NET-1 promotes metastasis of lung squamous-cell carcinoma by activating EMT

AIM: To explore the effect of neuroepithelial cell transforming gene-1 (NET-1) expression on the metastasis of lung squamous-cell carcinoma (LSC) and the underlying molecular mechanism. METHODS: Immunohistochemistry was used to detect the expression of NET-1 protein in 53 cases of lung squamous-cell carcinoma (LSC group), 24 cases of normal lung epithelium (NLE group) and 27 cases of lung squamous intraepithelial lesions (SIL group). The correlation of clinical and pathological factors was analyzed. The protein expression of NET-1 in human lung squamous-cell carcinoma cell lines H226, H1703, H2170, SK-MES-1, H520 and YTMLC-90 was determined by Western blot. The RNA interference recombinant adenovirus against NET-1 gene (Ad-NET-siRNA) and Ad-control with control sequence were constructed and infected with human lung squamous cell carcinoma cell YTMLC-90 to silence the expression of NET-1 gene. The protein expression of NET-1, E-cadherin, vimentin and Snail1 in the BEAS-2B cells and the YTMLC-90 cells was determined by Western blot. The mRNA expression of E-cadherin and vimentin in each group of the cells was detected by qPCR. The invasive ability of the cells in each group was detected by Transwell chamber assay. RESULTS: The positive expression rate of NET-1 in LSC group was significantly higher than that in NLE group and SIL group(P<0.05). The distribution of NET-1 protein positive expression population was correlated with histological grade, lymph node metastasis, and TNM stage. The NET-1 expression rate of LSC with lymph node metastasis was significantly higher than that without lymph node metastasis. Over-expression of NET-1 protein in YTMLC-90 cells was observed. The expression of E-cadherin was decreased, and the protein expression of vimentin and Snail1 was increased in YTMLC-90 cells. Knock-down of NET-1 expression increased the expression of E-cadherin, and decreased the expression of vimentin and Snail1 in the YTMLC-90 cells. CONCLUSION: The expression of NET-1 promotes the lymphatic metastasis of lung squamous-cell carcinoma. This promotion may be achieved through the activation of epithelial-mesenchymal transition (EMT) by NET-1 expression.     

Progress on genomic aberrations in esophageal squamous-cell carcinoma

Esophageal squamous-cell carcinoma (ESCC) is one of the most common malignancies with poor prognosis in China. Since most clinical confirmation of the patients with ESCC is diagnosed at an advanced stage or with lymph node metastasis, the treatment effect was very poor. With the applications of high-throughput microarray and whole-genome sequencing or whole-exome sequencing, several novel cancer-related genes have been identified and revealed, and these genes may become new biomarkers or therapeutic targets. This review is to summarize the research progress in ESCC genome reported recently.     

Expression of TSTA3 in esophageal squamous-cell carcinoma and its significance

AIM To investigate the expression of TSTA3 in esophageal squamous cell carcinoma (ESCC) and the effects of TSTA3 on the proliferation, invasion and migration abilities of human ESCC cell lines KYSE150 and KYSE450. METHODS The expression of TSTA3 was detected by immunohistochemistry in 45 cases of ESCC and matched adjacent tissues. The mRNA expression levels of TSTA3 in ESCC cells were detected by qPCR. Over-expression of TSTA3 in KYSE150 cells and KYSE450 cells was carried out by lentivirus infection. The effects of TSTA3 on the viability and colony formation ability of ESCC cells were examined by MTT assay and colony formation assay. Transwell assays were performed to detect the effects of TSTA3 on migration and invasion abilities of ESCC cells. The effect of TSTA3 on core fucosylation modification of ESCC cells was analyzed by flow cytometry. RESULTS The expression of TSTA3 in the ESCC tissues was significantly higher than that in matched adjacent tissues (P<0.01). Over-expression of TSTA3 had no effect on the proliferation of ESCC cells (P>0.05), but promoted the migration and invasion of ESCC cells (P<0.01). Moreover, over-expression of TSTA3 increased the core fucosylation modification level of ESCC cells (P<0.01). CONCLUSION TSTA3 may promote the development and progression of ESCC via regualting fucosylation modification level, and serve as a biomarker for early diagnosis and treatment of ESCC.     

