 did not cause a significant reduction in cellular proliferation, whereas the expression of Nkx3.1 enhanced the 17beta-estradiol anti-proliferative effect in PC3 cells. Nkx3.1 expression promoted 17beta-estradiol-induced apoptosis of PC3 cells, as shown by analysis of Bcl-2, Bax, Caspase-3 and poly (ADP-ribose) polymerase expression.

CONCLUSIONThe present study demonstrates that re-expression of Nkx3.1 enhances 17beta-estradiol anti-tumor action in PC3 human prostate cancer cells. The in vitro study suggests that re-expression of Nkx3.1 is worthy of further consideration as an adjuvant treatment of androgen independent prostate cancer with estrogen anti-tumor therapies.

Adenocarcinoma ; drug therapy ; genetics ; pathology ; Androgen-Insensitivity Syndrome ; drug therapy ; genetics ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Drug Screening Assays, Antitumor ; Estradiol ; pharmacology ; Flow Cytometry ; Gene Expression Regulation, Neoplastic ; drug effects ; genetics ; Homeodomain Proteins ; genetics ; metabolism ; Humans ; Male ; Prostatic Neoplasms ; drug therapy ; genetics ; pathology ; Transcription Factors ; genetics ; metabolism ; Transfection