ObjectiveTo study the expression of matrilysin in gastric cancer and to evaluate the correlation between its expression and invasion, metastasis, and prognosis. MethodsA total of 52 patients with gastric cancer were selected and followed up. The expressions of matrilysin in gastric primary focus, normal gastric mucosa, and metastatic lymph nodes were examined by reverse transcriptionpolymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry, respectively. The correlations between matrilysin expression and tumor invasion, metastasis, and prognosis were assessed. ResultsThe expressions of matrilysin in gastric primary focus and metastatic lymph nodes significantly increased, while decreased or loss in normal gastric mucosa (Plt;0.001). The higher concordance was seen between the levels of mRNA and protein (Plt;0.001). Among patients with infiltrating type, penetrated serosa, area of serosa involved more than 20 cm2, and metastatic lymph nodes more than 7, the expression of matrilysin was significantly higher (Plt;0.01). The survival rate of patients with matrilysin higher expression (34.1%) was significantly lower than that with matrilysin lower expression (55.6%), χ2=9.778， P=0.002. Conclusions Up-regulated expression of matrilysin plays an important role in tumor invasion, metastasis, and poor prognosis, and it is a good molecular marker to reflect the biological behaviors of gastric cancer.
Objective To explore the effect of minimally invasive and mini-incision surgery (MIS) in total hip arthroplasty (THA) on late osteonecrosis of femoral head (ONFH). Methods From March 2003, Eighteen patients (22 hips) with ONFH underwent MIS in THA. Their ages ranged from 24to 57 years, including 13 males and 5 females. The mean body mass index ranged from 17.1 to 30.1(24.6 on average). The Harris hip score was 46 points before operation. Modified posterior-lateral approach was adopted, and the MIS THA was performed by cementless prosthesis. As a comparison, 18 patients (22 hips) were performed by conventional THA at the same period. The data, including bleeding volume during operation, incision length, operative time, and postoperative function recovery, were compared. Results Follow-ups were done for 6 to 20 months (11 months on average). Dislocation occurred in one patient that underwent conventional THA 2 days after operation. No complication occurred in MIS THA group. The incision lengths ranged from 8.7 to 10.5 cm (9.3 cm on average) in MIS THA group, being statistically different (Plt;0.01). There was no significant difference in Harris scoring of the function between the two groups both before the operation and after the operation (Pgt;0.05). The operative time was almost the same, but the bleeding volume in MIS THA group was less (Plt;0.05). The function recovery was faster in MIS THA group.Conclusion The MIS THA is an alternative to the treatment of late ONFH. The advantages of MIS THA are fewer trauma, less bleeding volume, and faster recovery. The MIS THA should be performed by surgeons with rich experiences in THA and hospitals with necessary instruments.
ObjectiveTo investigate the influence of heat shock protein A2 (HSPA2) on the biological behavior of pancreatic adenocarcinoma cells and its mechanism. MethodsThe expressions of HSPA2 were determined in the human pancreatic adenocarcinoma cell lines (PANC-1, BxPC-3, and AsPC-1) using the Western blot. Subsequently, the cells with the lowest and highest HSPA2 expressions among these three lines were selected for conducting overexpression and knockdown experiments targeting HSPA2, respectively. The cellular proliferation, cell clonogenesis, migration, and invasion capabilities were assessed using MTT, clonogenic assay, and Transwell assay, respectively. Additionally, the impact of HSPA2 on the expression of key markers of epithelial-mesenchymal transition (EMT) was examined using the Western blot. The potential target molecules of HSPA2 were identified through immunoprecipitation assay and mass spectrometry. The rescue experiments further explored the regulatory relation between the HSPA2 and its target molecules. The influence of HSPA2 on pancreatic adenocarcinoma growth was investigated through establishment of xenograft tumor model in nude mice. ResultsThe HSPA2 exhibited the lowest expression in the PANC-1 cells and the highest expression in the AsPC-1 cells among the three cell lines. Subsequent functional studies demonstrated that the overexpression of HSPA2 in the PANC-1 cells markedly promoted proliferation, cell clonogenesis, migration, and invasion, while the knockdown of HSPA2 expression in the AsPC-1 cells markedly inhibited these processes. The Western blot analysis further showed that the HSPA2 overexpression downregulated E-cadherin expression and upregulated N-cadherin and Vimentin expressiones, whereas the HSPA2 knockdown produced opposite effects. The rescue experiments indicated that the HSPA2 promoted the EMT in pancreatic adenocarcinoma cells by upregulating Yes associated protein (YAP). The subcutaneous xenograft tumor experiments in the nude mice showed that the HSPA2 knockdown inhibited tumor growth. ConclusionThe results of this study suggest that HSPA2 promotes EMT via upregulating YAP, which facilitates proliferation, migration, and invasion of pancreatic adenocarcinoma cells.
