Objective To research the expressions of miR-196b and HoxB8 mRNA in colorectal cancer and theircorrelation with clinicopathologic features，and to explore the relationship between miR-196b and HoxB8 in vivo. Methods Expressions of RNA （including miR-196b and HoxB8 mRNA） and HoxB8 protein were detected respectively by using quantitative real-time reverse transcriptase PCR and Western blot in 30 cases of colorectal cancer and corresponding normalmucous membrane tissues. Results In colorectal cancer tissues，expressions of miR-196b and HoxB8 mRNA were higher than those of the corresponding normal mucous membrane tissues （P＜0.05）. Expression of miR196b mRNA was assoc-iated with lymph node metastasis，neoplasm stages （Ⅰ＋ⅡandⅢ＋Ⅳ），and distant metastasis （P＜0.05），on the otherhand，no significant differences were observed regarding tumor site，size，gross type，depth of invasion，tissue differentiation，age，and sex （P＞0.05）. Expression of HoxB8 mRNA was no significant differences concerning lymph node metastasis，tumor stages （Ⅰ＋Ⅱ，Ⅲ＋Ⅳ），distant metastasis，tumor site，size，gross type，depth of invasion，tissue differentiation，age，and sex （P＞0.05）. The expression of miR-196b mRNA was negatively correlated with HoxB8 mRNA expression （r=-0.458，P＜0.05），and HoxB8 protein expression with no obvious correlation （r=-0.236，P＞0.05） in colorectal cancer tissues. Conclusions The expressions of miR-196b and HoxB8 mRNA in colorectal cancer tissues are higher，the high expression of miR-196b mRNA is related to the tumorigenesis and progression of colorectal cancer as well as correlated with prognosis in colorectal cancer. The miR-196b inhibits the expression of HoxB8 mRNA by binding to the3′-UTR of target HoxB8 mRNA.
ObjectiveTo investigate the expressions of chemokine receptor CXCR4 and CCR7 in thyroid cancer and its clinicopathologic significance. MethodsFifty-five patients with thyroid cancer were selected in the Affiliated Hospital of North Sichuan Medical College from 2006 to 2009, and 30 patients with thyroid adenoma were selected in the same hospital during 2009. The expressions of CXCR4 and CCR7 were detected in all the selected cases samples (including thyroid cancer and thyroid adenoma) by immunohistochemical SP technique. ResultsThe positive expression rates of CXCR4 and CCR7 in the thyroid cancer were higher than those in the thyroid adenoma (Plt;0.01), which in the thyroid cancer with clinical stage Ⅲ+Ⅳ were higher than those of the clinical stage Ⅰ+Ⅱ (Plt;0.05). The positive expression rate of CCR7 in the thyroid cancer with lymph node metastasis was higher than that of the thyroid cancer without lymph node metastasis (Plt;0.05), which of CXCR4 in the patients with thyroid cancer was independent of lymph node metastasis (Pgt;0.05), and which of CXCR4 and CCR7 were also independent of the age and gender of the patients with thyroid cancer (Pgt;0.05). The positive expressions of CCR7 and CXCR4 in all the patients with thyroid cancer was positively correlated (rs=0.491, P=0.000). ConclusionsCXCR4 and CCR7 are involved in the coordination of thyroid cancer progression. They can be used as prognostic indicators of thyroid cancer. High expression of CCR7 is prone to lymph node metastasis of thyroid cancer.
Mesenchymal stem cells (MSC) are considered to have important value in the treatment of various diseases because of their low immunogenicity, transferability, and strong tissue repair capacity. Stromal cell derived factor-1 (SDF-1) and its receptor CXC chemokine receptor 4 (CXCR4) pathway plays an important role in migration of MSC. The induction of homing of MSC to retina by regulating SDF-1/CXCR4 may exert the curative effect on diabetic retinopathy to greatest exent.
ObjectiveTo systematically review the relationship between the expression of CXCL12/CXCR4 and pancreatic cancer.MethodsPubMed, EMbase, The Cochrane Library, Wiley Online Library, CNKI, VIP, WanFang Data and CBM databases were electronically searched to collect case-control studies on CXCL12/CXCR4 expression in pancreatic cancer from inception to February 1st 2020. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies; then, meta-analysis was performed by using RevMan 5.3 software.ResultsA total of 21 case-control studies involving 1 677 cases and 1 690 controls were included. The results of meta-analysis showed that the expression of CXCR4 in pancreatic cancer tissue was higher than normal tissue (OR=21.40, 95%CI 5.70 to 80.31, P<0.01), in carcinoma of head of pancreas been higher than carcinoma of pancreatic body and tail, (OR=1.58, 95%CI 1.02 to 2.44, P=0.04), in pancreatic cancer with lymph node metastasis been higher than without lymph node metastasis (OR=3.14, 95%CI 1.98 to 4.99, P<0.01), in pancreatic cancer with high TNM stages (Ⅲ, Ⅳ) been higher than low TNM stages (Ⅰ, Ⅱ) (OR=3.67, 95%CI 1.98 to 6.81, P<0.01), in pancreatic cancer with distant metastasis been higher than without distant metastasis (OR=3.56, 95%CI 1.71 to 7.39, P<0.01), and in pancreatic cancer with vascular invasion was higher than without vascular invasion (OR=3.22, 95%CI 1.70 to 6.09, P<0.01). The expression of CXCR4 was not statistically correlated with age, gender, pancreatic cancer tissue and paracancerous tissue, pancreatic cancer tissue and paracancerous lymph nodes, differentiation degree. There was no statistical correlation between the expression of CXCL12 and the differentiation degree, and lymph node metastasis.ConclusionsIn pancreatic cancer, the high expression of CXCR4 is related to lymph node metastasis, high TNM stage, distant metastasis, vascular invasion indicate poor prognosis. Due to limited quality and quantity of the included studies, more high quality studies are required to verify above conclusions.