Expression of HDAC6 protein in cervical carcinoma tissues and its clinical significance

AIM:To investigate the protein expression of histone deacetylase 6(HDAC6) in cervical carcinoma tissues and its clinical value. METHODS:The method of immunohistochemistry was used to detect the protein expression of HDAC6 in 63 cases of cervical carcinoma tissues, 38 cases of cervical intraepithelial neoplasia(CIN) tissues and 63 cases of normal cervical epithelial tissues. The relationships between the protein expression of HDAC6 and clinical pathological features were analyzed. The protein expression of HDAC6 in randomly selected 4 cases of cervical carcinoma tissues and paired normal cervical epithelial tissues was detected by Western blotting. RESULTS:Positive rates of HDAC6 protein expression in cervical carcinoma tissues were significantly higher than that in CIN tissues or normal cervical epithelial tissues, and there were obvious differences among the 3 groups(P<0.05). The protein expression of HDAC6 was not related to age and histological differentiation(P>0.05), but closely associated with clinical stages, invasive depth and lymph node metastasis(P<0.01 or P<0.05). Furthermore, the result of Western blotting demonstrated that the protein level of HDAC6 in cervical carcinoma tissues was markedly higher than that in normal cervical epithelial tissues. CONCLUSION:HDAC6 may be an important molecular marker for evaluating malignant degree and prognosis of cervical carcinoma.     

Effect of BMP9 over-expression on migration and invasion of human lung squamous-cell carcinoma NCI-H520 cells

AIM: To investigate the effect of bone morphogenetic proteins 9(BMP9) on the migration and invasion abilities of human lung squamous-cell carcinoma NCI-H520 cells and its mechanism. METHODS: The expression of BMP9 at mRNA and protein levels in the NCI-H520 cells and human bronchial epithelial (HBE) cells was detected by RT-PCR and Western blot. The NCI-H520 cells were transfected with the recombinant adenovirus AdBMP9 and the expression of BMP9 at mRNA and protein levels was validated by RT-PCR and Western blot. The migration and invasion abilities of the NCI-H520 cells were determined by wound-healing and Transwell assays. The mRNA and protein levels of the migration-related factor matrix metalloproteinase 2(MMP2) were detected by RT-PCR and Western blot. The level of phosphorylated Smad1/5(p-Smad1/5) was detected by Western blot. Meanwhile, NCI-H520 cells were treated with BMP specific antagonist AdNoggin and AdBMP9. The level of p-Smad1/5 and the cell migration ability were measured by Western blot, wound-healing and Transwell assays. RESULTS: The expression of BMP9 at mRNA and protein levels was lower in NCI-H520 cells than that in HBE cells. After AdBMP9 was stably transfected into the NCI-H520 cells, the expression of BMP9 at mRNA and protein levels was significantly up-regulated, cell migration and invasion abilities were significantly decreased, and the mRNA and protein levels of MMP2 were decreased. Meanwhile, the level of p-Smad1/5 was increased. Noggin reversed BMP9-caused the increase in p-Smad1/5 and the decrease in cell migration ability. CONCLUSION: Over-expression of BMP9 inhibits the migration and invasion abilities of lung squamous-cell carcinoma NCI-H520 cells. The activation of BMP-Smad signaling pathway may be involved in this inhibitory process.     

Effect of long non-coding RNA-671 on proliferation and invasion of esophageal squamous-cell carcinoma cells

AIM: To detect the expression of long non-coding RNA-671 (lnc671) in esophageal squamous-cell carcinoma cell lines and to investigate the effect of lnc671 on the malignant phenotype of esophageal squamous-cell carcinoma cells. METHODS: The level of lnc671 in the esophageal squamous-cell carcinoma cells was detected by RT-qPCR. Specific lnc671 small interfering RNA (siRNA) used to explore the effects of lnc671 on proliferation, colony formation, invasion and migration abilities of esophageal squamous-cell carcinoma cells. RESULTS: The database of GEPIA analysis showed that increased expression of lnc671 was associated with shorter survival in the patients of esophageal cancer (P<0.05). Compared with normal immortalized esophageal epithelial cells, lnc671 was highly expressed in a variety of esophageal squamous-cell carcinoma cell lines. lnc671 knock-down significantly inhibited the growth, colony formation ability, migration and invasion abilities of esophageal squamous-cell carcinoma cells(P<0.01). CONCLUSION: The expression of lnc671 is increased in various esophageal squamous-cell carcinoma cell lines. Knock-down of lnc671 expression inhibits the malignant phenotype of esophageal squamous-cell carcinoma cells.     

