Transcriptome Analysis of Xianlian Jiedu Prescription in Intervention of Colorectal Carcinoma Due to Dampness， Heat， Stasis， and Toxin in Mice / 中国实验方剂学杂志

ObjectiveTo analyze the transcriptome characteristics of Xianlian Jiedu prescription （XLJDP） in the intervention of colorectal carcinoma by high-throughput cDNA-sequencing （RNA-seq）. MethodNinety male C57BL/6 mice were randomly divided into the control group， colorectal carcinoma due to dampness， heat， stasis， and toxin model group， and XLJDP group， with 30 mice in each group. Mice in the model group and XLJDP group were fed a high-fat diet and provided with azoxymethane and dextran sodium sulfate （AOM/DSS） for inducing colorectal carcinoma. Those in the XLJDP group were further treated with intragastric administration of 12.9 g·kg-1 XLJDP since the day of modeling for 112 days. The colorectal tissues were collected from each group 4 h after the last drug treatment and stained with hematoxylin-eosin （HE） and methylene blue for observing the pathological changes. The total RNA was extracted from colorectal tissues for RNA-Seq-based transcriptome profiling， followed by gene oncology （GO） and Kyoto encyclopedia of genes and genomes （KEGG） pathway enrichment analysis and the screening and verification of differentially expressed genes. ResultCompared with the model group， XLJDP significantly relieved the colorectal congestion and edema and decreased tumor number and volume in mouse colorectal tissues. The methylene blue staining results indicated that XLJDP significantly suppressed the development of aberrant crypt foci （ACF，P<0.01）. As revealed by HE staining， XLJDP significantly alleviated the injury and dysplasia of colorectal tissues. Transcriptome analysis identified 615 differentially expressed genes （446 up-regulated and 169 down-regulated） between the model group and the blank group and 54 differentially expressed genes （29 up-regulated and 25 down-regulated） between the XLJDP group and model group. XLJDP mainly affected the expression of NIMA-related protein kinase 7 gene （Nek7， P<0.01）， Mucin 16 （Muc16， P<0.01）， SiahE3 ubiquitin protein ligase family member 3 （Siah3， P<0.01）， regenerating islet-derived protein 3-gamma （Reg3g， P<0.01）， RNA polymerase Ⅱ elongation factor-associated factor 2 （Eaf2， P<0.01）， transforming growth factor‐alfa gene （TGF-α， P<0.05）， secretoglobin family 1A member 1 （Scgb1a1， P<0.05）， family with sequence similarity 227 member B （Fam227B， P<0.05）， cytochrome P450 family 2 subfamily c polypeptide 40 （Cyp2c40， P<0.01）， and ankyrin repeat and EF-hand domain containing protein 1 （Ankef1， P<0.05）. Enrichment analysis showed that intestinal epithelial cell proliferation， metabolism of xenobiotics by cytochrome P450， and arachidonic acid metabolism signaling pathway were significantly enriched. ConclusionXLJDP is able to interfere with colorectal tumorigenesis and development due to dampness， heat， stasis， and toxin in mice， which has been proved by transcriptome analysis to be related to the regulation of metabolism-related pathways.

Chemerin, a pro-inflammatory adipokine, regulates chondrocyte proliferation and metabolism by increasing production of nitric oxide / 中国组织工程研究