Objective
To investigate the effect of human placental-derived mesenchymal stem cells (PMSCs) on immunological rejection in mouse allogeneic skin transplantation.
Methods
The placenta fetal tissues from voluntary donors were used to isolate and culture the PMSCs, and the 3rd passage PMSCs were used in the experiment. Thirty Vr
∶
CD1 (ICR) mice at age of 1-2 days were used as skin donors for allogeneic skin transplantation. Thirty C57BL/6 mice at age of 6-8 weeks as recipients were made back skin defect of 12 mm in diameter and were randomly divided into 3 groups (n=10): group A, autograft; group B, allogeneic graft + PBS tail vein injection; and group C, allogeneic graft + human PMSCs (1 × 105 cells/mouse) tail vein injection. The flap survival was observed. At 7 days after skin transplantation, blood leukocyte counting, abdominal fluid macrophage activation, and the expression levels of interleukin 4 (IL-4), interleukin 17 (IL-17), and interferon γ (INF-γ) in blood and spleen were detected by ELISA and RT-PCR, respectively.
Results
The flap survival time was significantly longer in group A [(58.33 ± 4.04) days] than in groups B and C [(3.80 ± 0.92) days and (6.80 ± 0.82) days] (P lt; 0.05), and in group C than in group B (P lt; 0.05). At 7 days after transplantation, the blood leukocyte number was (6.32 ± 0.45) × 109/L in group A, (7.45 ± 0.52) × 109/L in group B, and (6.35 ± 0.39)× 109/ L in group C, and it was significantly more in group B than in groups A and C (P lt; 0.05). The macrophage activation rate of the abdominal fluid was 6.87% ± 2.40% in group A, 7.84% ± 0.44% in group B, and 15.98% ± 2.87% in group C; group C was significantly higher than groups A and B (P lt; 0.01). ELISA results showed that there was no significant difference in the concentrations of IL-4 among 3 groups (P gt; 0.05). Compared with group B, the concentrations of IL-17 and IFN-γ were significantly reduced in group C (P lt; 0.05), while the concentration of IFN-γ was significantly increased in group B when compared with group A (P lt; 0.05). RT-PCR results showed that there were significant differences in the expressions of IL-4, IL-17, and IFN-γ mRNA between groups B, C and group A (P lt; 0.05); the expressions of IL-4 and IFN-γ mRNA were significantly lower in group C than in group B (P lt; 0.05).
Conclusion
Human PMSCs transplantation can suppress the acute immunological rejection in allogeneic skin transplantation. The possible mechanism may be partially related to the inhibitory effect on the secretion of IL-17 and IFN-γ.
Objective To analyze the variation of intestinal microflora in patients with colorectal cancer by SYBR GreenⅠreal-time fluorescence quantitative PCR and reveal the role and significance of intestinal microflora in the colorectal cancer-associated molecular pathogenesis. Methods A set of 16S rRNA gene group of species-specific primers for Bifidobacterium spp., Lactobacillus group, Escherichia coli, and ddl gene-targeted species-specific primers for Enterococcus faecalis and feces Enterococcus were designed. Patients with colorectal cancer (colorectal cancer group, n=30) and healthy volunteers (normal control group, n=30) were included and whose feces were collected to extract bacterial genome DNA. SYBR GreenⅠ real-time fluorescence quantitative PCR was used to analyze the five mentioned bacterial amounts. Results Level of Bifidobacterium spp. (4.52±0.49) and Lactobacillus group (5.46±0.12) in colorectal cancer group were significantly lower than those （9.25±0.83 and 7.45±0.37） of normal control group (Plt;0.05), whereas levels of Escherichia coli (5.82±0.47), Enterococcus faecalis (10.6±0.30) and feces Enterococcus (5.74±0.16) in colorectal cancer group were significantly higher than those （4.68±0.32, 4.95±0.24, and 5.03±0.43） of normal control group (Plt;0.05). Conclusions The fecal microflora composition of patients with colorectal cancer is significantly decreased in Bifidobacterium spp. and Lactobacillus group, whereas increased in Escherichia coli, Enterococcus faecalis, and feces Enterococcus. These data underline that the occurrence and progress of colorectal cancer may be related to intestinal microflora.