FAM3C activates Akt to promote viability of oral squamous-cell carcinoma cells

AIM: To investigate the expression and roles of family with sequence similarity 3, member C (FAM3C) in oral squamous-cell carcinoma cells. METHODS: The mRNA and protein expression levels of FAM3C in dysplastic oral keratinocyte (DOK) and oral squamous-cell carcinoma WSU-HN6 cells were detected by RT-qPCR and Western blot. The WSU-HN6 cells were treated with siFAM3C or FAM3C antibody. After 24, 48 and 72 h, the viability of WSU-HN6 cells was measured by CCK-8 assay, and the activation of protein kinase B (Akt) was detected by Western blot. Adenovirus was used to mediate over-expression of FAM3C in the DOK cells. The DOK cell viability was measured by CCK-8 assay after adenovirus infection for 24, 48 and 72 h, and the activation of Akt was detected by Western blot. RESULTS: Compared with the DOK cells, the mRNA and protein levels of FAM3C were significantly increased in the WSU-HN6 cells (P<0.05). The viability of WSU-HN6 cells transfected with siFAM3C was significantly inhibited at 48 h and 72 h (P<0.05). siFAM3C treatment inhibited the activation of Akt (P<0.05). FAM3C antibody treatment also suppressed the viability of the WSU-HN6 cells at 48 h and 72 h and the activation of Akt (P<0.05). Over-expression of FAM3C in the DOK cells promoted the cell viability at 48 h and 72 h and activated Akt (P<0.05). CONCLUSION: FAM3C might promote oral squamous-cell carcinoma cell growth by activating Akt.     

Silencing of FoxM1 induces apoptosis of oral squamous-cell carcinoma cells by promoting mitochondrial release of cytochrome C

AIM: To study the effect of forkhead box protein M1 (FoxM1) silencing on apoptosis of oral squamous-cell carcinoma. METHODS: Oral squamous-cell carcinoma SCC9 cells were infected with FoxM1-shRNA lentivirus or negative control lentivirus. The silencing effect was measured by RT-qPCR and Western blot. The changes of cell viability effect was measured by MTT saay. The cell colony formation ability was measured by plate experiment. Flow cytometry was used to analyze the changes of apoptotic rate. Western blot was used to measure the protein levels of cleaved caspase-3 and cleaved caspase-9 in the cells. The changes of mitochondrial membrane potential were measured by JC-1 method. Western blot was used to measure the protein level of cytochrome C in the mitochondria and cytoplasm. RESULTS: Infection with FoxM1-shRNA lentivirus successfully reduced the expression of FoxM1 in oral squamous-cell carcinoma cells (P<0.05). Negative control lentivirus had no effect on the expression level of FoxM1 in the cells. The cell viability was reduced by FoxM1 silencing, and the ability of cell colony formation was also decreased. The apoptotic rate and the protein levels of cleaved caspase-3 and cleaved caspase-9 were all increased (P<0.05), and the mitochondrial membrane potential was decreased. The protein level of cytochrome C in the cytoplasm was increased, while the protein level of cytochrome C in the mitochondria was decreased (P<0.05). CONCLUSION: Silencing of FoxM1 induces the apoptosis of oral squamous-cell carcinoma cells by decreasing the mitochondrial membrane potential and promoting the release of cytochrome C from mitochondria.     

Effects of miRNA-25 on proliferation of human esophageal squamous-cell carcinoma cell line TE1

AIM: To investigate the effects and mechanisms of microRNA-25(miRNA-25) on the proliferation of human esophageal squamous-cell carcinoma cell line TE1. METHODS: The abundance of miRNA-25 in different tissues was measured by RT-PCR. After silencing or over-expression of miRNA-25 with mimics or inhibitor in TE1 cells, the cell proliferation, cell cycle distribution and the expression of cyclin E1 and cyclin-dependent kinase 2(CDK2) at mRNA and protein levels were measured by CCK-8 assay, BrdU detection, flow cytometry, RT-PCR and Western blot, respectively. RESULTS: miRNA-25 was prominent in esophageal mucosal tissue and highly expressed in TE1 cells (P<0.05). Over-expression of miRNA-25 increased TE1 cell proliferation, promoted the cell cycle progression and enhanced the entrance of the cells into S phase (P<0.05). Inverse results were obtained after down-regulation of miRNA-25(P<0.05). Furthermore, the expression of cyclin E1 and CDK2 at mRNA and protein levels was significantly increased after over-expression of miRNA-25, but decreased after down-regulation of miRNA-25(P<0.05). CONCLUSION: miRNA-25 enhances cell cycle transition by increasing the expression of cyclin E1 and CDK2, thus accelerating TE1 cell proliferation. This study provides a novel mechanism by which miRNA-25 increases the proliferation of human esophageal squamous-cell carcinoma cell line TE1, suggesting that down-regulation of miRNA-25 may be a potential new therapeutic strategy for treating esophageal squamous-cell carcinoma.     