ObjectiveTo investigate the effects of overexpression of alpha/beta hydrolase domain-containing protein 5 (ABHD5) on the invasion and migration of human colon cancer cell line HCT116 and the pathway of adenosine monophosphate-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR).MethodsThe expression of ABHD5 in colon cancer tissues and its relationship with clinicopathological features was analyzed by UALCAN database. HCT116 cells were cultured in vitro and transfected with ABHD5 recombinant plasmid, then they were divided into control group, negative transfection group and ABHD5 transfection group. Real time quantitative PCR (qRT-PCR) was used to detect the expression of ABHD5 mRNA in HCT116 cells. The proliferation of HCT116 cells was detected by CCK-8 method. Transwell assay was used to detect the invasion and migration of HCT116 cells. The expression of matrix metalloprotein 9 (MMP-9), E-cadherin, Snail, and AMPK/mTOR pathway proteins p-AMPK, AMPK, p-mTOR and mTOR were detected by Western blot.ResultsThe results of the UALCAN showed that compared with normal colon tissues, the expression of ABHD5 mRNA in colon cancer tissues was decreased (P<0.05), and which in the adenocarcinoma and the N1 stage was lower than that of the mucinous adenocarcinoma (P<0.05) and N0 stage (P<0.05), respectively. Compared with the control group and the negative transfection group, the expression of ABHD5 mRNA in the ABHD5 transfection group was increased (P<0.05), the proliferation inhibition rate of HCT116 cells in the ABHD5 transfection group was increased (P<0.05), the numbers of migration and invasion cells in the ABHD5 transfection group were decreased (P<0.05), the expressions of MMP-9, Snail, p-mTOR and mTOR were reduced, and the expressions of E-cadherin, p-AMPK and AMPK were increased (P<0.05).ConclusionsThe overexpression of ABHD5 can inhibit the invasion and migration of colon cancer HCT116 cells, activate AMPK, and inhibit the expression of mTOR. It suggests that ABHD5 may play a role in inhibiting colon cancer by affecting AMPK/mTOR pathway.