ObjectiveTo observe clinical phenotypes and analyze the pathogenic genes of Leber congenital amaurosis (LCA). MethodsA retrospective clinical study. From 2019 to 2020, 2 patients diagnosed with LCA by genetic testing in Tianjin Medical University Eye Hospital and their 6 unaffected family members were enrolled in the study. Two patients were from 2 unrelated families, both were probands. The patient's medical history was inquired in detail, slit lamp microscopy, ultra-widefield fundus photography, autofluorescence, and flash visual evoked potential (F-VEP) were performed. Peripheral vein blood (3-5 ml) was collected and genomic DNA was extracted from all study subjects. A total of 381 pathogetic genes associated with inherited retinal diseases, were selected by targeted exome sequencing capture strategy. Sanger sequencing was used to verify suspected pathogenic mutations. Candidate pathogenic mutations were identified after bioinformatics analysis. Sanger sequencing, real-time quantitative polymerase chain reaction and family co-identification were used to confirm the final mutations. ResultsTwo patients were male, aged 3 and 27 years. One case had vision loss in both eyes, accompanied by nystagmus and acupressure eye sign since childhood. The clinical hallmark of the proband (F1-Ⅱ-3) in F1 includes clearly boundary of optic disc, normal retinal blood vessels and macular fovea. The implied period of the maximum forward wave in both eyes of F-VEP was roughly normal, and its amplitude decreased significantly. The phenotype of the proband (F2-Ⅱ-1) in F2 includes optic nerve head pallor, bone-spicule intraretinal pigmentation, “gold-foil maculopathy”, retina patchy hypo-autofluorescence in both eyes. There was no abnormal phenotype in the eyes of the family members. According to the genetic diagnosis, the proband (F1-Ⅱ-3) carried the GUCY2D gene c.835G>A (p.D279N) (M1) and exon 9-19 deletion (M2) compound heterozygous mutations, in which M1 was derived from healthy mother and M2 was derived from healthy father. The proband (F2-Ⅱ-1) carried CRB1 gene c.1576C>T(R526X) (M3) and c.1522T>C (C508R) (M4) compound heterozygous mutations, in which M3 from the healthy father, M4 from the healthy mother. M2 and M4 were novel mutations. ConclusionGUCY2D gene mutations lead to LCA1 type in the F1 family, CRB1 gene mutations lead to LCA8 type in the F2 family; there are significant different phenotypes caused by different pathogenic genes.
Objective To explore the expression of chemokine receptor CCR7 in thyroid papillary microcarcinoma tissues and the relationship with clinicopathological features. Methods The CCR7 expressions in 31 cases of thyroid papillary microcarcinoma, 34 cases of thyroid papillary carcinoma which diameter＞1cm, 34 cases of nodular goiter, and 12 cases of thyroid papillary microcarcinoma contralateral normal thyroid tissues were detected by using immunohistochemistry S-P method. Results The expression positive rates of CCR7 in thyroid papillary microcarcinoma and papillary thyroid carcinoma which diameter＞ 1cm were both 100%, the difference had not statistically significant （P＞0.05）. In nodular goiter and normal thyroid tissues, the expression positive rate of CCR7 was 64.7% and 33.3%, respectively, and compared with thyroid papillary microcarcinoma, the difference had statistically significant （P＜0.05）. There were not relations between the expression of CCR7 and patient’s gender, age, capsule invasion, and lymph node metastasis （P＞0.05）. Conclusions The CCR7 in thyroid papillary microcarcinoma and thyroid papillary carcinoma which diameter＞ 1cm are both high expressions, and have the same bionomics, both prone to cervical lymph node meta-stasis, and the radical neck dissection （central area） are both need to take.
ObjectiveTo observe the changes of eotaxin-1(CCL11), eotaxin-2(CCL24)and eotaxin-3(CCL26)in ranibizumab treated light-injured human retinal pigment epithelium (RPE) cells ARPE-19 and investigate the effects of vascular endothelial growth factor (VEGF) antagonist to the expressions of eotaxins.
MethodsCultured human RPE cells(8th-12th generations)were divided into light-injured group, ranibizumab treated group and normal control group. Cells of the three groups were exposed to the blue light at the intensity of(600±100) Lux for 12 h to establish the light injured model, while cell culture dishes of the normal control group were wrapped with double-layer foil. The cells of ranibizumab treated group were treated with VEGF-A antagonist(ranibizumab)at the final concentration of 0.125 mg/ml for 24 hours directly after the illumination. The mRNA and protein of VEGF-A, eotaxin-1, eotaxin-2, eotaxin-3, NF-κB were determined by Real time-PCR, enzyme-linked immunosorbent assay, Western blot, immunohistochemical staining at 0, 3, 6, 12, 24 hours after light damage.
ResultsThe mRNA and protein level of VEGF-A, eotaxin-1, eotaxin-2, eotaxin-3, NF-κB in the light-injuried group increased significantly compared to that in normal control group (P < 0.05). After treating with ranibizumab, the expression of eotaxin-1, eotaxin-2, eotaxin-3, NF-κB were significantly suppressed (P < 0.05).
ConclusionThe suppression of over-expression of VEGF in human RPE may down-regulate the expression of eotaxins, via the suppression of NF-κB.
