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OBJECTIVE@#To investigate the effect of Porphyromonas gingivalis (Pg) infection on IFNGR1 palmitoylation and biological behaviors of esophageal squamous cell carcinoma (ESCC) cells and the clinical implications.@*METHODS@#The expression levels of IFNGR1 protein in ESCC cell lines KYSE30 and KYSE70 were detected using Western blotting at 24 and 48 h after Pg infection, and 2-BP was used to detect IFNGR1 palmitoylation in the cells. KYSE70 cells with wild-type IFNGR1 (IFNGR1-WT cells) and with IFNGR1-C122A palmitoylation site mutation induced by site-specific mutagenesis (IFNGR1-C122A cells) were both infected with Pg, and the changes in palmitoylation of IFNGR1-C122A were analyzed using immunofluorescence and Click-iT assays. The changes in proliferation, migration and invasion ability of the infected cells were evaluated using plate cloning assay, scratch assay and Transwell assay, and IFNGR1 co-localization with lysosomal marker LAMP2 was dected using immunofluorescence assay. Immunohistochemistry was used to detect Pg infection and IFNGR1 protein expression in 50 ESCC tissues, and their correlation with the clinicopathological characteristics and survival outcomes of the patients was analyzed.@*RESULTS@#Pg infection down-regulated the protein expression of IFNGR1 in ESCC and promoted IFNGR1 palmitoylation at site 122. In IFNGR1-WT cells, Pg infection significantly enhanced cell proliferation, migration and invasion (P < 0.05). Similarly, Pg also significantly promoted proliferation, migration and invasion of IFNGR1-C122A cells, but to a lesser extent as compared with the wild-type cells (P < 0.05). Immunofluorescence assay showed that Pg and ZDHHC3 promoted IFNGR1 degradation within the lysosome. Immunohistochemical studies of the ESCC tissue samples showed a negative correlation between IFNGR1 and Pg expression, and a reduced IFNGR1 expression was correlated with a poorer survival outcome of the patient.@*CONCLUSION@#Pg infection enhances IFNGR1 palmitoylation to promote progression of ESCC, and elimination of Pg and inhibiting IFNGR1 palmitoylation may effectively control ESCC progression.
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Humanos , Neoplasias Esofágicas , Porphyromonas gingivalis , Lipoilación , Carcinoma de Células Escamosas de Esófago , LisosomasRESUMEN
Objective:To explore the effects of human-derived fibrin glue on prevention of postoperative complications of endoscopic submucosal dissection (ESD) in early esophageal squamous cancer and precancerous lesions.Methods:A total of 210 patients with early esophageal squamous cancer or precancerous lesions who underwent ESD at Department of Gastroenterology, Zhongda Hospital Affiliated to Southeast University from April 2017 to April 2020 were included in this retrospective study. Seventy-three cases (79 esophageal lesions) where human-derived fibrin glue was used before retrieving endoscope were included in the observation group, while 137 cases (156 esophageal lesions) where fibrin glue was not used were included in the control group. The postoperative complications and pain were compared between the two groups.Results:Clinical data including general information, longitudinal length, Paris type, pathological type, invasion depth, circumferential range, area of resection, duration of operation and local steroid used were similar between the two groups ( P>0.05). The incidences of perforation, delayed bleeding and esophageal stenosis in the observation group were 2.7% (2/73), 1.4% (1/73), and 16.4% (12/73), respectively, and were 2.9% (4/137), 1.5% (2/137), and 13.1% (18/137), respectively in the control group. There were no significant differences between the two groups ( P>0.05). The incidence of postoperative pain in the observation group was 53.4% (39/73), which was significantly lower than that in the control group of 70.8% (97/137) ( χ2=6.302, P=0.012). The incidences of mild, moderate and severe pain in observation group on the day of ESD were 9.6% (7/73), 6.8% (5/73) and 5.5% (4/73), respectively, and 27.0% (37/137, χ2=8.724, P=0.003), 17.5% (24/137, χ2=4.554, P=0.033) and 0.7% (1/137, χ2=2.805, P=0.094), respectively in the control group. The incidences of mild, moderate and severe pain in the observation group on the first day after the operation were 26.0% (19/73), 5.5% (4/73) and 6.8% (5/73), respectively, and 29.2% (40/137, χ2=0.237, P=0.626), 14.6% (20/137, χ2=3.912, P=0.048) and 4.4% (6/137, χ2=0.193, P=0.660), respectively in the control group. The corresponding incidences on the second day after the operation were 5.5% (4/73), 0 and 1.4% (1/73) in the observation group and 19.0% (26/137, χ2=7.087, P=0.008), 2.9% (4/137) and 0 in the control group, respectively. Conclusion:Human-derived fibrin glue shows no obvious preventive effect on post-ESD bleeding, perforation or stenosis in early esophageal cancer and precancerous lesions. However, it can significantly reduce the incidence of ESD-related postoperative pain, especially the incidences of mild and moderate pain.