BACKGROUND: The key pathological characteristics of osteoarthritis are manifested in the degeneration of the cartilage caused by inflammation, and chondrocytes are the only cells in cartilage tissues. Studies have shown that Chemerin can stimulate the migration of leukocytes to the inflammation site and increase the inflammation signal of chondrocytes, suggesting that Chemerin can play a role in arthritis. Our previous research indicated that the serum Chemerin level in patients with osteoarthritis was significantly increased, and the Chemerin level in the synovial fluid was related to the severity of osteoarthritis based on the Kellgren-Lawrence classification. Chemerin may be used as an inflammatory factor in osteoarthritis. OBJECTIVE: To investigate the effect of Chemerin on the proliferation and metabolism of chondrocytes. METHODS: The chondrocytes from neonatal mice were isolated by collagenase type II digestion, and then cultured. Cell growth curves were established and the range of concentrations of Chemerin that exhibited toxicity to normal chondrocytes was screened using an MTT assay. Subsequently, 10 μg/L interleukin-1β was used to stimulate the chondrocytes in order to establish an in vitro model of osteoarthritis induction. After the chondrocytes had been cultured in the presence of the drug for 2 days, cell morphology, proliferation and metabolism were evaluated by hematoxylin-eosin staining and diacetate fluorescein/ propidium iodide staining. In addition, the expression of inducible nitric oxide polymerase was analyzed by measuring the secretion of nitric oxide. Furthermore, qRT-PCR was used to quantify mRNA expression of proteoglycan, type II collagen α1, matrix metalloprotease-13 and nitric oxide synthase 2. RESULTS AND CONCLUSION: The chondrocytes cultured in vitro exhibited healthy activity and morphology. Furthermore, chemerin (50 μg/L) and interleukin-1β (10 μg/L) were able to reduce the synthesis of extracellular matrix, enhance the secretion of nitric oxide and increase chondrocyte apoptosis. More importantly, the qRT-PCR results indicated that Chemerin and interleukin-1β caused similar effects, by which the expression of cartilage-specific genes was downregulated and catabolism-related genes upregulated. As a pro-inflammatory factor, Chemerin can increase the generation of nitric oxide in chondrocytes, regulate cell metabolism, stimulate cell apoptosis and act synergistically with interleukin-1β.

Research progress of breast cancer metabolic reprogramming and microenvironment remodeling / 中国药科大学学报

@#As numerous connections between oncogenic signalling pathways and metabolic activities emerge, the importance of metabolic reprogramming in cancer is being increasingly recognized. During tumorigenesis, breast cancer cells undergo metabolic reprogramming, which generally includes enhanced glycolysis, tricarboxylic acid cycle activity, glutaminolysis and fatty acid biosynthesis. The extension and functional importance of these metabolic alterations may diverge according to breast cancer subtypes.Besides, aberrant metabolism of breast cancer cells remodels tumor microenvironment, promoting cancer vascularization and inhibiting anti-tumor immunity, and thus accelerates tumor progression.This review addresses current knowledge on the metabolic reprogramming and breast cancer microenvironment, which provides some reference for the development of metabolic target drugs for each breast cancer subtype.

Effect of glutamine metabolism on chemoresistance and its mechanism in tumors / 浙江大学学报·医学版

The metabolic reprogramming of tumor cells is characterized by increased uptake of various nutrients including glutamine. Glutamine metabolism provides the required substances for glycolysis and oxidative phosphorylation and affects the homeostasis of carbohydrate，fat and protein metabolism to induce the chemoresistance of tumor cells. Combination of chemotherapeutic agents with inhibitors specific to different components of glutamine metabolic pathway has obtained favorable clinical results on various tumors. Glutamine metabolic pathway plays a role in drug resistance of tumor cells in various ways. Firstly，the dynamic change of glutamine transporters can directly affect intracellular glutamine content thereby causing drug resistance; secondly，tumor stromal cells including adipocyte，fibroblast and metabolite from tumor microenvironment would give rise to immune-mediated drug resistance; thirdly，the expression and activity of key enzymes in glutamine metabolism also has a critical role in drug resistance of tumors. This article reviews the effects of glutamine metabolic pathway in the development of tumor chemoresistance，in terms of transporters，tumor microenvironment and metabolic enzymes，to provide insight for improving the therapeutic efficacy for drug-resistant tumors.