Clinical significance of STMN1 expression in cervical cancer and effect of inhibition of its expression on viability and apoptosis of cervical cancer SiHa cells

AIM: To investigate the clinical significance of stathmin 1 (STMN1) expression in cervical cancer and the influence of its expression on the viability and apoptosis of cervical cancer cells. METHODS: Western blot was used to detect the protein expression of STMN1 in cervical cancer tissues, and the relationship between the expression and clinical characteristics of cervical cancer was analyzed. STMN1-siRNA was transfected into cervical squamous-cell carcinoma SiHa cells. The protein levels of STMN1, STAT3, p-STAT3 and survivin were determined by Western blot after transfection for 48 h. The cell viability was measured by MTT assay. The apoptosis was analyzed by flow cytometry. DCFH-DA probe was used to detect the level of reactive oxygen species (ROS). RESULTS: The protein expression of STMN1 in cervical cancer tissues was significantly higher than that in paracancerous tissues (P<0.01). The STMN1 protein expression level was not correlated with age and histological types of cervical cancer patients, but was related to clinical stage, histological differentiation and lymph node metastasis (P<0.01). Transfection with STMN1-siRNA significantly reduced the expression of STMN1 in SiHa cells. Compared with control group, the cell viability in STMN1-siRNA group was significantly decreased, the apoptotic rate and ROS content were increased, and the protein levels of p-STAT3 and survivin were down-regulated (P<0.01). However, no significant difference of the STAT3 protein level was observed between STMN1-siRNA group and control group. CONCLUSION: STMN1 is highly expressed in cervical cancer, and its expression is related to clinical stage, histological differentiation and lymph node metastasis. Inhibition of STMN1 expression reduces the viability and promotes apoptosis of cancer cells by down-regulating STAT3 signaling pathway.     

FERMT2 expression in hepatocellular carcinoma and its effect on cell growth

AIM: To identify the expression of fermitin family homolog 2 (FERMT2) in hepatocellular carcinoma (HCC) tissues and the effect of FERMT2 on the cell growth and related protein expression. METHODS: Real-time PCR and immunohistochemistry were used to detect FERMT2 expression in the HCC tissues. The technique of CRISPR/Cas9 was applied to construct stable FERMT2 knockout MHCC97H cell line. WST-1 assay and flow cytometry were used to measure the cell viability, cell-cycle distribution and cell apoptosis. Western blot was used to determine the expression of related proteins in the MHCC97H cells. RESULTS: In HCC tissues, the expression level of FERMT2 was higher than that in adjacent liver tissues (P<0.05). High expression of FERMT2 was significantly correlated with postoperative recurrence of tumor. Knockout of FERMT2 gene evidently inhibited MHCC97H cell viability and accelerated cell apoptosis. Meanwhile, the expression levels of proliferating cell nuclear antigen, cyclins, cyclin-dependent kinases 2 and anti-apoptotic factors were significantly downregulated in MHCC97H cells with FERMT2 knockout (P<0.05). CONCLUSION: FERMT2 may function as a promoter of hepatocarcinogenesis and progression via regulating the cell viability, cell-cycle distribution and cell apoptosis, which is related with the expression of cell cycle regulators and anti-apoptotic factors.     

Protein and mRNA expression of KAI1 metastasis suppressor gene and its clinical significance in cervical carcinoma