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Objective: Our study aims to investigate the radiation associated H3 modification in regulating OIP5-AS1 to lay foundation for developing therapeutic targets on reversing radiation resistance of esophageal squamous carcinoma. Methods: We recruited 137 ESCC patients from The First Affiliated Hospital of Xi'an Medical College. qRT-PCR and Western blotting were used for detecting the expressions of target genes. Wound healing assay and CCK8 assay were used to detect the migration and proliferation abilities. ChIP assay was used to detect the interaction between OIP5-AS1 and H3K27ac. Results: OIP5-AS1 was highly expressed in ESCC radiation resistant patients and promoted the migration and proliferation abilities of ESCC radiation resistant cells. H3K27ac was activated in ESCC radiation resistant cells and was enriched in the promoter region of OIP5-AS1. CBP was upregulated in ESCC radiation resistant cells; its inhibitor, C646, could suppress the enrichment of H3K27ac in the promoter region of OIP5-AS1. Results: OIP5-AS1 regulated radioresistance in ESCC. CBP promoted the interaction between H3K27ac and OIP5-AS1, thereby activating the expression of OIP5-AS1 and resulting in radioresistance.
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@#Objective To investigate the risk factors for lymph node metastasis (LNM) and prognosis of T1-stage esophageal squamous carcinoma (ESC). Methods Clinical data of 387 patients with T1-stage ESC who underwent surgical treatment in our hospital from March 2013 to March 2018 were collected. There were 281 males and 106 females aged 60 (41-80) years. The patients were divided into a lymph node metastasis group (n=77) and a non-metastasis group (n=310). The risk factors for LNM and prognosis were analyzed. Results Among 387 patients with T1-stage ESC, 77 (19.9%) patients had LNM. The incidence of LNM was 8.4% (8/95) in T1a-stage patients and 23.6% (69/292) in T1b-stage patients. Univariate analysis showed that tumor size, differentiation degree, depth of invasion and vascular tumor thrombus were associated with LNM (P<0.05). Multivariate logistic regression analysis showed that invasion depth of tumor [OR=2.456, 95%CI (1.104, 5.463), P<0.05] and vascular tumor thrombus [OR=15.766, 95%CI (4.880, 50.938), P<0.05] were independent risk factors for LNM. The follow-up time was 41 (12, 66) months. The 1-year, 3-year and 5-year survival rates were 98.71%, 89.67% and 86.82%, respectively. Univariate analysis showed statistically significant differences in tumor invasion depth, vascular tumor thrombus and LNM between the survival group and the death group. Cox analysis showed that LNM [OR=3.794, 95%CI (2.109, 6.824), P<0.05] was an independent risk factor for prognosis. Conclusion T1-stage ESC patients with deeper invasion or vascular tumor thrombus have a higher risk of LNM. The prognosis of T1-stage ESC with LNM is relatively poor.