Expression of Sirtuin 4 in Oral Squamous Cell Carcinoma and its Correlation with Clinicopathological Parameters

Introduction: SIRTs (Sirtuins) are class III histone deacetylase enzymes that use NAD+ as a co-substrate for their enzymaticactivities. In mammals, there are seven sirtuin proteins (SIRT1–SIRT7) among which SIRT4, SIRT3 and SIRT5 are mitochondrialsirtuins that regulate enzymes and other mitochondrial proteins to coordinate oxidative production of ATP with the availability ofenergy in the diet. SIRT4 is known to have tumor suppression activity in many human cancers. However, the role of SIRT4 inoral squamous cell carcinoma is not known. It is present at higher levels under nutrient-rich conditions, and inhibits glutaminecatabolism through ADP-ribosylation and hence repression of glutamate dehydrogenase (GDH) activity, a rate-limiting enzymein glutamine catabolism. Due to higher requirement of energy and bio-molecules for proliferation, cancer cell often resort tovarious metabolic pathways that are otherwise uncommon in normal cells. One of such mechanism is switching to Glutaminemetabolism. SIRT4 acts as a tumor suppressor by repressing glutamine utilisation by cells.Purpose: Study the role of SIRT4 in oral squamous cell carcinoma and evaluate its tumor suppressor role.Method: Here we studied expression of SIRT4 in oral cancer tissues by immuohistochemistry and compared it with that ofnormal tissue.Results: SIRT 4 was seen to significantly down regulated in oral squamous carcinoma.Conclusion: The present study suggests SIRT4 as a marker of tumor aggressiveness and as a therapeutic target for OSCC.

Study on hepatotoxicity mechanism of Euodiae Fructus based on network pharmacology / 中草药

Objective: To screen the main hepatotoxic components, predict the target of active components, and explore the mechanism of liver toxicity of Euodiae Fructus (EF). Methods: According to TCMSP database, PubChem database Pharmmapper server and Uniprot KB database information, active constituents of EF were screened, and targets of hepatotoxicity were predicted. The active component-acting target network of EF was constructed by Cytoscape software, while the function and metabolic pathways of target genes were analyzed by KOBAS 3.0 database. Results: Network analysis results demonstrated that 147 potential hepatotoxic components from EF, accompanied with 49 targets like F2, PIM1, MMP13 and MAOB, connecting with cell metabolism, catalytic activity, stimulate the reaction pathways may be associated with EF’s liver toxic effects. Conclusion: Based on network pharmacology methodology, this paper disclosed that many potential toxic components in EF may interact with cell metabolism, catalytic activity and other pathways through multiple targets, leading to produce hepatotoxicity in vivo as a result, which can provide new clues for further researches of the hepatotoxicity mechanism study of EF.

Supercooling organ preservation technology and its application / 器官移植

The main purpose of organ preservation in organ transplantation is to maintain tissue and cell activity of donor organs so as to gain time for allocation and transportation of the organ, preparation of the recipient and organization of staff and facilities. The main principles of organ preservation can be divided into normothermic mechanical perfusion and cryopreservation. Cryopreservation is the favourite organ preservation method in clinical practice currently. However, the metabolic activity still exists in donor organs preserved with current cryopreservation technique, which makes the long-term preservation of organs extremely difficult. The supercooling organ preservation is a new type of cryopreservation technology, which greatly prolongs the preservation time of organs. It is expected to become an important organ preservation technique in the future, and it will provide technical support for the establishment of "organ bank".

Research advancement in vascular endothelial cell metabolism and tumor angiogenesis / 药学学报

Vascular endothelial cells play a major role in maintaining the oxygen and nutrient supply to all tissues in the body. Endothelial cells, together with vascular endothelial growth factor, are also the driving forces of tumor angiogenesis, a process describing the growth of blood vessels from the existing vasculature in tumor tissues. Reprogramming of endothelial cell metabolism satisfied the needs for biomass and energy in the process of tumor angiogenesis, which are known to involve the aspects of glucose metabolism, amino acid metabolism, and fatty acid metabolism. Recently, with the increasing interest to understand the metabolic regulation in cancer, the investigation into the metabolism of endothelial cells has made progress. We herein review the role of endothelial cell metabolism in angiogenesis, with a particular focus on the metabolic regulation of endothelial cells in tumor angiogenesis, which hopes to provide insights for the intervention of tumor angiogenesis in cancer therapy.

