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You Y.,Pathological Examination and Research Center | You Y.,Luohe Medical College | Li H.,The Second Peoples Hospital of Neijiang City | Qin X.,Hubei University of Arts and Science | And 2 more authors.
Cellular Oncology | Year: 2016

Background: Recently, we identified the esophageal carcinoma related gene 4 (ECRG4) as a novel candidate tumor suppressor gene and a promising therapeutic target in nasopharyngeal carcinoma (NPC). In addition, we found that reduced ECRG4 expression in NPC was associated with promoter hypermethylation. The aim of the current study was to assess the expression status of the ECRG4 protein in breast cancer and to clarify its clinicopathological significance and potential prognostic implications. Methods: Western blotting was used to examine ECRG4 protein levels in 20 paired breast cancer tissues and adjacent noncancerous tissues. In addition, we performed ECRG4 immunohistochemistry on 113 clinicopathologically well-characterized breast cancer samples and assessed putative associations between its expression and overall patient survival rates. Results: We found that ECRG4 protein expression was significantly reduced in the breast cancer tissues compared to the noncancerous tissues. Clinicopathological analyses revealed that loss of ECRG4 protein expression, observed in 41.6 % (47/113) of the primary breast cancer tissues tested, was significantly correlated with lymph node metastasis (P = 0.026), advanced tumor stage (P = 0.042) and unfavorable overall survival (P = 0.004). Additional multivariate analyses revealed that ECRG4 protein expression may serve as an independent prognostic factor for the prediction of patient survival (P = 0.033). Conclusion: Our data suggest that loss of ECRG4 protein expression may be involved in tumor progression and may serve as a prognostic biomarker for breast cancer. © 2015, International Society for Cellular Oncology. Source


You Y.,Pathological Examination and Research Center | You Y.,Luohe Medical College | You Y.,Luohe Key Laboratory of Medical Bioengineering | Li H.,The Second Peoples Hospital of Neijiang City | And 5 more authors.
Cellular Oncology | Year: 2015

Background: Cyclin-dependent kinase 10 (CDK10) has recently been identified as a tumor suppressor and, concordantly, its encoding gene has frequently been found to be inactivated in various human cancers. Here, we examined the expression status of CDK10 in a panel of primary human breast cancers and evaluated its correlation with clinicopathological parameters and clinical outcome. Methods: Western blotting was used to assess CDK10 protein levels in 20 paired breast cancer tissues and adjacent noncancerous tissues. In addition, immunohistochemistry was performed in 128 formalin-fixed, paraffin-embedded tumor tissues. Associations of CDK10 expression with various clinicopathological parameters were evaluated and Kaplan-Meier survival analyses and Cox proportional hazards models were used to estimate its effect on patient survival. Results: We found that CDK10 protein expression was markedly decreased in cancer tissues compared to adjacent noncancerous tissues. Immunohistochemistry revealed decreased CDK10 levels in 65/128 (50.8 %) of the primary breast cancer tissues tested. These decreased levels were found to be significantly associated with lymph node metastasis (P = 0.003), advanced tumor stage (P < 0.001) and unfavorable overall survival (P < 0.001). Furthermore, multivariate analyses indicated that CDK10 expression may serve as an independent prognostic factor for survival (P = 0.001). Conclusion: Down-regulated CDK10 expression frequently occurs in breast cancers and correlates with disease progression and poor survival. CDK10 may serve as a prognostic biomarker for breast cancer. © 2015, International Society for Cellular Oncology. Source


Gao F.-L.,Zhengzhou University | Gao F.-L.,Pathological Examination and Research Center | Liu C.-L.,Pathological Examination and Research Center | Li W.-S.,Pathological Examination and Research Center | Zhao G.-Q.,Zhengzhou University
World Chinese Journal of Digestology | Year: 2010

AIM: To investigate the effects of B-cell-specific Moloney murine leukaemia virus insertion site 1 (Bmi-1) gene knock-down on cell senescence and migration in human gastric caner cell line BGC823. METHODS: Two pairs of complementary small hairpin RNA (shRNA) oligonucleotides targeting the Bmi-1 gene were devised, synthesized, annealed and cloned into the pRNAT-U6.2 vector. After DNA sequencing to verify the correct insertion of the shRNA sequences, the recombinant plasmids were transfected into BGC823 cells. The expression of Bmi-1 mRNA transcription-polymerase chain reaction (RT-PCR) and Western blot, respectively. The effects of Bmi-1 knockdown on cell senescence and migration were determined by β-Gal activity assay and Boyden chamber assay, respectively. RESULTS: The double-stranded shRNA oligonucleotides targeting the Bmi-1 gene were successfully cloned into the pRNAT-U6.2 vector. DNA sequencing results verified the correct insertion of the shRNA sequences. RT-PCR and Western blot analyses indicated that the expression levels of Bmi-1 mRNA and protein were significantly downregulated in cells transfected with the recombinant plasmids. Particularly, Bmi-1 protein expression was almost completely abolished in cells transfected with the recombinant vector harboring shRNA targeting the sequence GGAGGAGGTGAATGATAAA (nt 1 104-1 122). Compared with untransfected cells and cells transfected with the empty vector, the average percentage of senescent cells increased and the number of cells passing through the Matrigel decreased in cells transfected with the recombinant vectors. CONCLUSION: ShRNA-mediated silencing of the Bmi-1 gene can effectively promote cell senescence and reduce migration in human gastric caner cell line BGC823. Source


Gao F.-L.,Pathological Examination and Research Center | Gao F.-L.,Zhengzhou University | Li W.-S.,Pathological Examination and Research Center | Liu C.-L.,Pathological Examination and Research Center | And 2 more authors.
World Journal of Gastroenterology | Year: 2013

AIM: To evaluate the impact of Bmi-1 on cell senescence and metastasis of human gastric cancer cell line BGC823.METHODS: Two pairs of complementary small hair pin RNA (shRNA) oligonucleotides targeting the Bmi-1 gene were designed, synthesized, annealed and cloned into the pRNAT-U6.2 vector. After DNA sequencing to verify the correct insertion of the shRNA sequences, the recombinant plasmids were transfected into BGC823 cells. The expression of Bmi-1 mRNA and protein was examined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. The effects of Bmi-1 knockdown on cell senescence and metastasis were determined by the β-Gal activity assay and Boyden chamber assay, respectively.RESULTS: The double-stranded oligonucleotide fragments of Bmi-1 short interfering RNA (siRNA) cloned into pRNAT-U6.2 vector conformed to the inserted sequence. RT-PCR and Western blotting indicated that the expression levels of Bmi-1 gene mRNA and protein were markedly decreased in transfected BGC823 cells with pRNAT-U6.2-si1104 and pRNAT- U6.2-si1356, especially in transfected BGC823 cells with pRNAT-U6.2-si1104, compared with two control groups (empty vector and blank group). In particular, Bmi-1 protein expression was almost completely abolished in cells transfected with the recombinant vector harboring shRNA targeting the sequence GGAGGAGGTGAATGATAAA (nt1104-1122). Compared with untransfected cells and cells transfected with the empty vector, the mean percentage of senescent cells increased and the number of cells passing through the Matrigel decreased in cells transfected with the recombinant vectors.CONCLUSION: Silencing Bmi-1 by RNA interference can increase the senescent cell rate and effectively reduce the metastasis of gastric cancer cells. © 2013 Baishideng Publishing Group Co., Limited. All rights reserved. Source

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