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Objective To investigate the effect of histone deacetylase inhibitor trichostatin A (TSA) on the migration of human esophageal squamous carcinoma cells(ESCC) and the possible mechanism. Methods KYSE-150 cells and EC9706 cells were cultured and Transwell assay was performed to detect the role of TSA alone and combined with protein kinase C (PKC) inhibitor AEB071 on cell migration; the images of morphology after cells treatment with TSA or combination of AEB071 with TSA; Western blotting was conducted to examine the protein level of epithelial-mesenchymal transition (EMT) related signaling molecules. Results TSA promoted the migration of ESCC cells significantly, and PKC inhibitor AEB071 partly inhibited the effect of TSA-promoted ESCC cells migration. Treatment with TSA resulted in the cell morphology transitioned from epithelia oval-like to mesenchymal spindle-like, indicating the EMT. AEB071 partially rescued ESCC cells morphological changes which TSA induced. Western blotting showed that TSA reduced the expression of E-cadherin and augmented the expression of vimentin, β-catenin, Slug and acH3, whereas AEB071 obviously blocked the EMT-related protein level changes which induced by TSA. Conclusion TSA promotes ESCC cells migration via inducing EMT process and the mechanism may be mediated by PKC signaling pathway.
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Objective Vascular endothelial growth factor C (VEGFC) and cortactin (CTTN) have been found to be closely related to the growth of esophageal squamous cell carcinoma (ESCC), but their specific relationship has not been clearly defined up to the present time. This study aimed to investigate the effects of VEGFC and CTTN on the proliferation and apoptosis of ESCC cells. Methods Human ESCC TE1 cells were treated with normal culture medium (the blank control group), MATE transfection reagent ( the MATE group), negative control RNA and MATE reagent (the negative control group), positive control RNA and MATE reagent (the positive control group), VEGFC siRNA and MATE transfection reagent (the VEGFC siRNA group), and CTTN siRNA and MATE transfection reagent (the CTTN siRNA group). The proliferation of the ESCC TE1 cells in different groups was detected by CCK-8 assay and their apoptosis determined by flow cytometry. Results Compared with the blank control group, the ESCC cells of the VEGFC siRNA and CTTN siRNA groups showed significantly decreased expressions of VEGFC mRNA (1.00 ± 0.00 vs 0.13 ± 0.01, P < 0.05) and CTTN mRNA (1.00 ± 0.00 vs 0.29 ± 0.02, P < 0.05). The proliferation rate of the ESCC cells was remarkably lower in the VEGFC siRNA and CTTN siRNA than in the other groups (P < 0.05), and even lower in the VEGFC siRNA than in the CTTN siRNA group ([31.26 ± 5.25]% vs [46.99 ± 4.82]%, P < 0.05), but their apoptosis rate was markedly higher in the former than in the latter group ([48.41 ± 5.37]% vs [36.78 ± 4.29]%, P < 0.05). Conclusion Interfering with the expressions of VEGFC and CTTN can inhibit the proliferation and promote the apoptosis of ESCC cells, and VEGFC has an even better effect than CTTN.
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Objective To explore the effect of oridonin (ORI) on proliferation, apoptosis, cell cycle and migration of esophageal squamous carcinoma cell (ESCC) lines KYSE-150 and KYSE-450. Methods The effect of ORI on the proliferation and clony formation of esophageal cancer cells were detected by MTT and colony formation assays. Flow cytometry was performed to examine the impact of ORI on cell apoptosis and cell cycle. Transwell assay was applied to detect the role of ORI on cell migration. The effect of ORI on the expression of anti-apoptotic protein Bcl-2, cell cycle inhibitory protein p21Cip1/Waf1, epithelial-mesenchymal transition (EMT) related markers were examined by Western blotting. Results ORI had a significant inhibitory effect on the proliferation, migration and clone formation of KYSE-150 and KYSE-450 cells (P<0. 05) in a time and dose-dependent manner. With the increase of ORI concentration, apoptosis rate and the proportion of cells in G2/M phase increased significantly (P<0. 05), and the proportion of cells in G0/G1 phase decreased significantly (P < 0. 0 5). Bcl-2, vimentin and p-catenin were down-regulated and p21Cipl/Wafl, Ecadherin were up-regulated after treatment of ORI on ESCC cells for 48 hours. Conclusion ORI may inhibit ESCC cell proliferation and clony formation by inducing apoptosis and resting cells in G2/M phase, and suppress ESCC cell migration via inhibiting EMT process.