Progress in roles and mechanisms of deacetylase SIRT7 / 生物工程学报

As a member of the Sirtuins family in mammals, SIRT7 locates in nucleus and is a highly specific H3K18Ac (acetylated lysine 18 of histone H3) deacetylase. Recent studies showed that SIRT7 could participate in the ribosomal RNA transcription, cell metabolism, cell stress and DNA damage repair through various signaling pathways. In addition, SIRT7 is also closely related with aging, heart disease and fatty liver. In particular, SIRT7 plays important roles in the regulation of initiation and development of various tumors, such as liver cancer, gastric cancer, breast cancer, bladder cancer, colorectal cancer, and head/neck squamous cell carcinoma. This review describes the cellular and molecular functions of SIRT7, and systematically summarizes recent progress of SIRT7 in human disease.

Mechanism research of curcumin on cancer cells based on cell metabolic profiling / 中国中药杂志

In this study, gas chromatography coupled with mass spectrometry(GC-MS) was used to analyze the changes of 12 kinds of cancer cells treated by curcumin. The related differential metabolites were screened and the metabolic pathways were analyzed to explore the anti-tumor mechanism of curcumin. Methyl thiazol tetrazolium(MTT) assay was used to detect the 50% inhibiting concentration(IC_(50)) of curcumin on 12 human tumor cells. After treatment with curcumin for 48 h, the cells were collected and analyzed by GC-MS, followed by pathway analysis and multivariate data analysis including principal component analysis(PCA), orthogonal partial least squares discriminant analysis(OPLS-DA) and One-way analysis of variance(ANOVA),etc. Overall, 34 metabolites showed significant concentration changes after intervention for 48 h, mainly involving multiple metabolic pathways, including lysine degradation, glycine, serine and threonine metabolism, arginine and proline metabolism, cysteine and methionine metabolism, aminoacyl-tRNA biosynthesis, primary bile acid biosynthesis, lysine biosynthesis. In this study, the anti-tumor mechanisms of curcumin interfering with energy metabolism, amino acid metabolism, microtubule system, protein synthesis and oxidative stress response of tumor cells were analyzed from the perspective of metabolism, providing a new reference for further tumor pharmacology study.

Advances in multi-scale analysis and regulation for fermentation process / 生物工程学报

Industrial fermentation focuses on realizing the uniform of high titer, high yield, and high productivity. Multi-scale analysis and regulation, including molecule level, cell level, and bioreactor level, facilitate global optimization and dynamic balance of fermentation process, which determine high efficiency of biosynthesis, targeted directionality of bioconversion, process robustness, and well-organized system. In this review, we summariz and discuss advances in multi-scale analysis and regulation for fermentation process focusing on the following four aspects: 1) kinetic modeling of metabolic pathways, 2) characteristic of cell metabolism, 3) co-coupling fermentation and purification, and 4) bioreactor design. Integrating multi-scale analysis of fermentation process and integrating multi-scale regulation are expected as an important strategy for realizing highly efficient fermentation by industrial microorganisms.

Câncer de mama: Reprogramação do metabolismo tumoral / Breast Cancer: tumoral metabolism reprogramming

O câncer de mama é a neoplasia de maior incidência em mulheres de todo o mundo, cuja mortalidade se deve principalmente ao desenvolvimento de metástases (condição patológica em que as células tumorais conseguem atravessar a matriz extracelular e se estabelecer em outros tecidos). Devido à importância epidemiológica dessa doença, estudos têm sido realizados em busca de uma melhor compreensão dos processos que atuam na carcinogênese e/ou tumorigênese e que, consequentemente, levam ao desenvolvimento de novas formas de diagnóstico e tratamento que sejam cada vez mais efetivos. Para manter a alta taxa de proliferação e desenvolver um perfil agressivo, características que são observadas em células tumorais, diversas alterações no metabolismo celular se tornam necessárias. O metabolismo tumoral começou a ser descrito por Otto Warburg em 1920, onde afirma que células cancerosas metabolizam glicose de forma diferente das células normais através da glicólise aeróbica. Dados recentes mostram que as alterações também ocorrem no metabolismo lipídico, apontando para uma reprogramação celular. A possibilidade de novos alvos farmacológicos inseriu o metabolismo como alvo das pesquisas recentes. Entretanto, e apesar do avanço, 90 anos depois da descoberta feita por Warburg, os estudos ainda não conseguiram esclarecer por completo como o metabolismo tumoral funciona, demonstrando assim a necessidade de mais pesquisas. Tendo em vista este cenário, essa revisão tem como objetivo documentar e discutir os principais resultados obtidos até o momento, como apontar e sugerir áreas de investigação. (AU)