Objectives To explore the effects of curcumin and cisplatin on A549 lung cancer cell invasion and metastasis, and explore the influence of the two drugs on matrix metalloproteinase 9 (MMP-9) and E-cadherin protein. Methods MTT assay was performed to detect the effects of curcumin, cisplatin alone and the combination on A549 lung cancer cell proliferation. Transwell assay was performed to detect the effects of curcumin, cisplatin alone and the combination on the invasion and metastasis of lung cancer cells. Western blot was used to detect the protein expression of MMP-9 and E-cadherin. Results The proliferation inhibition of A549 lung cancer cell rate in 5, 10, 20, 40 μmol/L of curcumin was 6.50%±1.06%, 11.70%±0.88%, 22.97%±0.82%, 27.93%±0.94%, respectively. Compared with control group, the proliferation inhibition rates in four different curcumin groups were significantly increased (all P<0.01). The differences in the proliferation inhibition rates among four different curcumin groups were statistically significant (allP<0.05). The proliferation inhibition rates of A549 lung cancer cell in 1, 2, 4 mg/L of cisplatin were 7.12%±0.86%, 20.07%±1.14%, 26.88%±0.51%, respectively. Compared with control group, the proliferation inhibition rates in three different cisplatin groups were significantly increased (allP<0.01). The differences in the proliferation inhibition rates among three different cisplatin groups were statistically significant (allP<0.01). The proliferation inhibition rates of A549 lung cancer cell in curcumin (20 μmol/L) combined with cisplatin (1, 2, 4 mg/L respectively) were 28.37%±0.57%, 39.72%±0.64%, 46.27%±0.86%, respectively. Compared with control group and curcumin or cisplatin used alone, the proliferation inhibition rates of three combined groups were significantly increased (allP<0.01). The invasion inhibition rates of A549 lung cancer cell in curcumin group (20 μmol/L), cisplatin group (2 mg/L) and combined group (curcumin 20 μmol/L plus cisplatin 2 mg/L) were 38.62%±0.23%, 36.52%±0.33%, 63.78%±0.59%, respectively. Compared with control group and curcumin or cisplatin used alone, the invasion inhibition rates of combined group were significantly increased (allP<0.01). The protein grey values for curcumin group (20 μmol/L), cisplatin group (2 mg/L) and combined group (curcumin 20 μmol/L plus cisplatin 2 mg/L) were 0.768±0.047, 0.654±0.104, 0.684±0.008, 0.444±0.104 (MMP-9) and 0.603±0.170, 0.792±0.050, 0.784±0.045, 0.879±0.110 (E-cadherin), respectively. Compared with control group and curcumin or cisplatin used alone, the protein grey values of combined group were significantly different (allP<0.01 orP<0.05). Conclusions Curcumin and cisplatin combination can inhibit the invasion and metastasis of lung cancer A549 cells. Its mechanism may be related to downregulating MMP-9 and upregulating E-cadherin.
Objective To examine the effects of newly designed LY52 on the expression of matrix metalloproteinases and invasive ability of hepatocellular carcinoma HepG2 cells. Methods The effects of LY52 on the proliferations of HepG2 cells were detected by MTT assay. Gelatin zymography and Western blot were used to detect the effects of LY52 on matrix metalloproteinase-2 expression in the cell line. Transwell chamber assay was used to detect the effects of LY52 on the invasion of the cells. Results No obvious inhibitory or cytotoxicity effects of LY52 was found in lower concentrations (lt;200 μg/ml) of LY52. Gelatin zymography and Western blot showed that matrix metalloproteinase-2 expression were inhibited by LY52 in a dose-dependent manner in HepG2 cells. Furthermore, transwell chamber assay showed that LY52 could significantly inhibit the invasion of the cell line in a dose-dependent manner.Conclusion The results suggest that LY52 may inhibit the invasion of hepatocellular carcinoma cells by suppressing the matrix metalloproteinase-2 activity.
目的 观察鼻内镜下三种不同微创手术治疗非侵袭型真菌性上颌窦炎的疗效及氟康唑冲洗术腔的临床意义。 方法 回顾性分析我科2006年1月－2010年12月收治的284例非侵袭型真菌性上颌窦炎住院患者资料。患者分别采用单纯鼻内镜下上颌窦窦口开放术（术式1）、鼻内镜下上颌窦窦口开放联合经唇龈沟上颌窦前壁开窗（术式2）、以及鼻内镜下上颌窦窦口开放联合下鼻道开窗（术式3）进行治疗；术式3治疗的患者术后定期换药时，分别使用生理盐水或氟康唑反复冲洗鼻腔和上颌窦。所有患者门诊随访至少半年。 结果 在本组接受术式1、术式2和术式3治疗的患者分别有51例、45例和188例。上述三种术式治疗的患者中，分别有15例，9例和6例患者出现复发，复发率分别为29.6%、20.0%和3.2%；其中术式3治疗的患者复发率显著性低于术式1或术式2治疗的患者（P＜0.05）。在术式3治疗的患者中，生理盐水和氟康唑冲洗的伤口愈合时间分别为3.8周和 3.7周，两种冲洗方式对伤口的愈合影响差异无统计学意义（P＞0.05）。 结论 鼻内镜下上颌窦窦口开放联合下鼻道开窗是治疗非侵袭型霉菌性上颌窦炎的最佳方式，且伤口愈合时间与冲洗液种类无关。
【Abstract】Objective To investigate the correlation of adhesive molecule expressions with potential of invasion and metastasis in papillary thyroid carcinoma (PTC). Methods S-P immunohistochemical method was used to detect CD44v6 and E-cadherin expression in 58 cases of PTC. Results The positive rates of CD44v6 and E-cadherin in PTC were 72.40%and 41.4% respectively. There was a positive correlation between CD44v6 expression and tumor invasive and metastatic potential in PTC (P＜0.05), and a reverse correlation between E-cadherin expression and the potential (P＜0.01).Moreover,there was a reverse correlation between the CD44v6 and E-cadherin expression in PTC(P＜0.05). Conclusion These data show a correlation between the adhesive molecule expression and the potential of invasion and metastasis in PTC. CD44v6 and E-cadherin may be prognostic indicators in PTC.