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BACKGROUND: Death domain-associated protein (DAXX), originally identified as a pro-apoptotic protein, is now understood to be either a pro-apoptotic or an anti-apoptotic factor with a chromatin remodeler, depending on the cell type and context. This study evaluated DAXX expression and its clinical implications in squamous cell carcinoma of the esophagus. METHODS: Paraffin-embedded tissues from 60 cases of esophageal squamous carcinoma were analyzed immunohistochemically. An immune reaction with more than 10% of tumor cells was interpreted as positive. Positive reactions were sorted into 2 groups: reactions in 11%–50% of tumor cells and reactions in more than 51% of tumor cells, and the correlations between expression and survival and clinical prognosticators were analyzed. RESULTS: Forty-three of the 60 cases (71.7%) showed strong nuclear DAXX expression, among which 19 cases showed a positive reaction (31.7%) in 11%–50% of tumor cells, and 24 cases (40.0%) showed a positive reaction in more than 51% of tumor cells. A negative reaction was found in 17 cases (28.3%). These patterns of immunostaining were significantly associated with the N stage (p=0.005) and American Joint Committee on Cancer stage (p=0.001), but overall survival showed no significant difference. There were no correlations of DAXX expression with age, gender, or T stage. However, in stage IIB (p=0.046) and stage IV (p=0.014) disease, DAXX expression was significantly correlated with survival. CONCLUSION: This investigation found upregulation of DAXX in esophageal cancer, with a 71.7% expression rate. DAXX immunostaining could be used in clinical practice to predict aggressive tumors with lymph node metastasis in advanced-stage disease, especially in stages IIB and IV.
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Carcinoma de Células Escamosas , Cromatina , Neoplasias Esofágicas , Esófago , Articulaciones , Ganglios Linfáticos , Metástasis de la Neoplasia , Regulación hacia ArribaRESUMEN
Objective To screen predictors for the prognosis of patients with inoperable locally advanced esophageal squamous carcinoma (LAESC) who are undergoing concurrent radiochemotherapy and establish a preliminary scoring system. Methods The data of 75 patients with inoperable LAESC who were undergoing intensity-modulated radiation therapy and concurrent chemotherapy were collected and analyzed to determine whether the prognosis was associated with medical history,vital signs,and the results of routine blood test and liver and kidney functions test before and at the end of radiochemotherapy. The prediction efficacy of the model was assessed using the receiver-operating characteristic curve. The degree of fitting was tested using the Hosmer-Lemeshow goodness-of-fit test. Results Seventy-five patients with LAESC were included. The univariate analysis indicated that the prognosis of the patients with LAESC who were undergoing concurrent radiochemotherapy was associated with weight loss of more than 5％,poor dietary habit,and significant decrease in white blood cell count (P = 0.047,0.074,and 0.074). The multivariate Cox model was conducted,and a scoring system for prediction of prognosis was established. The scores were 1.5 for weight loss of more than 5％,1.0 for poor dietary habit,and 1.0 for a significant decrease in white blood cell count (more than 2.0×109/L). A total score of more than 2.25 indicated a high mortality risk,with a sensitivity of 0.559 and a specificity of 0.805. Conclusion The simple and practical scoring system for prediction of prognosis of patients with LAESC in this study could generally predict the mortality risk of patients with inoperable LAESC who are undergoing concurrent radiochemotherapy.