Breast cancer is the most prevalent neoplasm in women worldwide, whose mortality is mainly due to the development of metastasis (pathological condition in which cancer cells can cross the extracellular matrix and settle in other tissues). Due to the epidemiological importance of this disease, studies have been carried out in order to better understand the processes involved in carcinogenesis and/or tumorigenesis and, consequently, allow the development of new forms of diagnosis and treatment that are increasingly effective. To maintain the high proliferation rate and develop an aggressive profile, features that are observed in tumor cells, several changes in cellular metabolism become necessary. Tumor metabolism began to be described by Otto Warburg in 1920, where he states that cancer cells metabolize glucose differently from normal cells through aerobic glycolysis. Recent data show that changes also occur in lipid metabolism, pointing to cellular reprogramming. The possibility of new pharmacological targets, inserted the metabolism as a target of recent research. However, despite the breakthrough, 90 years after Warburg discovery, studies have not yet been able to fully clarify how tumor metabolism works, demonstrating the need for more research. In view of this scenario, this review aims to document the main results obtained so far and to discuss those aspects that are not yet well understood. (AU)

Advances in sepsis induced immunosuppression and immunomodulation therapy / 中华危重病急救医学

Immunosuppression plays a vital role in the pathophysiological mechanism of sepsis, and it is the main cause of death in patients with sepsis during the later phase. Sepsis induced immunosuppression is gradually recognized. Its underlying mechanisms involve immune cell apoptosis, autophagy, cell metabolism reprogramming, endotoxin tolerance, central nervous system regulation, and epigenetic regulation. New approaches that target the host immune response and reconstruct the immune balance are the keys to improve the prognosis of patients with sepsis. With the help of immune status monitor, novel immunomodulatory agents, such as thymosin α1, γ- interferon (IFN-γ), interleukin-7 (IL-7), granulocyte-macrophage colony stimulating factor (GM-CSF) and anti-programmed death receptor 1 (PD-1) antibody, are expected to become a new strategy for the treatment of sepsis in future.

Red LED Photobiomodulates the Metabolic Activity of Odontoblast-Like Cells

Abstract Phototherapy has been indicated as an adjunctive treatment for tissue repair, including the pulp tissue. However, there are no defined irradiation parameters, which is a great challenge to the clinical use of phototherapy. The aim of this study was to evaluate the effect of phototherapy with red LED on odontoblast-like MDPC-23 cells, using different parameter settings. Cells were seeded (104 cells/cm²), incubated for 12 h in complete DMEM and then the culture medium was replaced by DMEM supplemented with 0.5% FBS. After 12 h incubation, irradiations were performed (630±10 nm) using a LEDTable device with a 20 or 40 mW/cm² power density and 2 J/cm² energy dose. The cells were irradiated 1 or 3 times, at 1 min intervals. Non-irradiated cells served as control. The cells were evaluated for viability (MTT assay), total protein dosage (Lowry method) and number of viable cells (Trypan blue). The data (n=12 per group) were submitted to Kruskal-Wallis and Mann-Whitney tests (p=0.05). A single irradiation with 20 or 40 mW/cm² enhanced cell viability, which was negatively affected after 3 consecutive irradiations. Cells irradiated only once with 20 mW/cm² produced more proteins compared with those irradiated with 40 mW/cm². Reduction in the number of viable cells occurred only after 3 consecutive irradiations with 40 mW/cm². In conclusion, red LED was capable of biomodulating the metabolic activities of cultured MDPC-23 odontoblast-like cells. The best cell biostimulation was obtained when a single irradiation with 2 J/cm2 energy dose and 20 mW/cm2 power density was delivered to the pulp cells.