AIM: To study the mRNA and protein expression of Kang ai1 (KAI1) tumor suppressor gene and to determine the relationship between KAI1 and invasiveness and metastasis of cervical cancer. METHODS: The expression of KAI1 metastasis suppressor was detected by immunohistochemistry in paraffin slides and by real-time quantitative polymerase chain reaction (RT-PCR) in fresh tissue. The samples included 20 cases of normal cervical tissues, 20 cases of cervical intraepithelial neoplasia (CIN) and 40 cases of cervical carcinoma. The results of the gene expression combined with the pathological and clinical data were also analyzed. RESULTS: The expression of KAI1 protein and mRNA was related to the tissue differentiation of cervix. The positive rates of KAI1 expression were the highest in the normal cervical tissue, the middle in CIN and the lowest in cervical carcinoma with significant difference among three groups (P<0.01). The expression of KAI1 protein was not related with the grade of CIN (P>0.05). However, both mRNA and protein expression of KAI1 were related to the differentiation and the clinical stages of cervical cancer (P<0.01) and also related to the metastasis of the cancer. The positive rates between the non-lymphatic metastasis and lymphatic metastasis (P<0.05) were significant different. Cox regression and logistic regression showed that the tissue differentiation, clinical stages, lymphatic metastasis and expression of KAI1 were all related factors with recurrence and prognosis of cervical cancer. CONCLUSION: The down-regulation of KAI1 tumor suppressor gene at both mRNA and protein levels is related to the differentiation, clinical stages and metastasis of cervical cancer, indicating that the expression of KAI1 is a prognostic factor for cervical cancer.     

Effects of Smo gene silencing on cell activity and apoptosis of human cervical carcinoma HeLa cells

AIM: To investigate the effect of Hedgehog (Hh) signaling pathway on the viability and apoptosis of cervical carcinoma cells by shRNA technique to knock down Smoothened (Smo) gene. METHODS: Smo shRNA was used to transfect the cervical carcinoma HeLa cells. The expression of Smo and Gli1 at mRNA and protein levels in the HeLa cells was determined by RT-PCR and Western blot, respectively. The effect of Smo gene silencing on the growth of the cells was measured by MTT assay. The apoptosis and cell cycle were determined by flow cytometry. RESULTS: Compared with control group, the mRNA and protein expression of Smo and Gli1 were evenly reduced obviously after transfected with Smo shRNA for 72 h (P<0.05). The viability of HeLa cells transfected with Smo shRNA was significantly inhibited. The percentages of the cells in G₀/G₁ phase and early apoptosis rate were obviously higher in Smo shRNA transfection group than those in control group. CONCLUSION: Smo gene silencing effectively inhibits the cell growth and induces the apoptosis of human cervical carcinoma cells.     

Roles of atypical chemokine receptors in progression and metastasis of tumor

Chemokines and their receptors have been implicated mostly in tumor progression and metastasis. Atypical chemokine receptors (ACKRs) comprise a group of 7-transmembrane domain proteins structurally similar to G protein-coupled receptors. However, ACKRs do not induce classical signaling via the typical G protein-mediated pathways. ACKRs efficiently internalize the cognate chemokine ligands and act as scavengers instead. ACJRs are composed of at least 3 members of chemokine receptors:Duffy antigen receptor for chemokines (DARC, also known as ACKR1), D6 (also known as ACKR2) and ChemoCentryx chemokine receptor (CCX-CKR, also known as ACKR4). These receptors bind to and/or internalize their chemoattractant ligands without activating signal transduction cascades leading to cell migration. In this review, we summarize the recent progress regarding the roles of ACKRs in the progression and metastasis of tumor.     

Progress of ELMO family on malignant tumor invasion and metastasis

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 malignant tumor cell invasion and metastasis. In this paper, we review the progress of the relationship between ELMO family and malignant tumor invasion and metastasis.     

Over-expression of SATB1 mediates invasion and metastasis of nasopharyngeal carcinoma cells through epithelial-mesenchymal transition

AIM:To analyze the high expression of special AT-rich sequence-binding protein 1 (SATB1) in nasopharyngeal carcinoma (NPC) and its role in tumor invasion and metastasis. METHODS:The method of immunohistochemistry was used to detect the expression of SATB1 and epithelial-mesenchymal transition (EMT)-related molecules E-cadherin and vimentin in 76 cases of NPC and 61 cases of nasopharyngeal chronic inflammation (NPI), and the correlations of over-expression of SATB1 with NPC patients' clinical parameters as well as the expression of E-cadherin and vi-mentin were analyzed. Variously differentiated NPC cell lines CNE1, CNE2Z and C666-1 were cultured in vitro, and then SATB1-overexpressing cell line was screened. After interfering with SATB1 expression by siRNA, the expression of EMT-related molecules and the change of cell invasiveness were analyzed. RESULTS:The expression of SATB1 in the nasopharyngeal tissue was dominantly localized in the nuclei. The positive rate of SATB1 in NPC group was significantly higher than that in NPI group (P<0.01). E-cadherin was membrane-positive in NPI epithelial cells, while membrane E-cadherin in NPC was decreased but cytoplasmic expression was increased. The positive expression rate of membrane E-cadherin in NPI was significantly higher than that of NPC (P<0.01). Vimentin was localized in cytoplasm and negative in NPI epithelial cells, but the positive rate in NPC parenchymal cells was significant higher than that in NPI (P<0.01). The high expression of SATB1 in NPC was not related to the patents' sex, age, clinical classification and N classification, but positively correlated with T and M classification (P<0.05). Besides, high expression of SATB1 was positively correlated with vi-mentin in NPC tissues (r=0.358, P=0.009). SATB1 expression in NPC cell lines was negatively correlated with the levels of cell differentiation. Knockdown of SATB1 expression in C666-1 cells with siRNA was accompanied by an increase in E-cadherin and a decrease in vimentin levels, as well as a decrease in cell invasiveness. CONCLUSION:High expression of SATB1 promotes the clinical progress of NPC through EMT mechanism.     