ObjectiveTo investigate the effect of eukaryotic initiation factor 6 (eIF6) expression on invasion and metastasis of colorectal cancer cells and Wnt/β-catenin signaling pathway.MethodsImmunohistochemistry was used to detect the expressions of eIF6 protein in colorectal cancer tissues and paracancerous tissue. Sw837 cell lines with overexpression/knockdown eIF6 were constructed by transfection and divided into control group, empty plasmid group, overexpression group and knockdown group respectively. Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) and Western blotting (WB) were used to verify the overexpression/knockdown of eIF6 in sw837 cells. WB was used to detect the expressions of β-catenin, glycogen synthase kinase-3β (GSK-3β), anaphase promoting complex (APC), zinc finger transcription factor SNAI (Snail), E-cadherin and Vimentin. Transwell invasion test, Scratch test and subcutaneous tumorigenesis test were used to detect the migration ability, invasion ability and tumorigenesis ability in vivo of cells. The pathological changes of the transplanted tumor were observed by HE staining.ResultsThe positive expression rate of eIF6 protein in cancer tissues was significantly higher than that in adjacent tissues (P<0.05). Compared with those in the control group, the protein expression levels of β-catenin, Snail and Vimentin in the overexpression group were higher, the protein levels of GSK-3β, APC and E-cadherin were lower, the ability of cell migration and invasion, and tumorigenicity in vivo were enhanced, the difference were statistically significant (P<0.05). The protein expression levels of β-catenin, Snail and Vimentin were lower in knockdown group, the protein levels of GSK-3β, APC and E-cadherin were higher, the ability of cell migration and invasion, and tumorigenicity in vivo were reduced, the difference were statistically significant (P<0.05).ConclusioneIF6 may promote the invasion and metastasis of colorectal cancer cells by activating Wnt/β-catenin signaling pathway.
Objective To comprehend the concept， pathology， molecular mechanisms， diagnosis， and treatmentof aggressive fibromatosis （AF）， and to find a novel way to cure aggressive fibromatosis. Method The literatures about the definition， molecular mechanisms， and clinical research of AF were reviewed and analized. Results AF is rare and benign fibromatous lesion that is the result of abnormal proliferation of myofibroblasts. The pathologic features of AF isa benign disease， but it has “malignant” biological behavior. The tumor often involved the surrounding organs and bloodvessels， and caused death of patients. For patients with clinical symptoms or complications， complete excision of thetumor is the treatment of choice. Even if the operation to ensure the negative margin also has a higher recurrence rate， soits treatment requires multidisciplinary treatment. Conclusions The mechanism of AF is very complex， and it’s mecha-nism is still unclear. Clinical management of patients with AF is difficult and controversial， at present， the most effective treatment for AF is operation resection. The effects of adjuvant radiotherapy， chemotherapy， and other treatment after operation for AF still need further study.