Resumo Fototerapia tem sido indicada como um tratamento adjuvante para o reparo de tecidos, incluindo o tecido pulpar. Entretanto, não há parâmetros de irradiação definidos, o que representa um grande desafio para o uso clínico da fototerapia. O objetivo deste estudo foi avaliar o efeito da fototerapia com LED vermelho em células MDPC-23 com fenótipo odontoblastóide, usando vários parâmetros. As células foram semeadas (104 células/cm2), incubadas por 12 h em DMEM completo e então o meio de cultura foi trocado por DMEM com 0,5% SFB. Após 12 h de incubação, as irradiações foram realizadas (630±10 nm) usando um dispositivo com densidade de potência de 20 ou 40 mW/cm2 e dose de energia de 2 J/cm2. As células foram irradiadas 1 ou 3 vezes, com intervalos de 1 min. Células não irradiadas serviram como controle. Foram avaliadas a viabilidade (ensaio de MTT), dosagem de proteína total (método de Lowry) e número de células viáveis (ensaio de Trypan blue). Os dados (n=12 por grupo) foram submetidos aos testes de Kruskal-Wallis e Mann-Whitney (p=0,05). Uma única irradiação com 20 ou 40 mW/cm2 aumentou a viabilidade celular, a qual foi negativamente afetada após 3 irradiações. Células irradiadas apenas uma vez com 20 mW/cm2 produziram mais proteínas comparadas com aquelas irradiadas com 40 mW/cm2. Redução no número de células viáveis ocorreu apenas após 3 irradiações com 40 mw/cm2. Em conclusão, o LED vermelho foi capaz de biomodular a atividade metabólica de células MDPC-23. A melhor bioestimulação celular foi obtida quando uma única irradiação com dose de energia de 2 J/cm2 e densidade de potência de 20 mW/cm2 foi administrada às células pulpares.

Dysregulation of glucose metabolism in tumorigenesis and tumor progression / 中国生化药物杂志

Dysregulation of cell metabolism, especially glucose metabolism, is implicated in tumorigenesis and tumor progression.Cancer cells uptake a large amount of glucose and prefer to perform glycolysis in the cytosol even under normal oxygen condition, which fuels fast cell growth and proliferation.Dysregulation of glucose metabolism leads to tumorigenesis and promotes cancer development.Conversely, the initiation and development of cancer reprograms glucose metabolism to confer cancer cells the ability to survive and proliferate.Oncogenes, tumor suppressors or non-coding RNAs could regulate glucose metabolism.Meanwhile, the enzymes and metabolites involved in glucose metabolism could regulate the expression of factors related to cancer.Enzymes, the direct executor of cell metabolism, play a key role in dysregulation of glucose metabolism, tumorigenesis and tumor development.

Expression of Ezrin and phos-ezrin in skin squamous carcinomas and its clinical significance / 中国医师杂志

Objective To investigate the expressions of Ezrin and phos-ezrin in squamous cell carcinomas (SCC),and to an alyze their clinic significance.Methods Immunohistochemistry was used to detect the expressions of Ezrin and phos-Ezrin in 20 cases of normal skin,31 cases of seborrheic Keratosis (SK),36 cases of basal cell carcinoma (BCC),and 37 cases of SCC.Results (1) The positive rates of Ezrin in normal skin (NS),SK,BCC,and SCC were 20.0％,25.8％,66.7％,and 89.2％,respectively.The positive reates of phos-Ezrin in NS,SK,BCC,and SCC were 10.0 ％,22.6％,77.8％,and 94.6％,respectively.Ezrin and phos ezrin in cancers were higher than that in noncancer tissues (P ＜ 0.01).(2) The expressions of Ezrin,and phos-Ezrin were closely correlated with the cutaneous tumor's type(R1 =0.87,r1 =0.89,P ＜ 0.01),malignant degree (patho-grading of SCC) (R2 =0.80,r2=0.86,P ＜ 0.01),metastasis via lymph node (R3 =0.89,r3 =0.91,P ＜ 0.01).Conclusions Ezrin and phos-Ezrin expressions were closely related to the types of tumor,malignant degrees,and metastasis.The combined-detection of Ezrin and phos-ezrin would provide a novel clue to predicting metastasis and prognosis of cutaneous tumor.