Expression of SCD-1 in cervical carcinoma and effect of its down-regulation on proliferation and apoptosis of cervical carcinoma cells

AIM:To examine the expression of stearoyl-CoA desaturase-1 (SCD-1) in normal cervical tissues, cervical squamous cell carcinoma tissues, and cervical carcinoma cell lines HeLa, SiHa and CaSki, and to investigate the effect of down-regulation of SCD-1 on the proliferation and apoptosis of cervical carcinoma cells. METHODS:The expression of SCD-1 was detected by Western blotting in normal cervical tissues, cervical squamous cell carcinoma tissues, and cervical carcinoma cell lines HeLa, SiHa and CaSki. SCD-1 siRNA and control siRNA were utilized to transfect CaSki cells by Lipofectamine 2000, and SCD-1 protein level was determined by Western blotting after transfection. Furthermore, CCK-8 and flow cytometry were utilized to investigate the changes of cell proliferation and apoptosis after transfection with SCD-1 siRNA in CaSki cells. Subsequently, the activities of caspase-3 and caspase-9 were analyzed by Caspase-Glo3/7 and 9 detection kit after transfection with SCD-1 siRNA in CaSki cells. Finally, the protein expression of Bcl-2 and Bax was detected by Western blotting. RESULTS:The protein expression of SCD-1 in cervical squamous cell carcinoma tissues was significantly higher than that in normal cervical tissues, and the protein expression of SCD-1 in the 3 cervical carcinoma cell lines was obviously higher than that in normal cervical tissues, in which CaSki cells displayed the highest SCD-1 protein level. In addition, the protein expression of SCD-1 in SCD-1 siRNA group was significantly lower than that in untreated group and control siRNA group. Compared with untreated group and control siRNA group, the proliferation of CaSki cells was markedly inhibited in SCD-1 siRNA group. Early apoptotic rate in SCD-1 siRNA group was evidently higher than that in untreated group and control siRNA group. The activities of caspase-3 and caspase-9, and the level of Bax protein were significantly elevated, and the protein level of Bcl-2 was obviously reduced after transfection with SCD-1 siRNA in CaSki cells. CONCLUSION: SCD-1 may play an important role in the occurrence and development of cervical carcinoma, and its down-regulation, which mediates cell proliferation inhibition and apoptosis, may be tightly associated with the activities of caspase-3 and caspase-9, and the protein expression of Bcl-2 and Bax.     

Ectopic hCG in endometrial carcinoma and its effect on COX-2 expression

AIM: To investigate the effect of human chorionic gonadotropin(hCG) on cyclooxygenase-2(COX-2) expression in endometrial carcinoma so as to study the function of ectopic hCG.METHODS: The ectopic β-hCG in JEC endometrial carcinoma cell lines was quantified by radioimmunoassay. By MTT assay, the effect of hCG on the cell viability of JEC cell lines and the inhibition of selective COX-2 inhibitor NS398 on JEC cell lines were examined. The effect of hCG on COX-2 expression was detected by Western blotting. RESULTS: The ectopic β-hCG release from cultured JEC cell lines were observed. HCG promoted the cell viability, upregulated the expression of COX-2 protein and increased the inhibition of selective COX-2 inhibitor NS398 in JEC cell lines. CONCLUSION: The ectopic hCG in JEC endometrial carcinoma cell lines increases cell proliferation, which may be mediated by upregulating the expression of COX-2 protein.