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Objective To compare the efficacy and safety of two concurrent chemoradiotherapy regimens between paclitaxel plus fluorouracil( TF) and cisplatin plus fluorouracil ( PF) in the treatment of locally advanced esophageal squamous carcinoma. Methods 103 patients with locally advanced esophagus carcinoma were treated in Affiliated Hospital of Jiangnan University from December 2014 to February 2016, and randomly assigned to either study group ( TF ) or control group ( PF ) according to random number table, of which 52 patients in the TF group while 51 patients in the PF group. The primary outcome was overall survival(OS), and secondary outcomes include progression-free survival(PFS), local progression-free survival( LPFS) and side effects. Results The 1-year OS for TF group was 76. 9％ versus 74. 5％ for PF group( P>0. 05 ) , and the 2-year OS for TF group was 59. 6％ versus 56. 9％ for PF group ( P >0. 05). The 1-year LPFS for TF group and PF group were 71. 2％ and 66. 7％ respectively(P>0. 05), and the 2-year LPFS for TF group and PF group were 61. 5％ and 58. 8％ respectively(P>0. 05). The 1-year PFS for TF group was 63. 5％ versus 62. 7％ for PF group ( P>0. 05 ) , and the 2-year PFS for TF group was 51. 9％ versus 39. 2％ for PF group ( P>0. 05 ) . The incidence rate of serious ( grade 3- 4 ) leukopenia for TF group was 36. 5％ versus 17. 6％ for PF group(χ2 =4. 642, P<0. 05). The incidence rate of serious (grade 3-4) acute radiation pneumonitis was 15. 4％ in the TF group, higher than that in the PF group with the rate of 3. 9％(χ2 =3. 859, P<0. 05), while the incidence rate of severe nausea and vomiting for PF group was 17. 6％ versus 1. 9％ for TF group(χ2 =7. 262, P <0. 05). The difference between the two groups was statistically significant. Conclusions Patients who were treated with two concurrent chemoradiotherapy regimens showed no difference in OS, PFS and LPFS. The regimen on the basis of Paclitaxel has higher risk of adverse effects incidence rates of hematological toxicity and acute radiation pneumonitis, while digestive system toxicity must be concerned when concurrent chemoradiotherapy is performed on the basis of cisplatin plus fluorouracil.
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Plumbagin (Plumbago zeylanica L.) has a wide spectrum of anticancer activity with a relatively lower toxicity. The molecular mechanisms of proliferation inhibition and apoptosis induction by plumbagin on esophageal squamous carcinoma cell lines may be important for the structure modification and clinical application of plumbagin. After treatment of KYSE-30, KYSE-70 and KYSE-140 cells with 0-20 μmol·L-1 of plumbagin for 24, 48, 72 h, CCK8 was used to examine the proliferation, Annexin V and PI immunofluorescence staining for apoptosis, real-time PCR and Western blot for FoxM1 mRNA and protein expression, dual-luciferase reporter gene assay for the transcriptional activity of FoxM1, respectively. In addition, the relationship between anti- tumor effect of plumbagin and FoxM1 was investigated in vivo. Plumbagin significantly inhibited proliferation and induced apoptosis of esophageal squamous carcinoma cell in vitro and in vivo. Moreover, plumbagin down-regulated the expression of FoxM1 through suppression of its gene transcription. Our findings suggest that plumbagin may inhibit the proliferation of esophageal squamous carcinoma cell in vivo and in vitro through down-regulating the expression of FoxM1.
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Objective To explore the expression of eukaryocyte initiation factors-4E (eIF-4E) in normal esophageal epithelium and different esophageal lesions tissue and its relationship with vascular endothelial growth factor (VEGF).Methods Thirty normal esophageal incisal margin tissues,32 atypical hyperplasia tissues,20 carcinoma in situ tissues and 117 esophageal invasive carcinoma tissues were selected from the biopsy specimens of the Department of Pathology,the First Affiliated Hospital of Xinxiang Medical University from March 2014 to March 2016.The expression of eIF-4E and VEGF were detected by immunohistochemistry method and the correlation between them was analyzed.Results The positive expression rate of eIF-4E in normal esophageal epithelium,atypical hyperplasia,carcinoma in situ and invasive carcinoma tissues was 0.0％ (0/ 30),9.4％ (3/32),45.0％ (9/20) and 80.3％ (94/117) respectively.There was no statistic difference in the positive expression rate of eIF-4E in normal esophageal epithelium and atypical hyperplasia tissues (P ＞ 0.05);there was statistic difference in the positive expression rate of eIF-4E in the other esophageal tissues(P ＜ 0.05).In 117 invasive carcinoma tissues,the positive expression rate of eIF-4E in metastatic carcinoma tissues (93.2％,55/59) was significantly higher than that in the non metastatic carcinoma tissues (67.2％,39/58) (P ＜ 0.05).The positive expression rate of eIF-4E in esophageal carcinoma tissues which invaded into shallow muscle layer,deep muscular layer and adventitia was 70.0％ (28/40),73.8％ (31/42) and 100.0％ (35/ 35) respectively;there was no statistic difference in positive expression rate of eIF-4E in the carcinoma tissues which invaded into shallow muscle layer and deep muscular layer(P ＞ 0.05);the positive expression rate of eIF-4E in the carcinoma tissues which invaded into shallow muscle layer and deep muscular layer was significantly lower than that in the carcinoma tissues which invaded into adventitia(P ＜0.01).The expression of eIF-4E in the esophageal invasive carcinoma tissues was positive VEGF(x2 =51.460,P ＜ O.05).Conclusion eIF-4E play an important role in the canceration of normal esophageal and the invasion,metastasis of esophageal carcinoma.The expression of eIF-4E is correlate with VEGF in esophageal carcinoma tissues.