Oct-4 expression in epidermal tumors / 中国医师杂志

Objective The aim of this study was to understand the role of specific markers of stem cells Oct-4 expression in the development of human epidermal non-melanoma cutaneous tumors.Methods The paraffin-embedded samples were retrieved from files of pathology department at our hospital,including 20 cases of skin squamous cell carcinomas (SCC),20 cases of basal cell carcinomas (BCC),20 cases of seborrhoeic keratosis (SK) and 20 cases of normal skin (from head,face,trunk,extremities).The expression of Oct-4 and PCNA were observed by immunohistochemical staining technique.Results Oct-4 protein was abnormally increased in SCC and BCC comparel to normal skin and SK ( P ＜0.05 ).However there were no significant difference of Oct-4 protein expression between SCC and BCC ( P ＞0.05).There were also no significantly different Oct-4 protein expression between Sk and the normal skin ( P ＞ 0.05 ),and no significantly different Oct-4 protein expression between SK and BCC( P ＞0.05 ).PCNA protein was abnormally increased in SCC and BCC compared to normal skin and SK ( P ＜0.01 ).There were significantly different PCNA protein expression between SCC and BCC( P ＜0.05).There were also significantly different PCNA protein expression between SK and the normal skin ( P ＜ 0.05 ).However there were no significant difference of PCNA protein expression between SK and BCC ( P ＞ 0.05 ).There were positive correlation between the expression intensity of Oct-4 and PCNA in SCC and BCC.Conclusions The abnormal expression of Oct-4 may have an important role in the development of BCC and SCC.Positive Oct-4 expression cells may be the tumor stem cell in SCC and BCC.There were positive correlation between the expression intensity of Oct-4 and PCNA in SCC and BCC.The over expression Oct-4 in BCC and SCC may play an important role in proliferation of tumor.

Expression and significance of Twist and E-cadherin and Vimentin in cervical squamous epithelial cancerization / 中国医师杂志

ObjectiveTo explore the expression rule and clinic significance of Twist and E-cadherin and Vimentin in cervical squamous epithelial cancerization.MethodsChronic cervicitis were used as control group,the expression of Twist (using hybridization in situ),E-cadherin and Vimentin( SABC immunohistochemical stain) in tissues of cervical intraepithelial neoplasia (CIN) and cervical squamous carcinoma were detected,and the correlations were analyzed.ResultsThe positive rate of Twist in group of chronic cervicitis,CIN Ⅰ,CINⅡ,CIN Ⅲ and cervical squamous carcinoma was 10.0％,28.1％,29.6％,42.9％ and 64.3％,respectively.The expression rate of Twist in cervical squamous carcinoma group was higher than other groups ( P ＜ 0.05 ).The positive rates of E-cadherin and Vimentin were 80.0％,68.8％,55.6％,51.4％,39.3％ and 0,6.3％,7.4％,31.4％,32.1％,respectively.The difference of E-cadherin and Vimentin expression between the cervical squamous carcinoma ( or CIN Ⅲ group) and the chronic cervicitis group was obvious ( P ＜0.05,respectively).The expression of Twist was negatively correlated with E-cadherin( r =-0.37,P ＜0.01 ),and it was positively correlated with Vimentin in all cases of CIN and cervical squamous carcinoma( r =0.23,P ＜0.05).ConclusionsThere is a close relationship between abnormal expression of Twist and cervical squamous epithelial cancerization.Twist may participate in the genesis of cervical squamous carcinoma through mediating the expression of E-cadherin and Vimentin in cervix tissue.