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Objective To study the expression and clinical significance of miR-183-5p, TβRⅠ and TβRⅡ in esophageal squamous cell carcinoma (ESCC). Methods The mRNA and protein expression of miR-183-5p, TβRⅠ and TβRⅡ were examined in ESCC cell lines ECA-109, TE-1, normal esophageal epithelial cells, tumor tissues and tumor-free tissues from 72 ESCC patients. Their clinical significance and the relationship between miR-183-5p and the latter two were analyzed. The effects of miR-183-5p on the expression of TβRⅠand TβRⅡ in ECA-109 cells and the cell functions of ECA-109 were also investigated. Results Compared with the normal esophageal epithelia cells, ESCC cell lines TE-1 and ECA-109 were statistically characterized by a high expression of miR-183-5p (all P<0.05) and low expression of TβRⅠand TβRⅡ(all P<0.05). The expression of miR-183-5p in ESCC tissues was higher than that in adjacent normal tissues, while the expressions of TβRⅠ and TβRⅡ were lower (all P< 0.05). The expression of miR-183-5p was closely related to sex, tumor differentiation, tumor staging, distant metastasis, lymphatic metastasis, and tumor location (all P<0.05). TβRⅠlevel was associated with sex, lymph node metastasis and tumor size (all P<0.05). Experimental data showed the negative correlation between the expression of miR-183-5p and TβRⅠin ESCC tissues (r= -0.521, P< 0.05). Over expression of miR-183-5p significantly inhibited the expression of TβRⅠ in ECA-109 cells (P< 0.05) and promoted the growth, invasion and metastasis of ECA-109 cells (P< 0.05). Low expression of miR-183-5p significantly promoted the expression of TβRⅠ in ECA-109 cells (P< 0.05), and suppressed the growth, invasion and metastasis of ECA-109 cells (P< 0.05). There was no significant change in the expression of TβRⅡ in the transfection experiments. Conclusion MiR-183-5p is closely related to the abnormal expression of TβRⅠ, which may exert an important role in the progression of lymphatic metastasis.
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Objective To investigate the role of autophagy in radiation-induced death process of human esophageal squamous carcinoma Eca-109 cells.Methods Esophageal carcinoma cell line Eca-109 was divided into 6 groups of control,5 mmol/L 3-Methyladenine treatment,10 mmol/L treatment,6 Gy irradiation,irradiation + 5 mmol/L drug,and irradiation + 10 mmol/L drug.Some cells were transferred with GFP-LC3 plasmid and the changes of autophagosome were obserred.After each treatment,the expression of autophagy marker LC3B was measured by Western Blot,cell viability was detected by MTT,morphological characteristics of apoptosis cells were stained with a fluorescein of Hoechst 33342 and the percentage of apoptotic cells and cell cycle distribution were measured by flow cytometry.Clonogenic survival were used to evaluate the cell radiosensitivity.Results Autophagy level was increased after radiation,and the LC3B Ⅱ expression and LC3B Ⅱ/LC3B Ⅰ ratio were significantly decreased by autophagy inhibitor 3-Methyladenine (F =25.64,P ＜ 0.05).The number of autophagosome fluorescent foci were significantly increased in the GFP-LC3 transfected cells after radiation,but reduced by 3-Methyladenine (F =127.36,P ＜ 0.05).Compared with radiation alone group,autophagy inhibition combined with radiation significantly decreased cell viability (F =129.54,P ＜ 0.05) and colony formation,increased apoptosis and the percentage of G2/M-phase cells.Conclusions 3-Methyladenine enhances the radiosensitivity of esophageal squamous carcinoma Eca-109 cells,suggesting that inhibition of autophagy could be used as an adjuvant treatment of radiotherapy in esophageal squamous carcinoma.
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OBJECTIVE: To explore the inhibitory effect of betulinc acid(BA) on esophageal squamous cell carcinoma (ESCC) KYSE170 cells and the mechanisms of the inhibitory effect. METHODS: Different concentrations of BA(0, 5, 10, 20, 40, 60, 80 and 100 μg·mL-1) were used to detect their effects and the inhibitory rate on the cells for 24 to 72 h. The clone formation test was used to detect the long term inhibitory effects of different BA concentration(0, 5, 20 and 40 μg·mL-1) on KYSE170 cells. Different concentrations of BA(10, 60 and 100 (μg·mL-1) for 24 and 48 h were used to detect the apoptosis rate of cells by flow cytometry. Different concentrations of BA(0, 10 and 40 μg·mL-1) for 24 h were used to detect the cell cycle of cells by flow cytometry. RESULTS: BA inhibited the growth of KYSE170 cells in a dose- and time-depentent manner. IC50 at 24, 48 and 72 h were (56.81±2.56), (39.73±2.77) and (29.28±3.05) μg·mL-1, respectively. The clone formation plating efficiencies were (89.56±5.00)%, (61.00±2.03)%, (31.33±3.51)% and (15.33±2.33)% when the drug concentrations were 0, 5, 20 and 40 μg·mL-1, respectively. With the increase of BA concentration and the prolong of BA incubation time the apoptosis rate increased significantly (P<0.05 or 0.01). After 0, 1 and 10 μg·mL-1 BA added for 24 h, the rate of Gl phase cells decreased, while the rate of S phase cells increased(P<0.01). CONCLUSION: BA can inhibit the growth of KYSE170 cell by inducing cell apoptosis and blocking cells to stay in S phase. Copyright 2012 by the Chinese Pharmaceutical Association.
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Objective To analyze the possible risk factors of esophageal stenosis after endoscopic mucosal resection (EMR). Methods From January 2008 to December 2009, a total of 219 procedures of esophageal EMR were performed to resect early esophageal squamous carcinoma and its precancerous lesions,and esophageal stenosis was observed in 9 cases. Data of these 9 patients ( stenosis group) were collected and compared with those of patients without stenosis ( control group, n = 202, 8 patients were excluded because of being diagnosed as squamous carcinoma with submucosal infiltration after EMR and being transfered to surgery). Results There was no significant difference between two groups in regard of gender, age, location of the lesion, length of the lesion or pathological diagnosis after EMR, while the rate of patients with mucosal defect larger than 3/4 circumference in stenosis group ( 8/9, 88.9% ) was significantly higher than that in control group (9/202, 4. 5%, P ＜ 0. 01 ). Conclusion In EMR for early esophageal squamous carcinoma and its precancerous lesions, post-EMR mucosal defect larger than 3/4 circumference is a risk factor for esophageal stenosis.
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Objective To study the expression of matrix metalloproteinase-9(MMP-9) and tissue inhibitor of metalloproteinase-1(TIMP-1), and its correlation with lymph node metastasis in esophageal squamous carcinoma(ESC). Methods The expressions of MMP-9 and TIMP-1 were detected in 78 cases of esophageal squamous carcinomas by using immunohistochemical SP method. Results The expression level of MMP-9 in high differentiated (grade Ⅰ～Ⅱ) and early stage (stageⅠ～Ⅱ) ESC was significantly lower than that in low differentiated(grade Ⅲ～Ⅳ) and late stage (stage Ⅲ～Ⅳ) ESC(P
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Objective:Toinvestigate the expression of RHAMMgene and TPX2 gene in esophageal squamous cell carcinoma(ESCC)and their relationships with clinicopathological factors.Methods:The expression of RHAMM gene and TPX2 gene were detected by reverse transcriptase polymerase chain reaction(RT-PCR)in ESCC tissues,para-cancer tissues,and matched esophageal normal mucosa tissues of 40 patients.Results:The positive expressions of RHAMM mRNA in ESCC tissues(65.0%)were significantly higher than those in para-cancer tissues(37.5%)and esophageal normal mucosa tissues(22.5%).Significant relationship was observed between positive expression of RHAMM mRNA and lymphnode metastasis(P