Search

Your search keyword '"Rongcheng, Luo"' showing total 2 results
Start Over Author "Rongcheng, Luo" Journal molecular cancer
2 results on '"Rongcheng, Luo"'

1. MiR-661 promotes tumor invasion and metastasis by directly inhibiting RB1 in non small cell lung cancer

Author

Feiye Liu, Yanjun Cai, Xiaoxiang Rong, Jinzhang Chen, Dayong Zheng, Lu Chen, Junyi Zhang, Rongcheng Luo, Peng Zhao, and Jian Ruan

Subjects
miR-661, Non small cell lung cancer, RB, E2F1, Metastasis, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Abstract Background Aberrant microRNA expression has been implicated in metastasis of cancers. MiR-661 accelerates proliferation and invasion of breast cancer and ovarian cancer, while impedes that of glioma. Its role in non small cell lung cancer (NSCLC) and underlying mechanism are worthy elucidation. Methods Expression of miR-661 was measured with real-time PCR in both NSCLC tissues and cell lines. The effects of miR-661 on migration, invasion and metastasis capacity of NSCLC were evaluated using wound healing, transwell assay and animal models. Dual reporter luciferase assay and complementary experiments were performed to validate RB1 as a direct target of miR-661 for participation in the progression of NSCLC. Results MiR-661 was upregulated in NSCLC tissues as compared to paired adjacent tissues and associated with shorter overall survival. Furthermore, miR-661 promoted proliferation, migration and metastasis of NSCLC. Then, we identified RB1 as a direct target of miR-661 through which miR-661 affected EMT process and metastasis of NSCLC. RB1 interacted with E2F1 and both could mediate EMT process in NSCLC. Conclusion MiR-661 promotes metastasis of NSCLC through RB/E2F1 signaling and EMT events, thus may serves as a negative prognostic factor and possible target for treatment of NSCLC patient.

Published
2017
Full Text
View/download PDF

2. Over-expression of cathepsin B in hepatocellular carcinomas predicts poor prognosis of HCC patients

Author

Jian Ruan, Weijia Fang, Xiaomin Rong, Peng Zhao, Haiyan Zheng, Junyi Zhang, Rongcheng Luo, and Xiaodong Rong

Subjects
Male, 0301 basic medicine, Oncology, Cancer Research, Carcinogenesis, Hepatocellular carcinoma, medicine.disease_cause, Cathepsin B, Phosphatidylinositol 3-Kinases, Prognostic marker, 0302 clinical medicine, Cell Movement, Mice, Inbred BALB C, Liver Neoplasms, Middle Aged, Prognosis, Immunohistochemistry, Treatment Outcome, Matrix Metalloproteinase 9, 030220 oncology & carcinogenesis, Molecular Medicine, Female, Signal Transduction, medicine.medical_specialty, Carcinoma, Hepatocellular, Mice, Nude, Biology, 03 medical and health sciences, Gentamicin protection assay, Cell Line, Tumor, Internal medicine, medicine, Carcinoma, Animals, Humans, Neoplasm Invasiveness, Proportional Hazards Models, Oncogene, Research, medicine.disease, Survival Analysis, 030104 developmental biology, Tumor progression, Cancer research, Proto-Oncogene Proteins c-akt
Abstract

Background Several studies have found that Cathepsin B (CTSB) is up-regulated in many tumor types and facilitates tumor progression. However, the role of CTSB in hepatocellular carcinoma (HCC) progression remains unclear. This study was aimed at investigating the expression and role of CTSB in HCC in a large set of samples and cell lines (MHCC-97H and MHCC-97 L), and evaluating the clinical and prognostic significance of CTSB protein in patients with HCC. Methods The expression of CTSB was examined in HCC tissue and cell lines by Western-blotting, Real-time PCR, and immunohistochemical staining. Wound healing assay and invasion assay were used to verify the effect of CTSB on the migration and invasion ability of HCC cell lines. Tumor formation assay in nude mice was used to analyze the effect of CTSB on the tumorigenicity of HCC cell lines. Results The status of CTSB protein in carcinoma tissues is much higher than that in paracarcinoma tissues. The overall survival of the patients with high CTSB expression was significantly shorter than the low CTSB expression group. High CTSB expression was significantly correlated with advanced clinical staging, histological grade, and tumor recurrence. In vitro and in vivo experiments demonstrated that over-expression of CTSB in MHCC-97 L cells promoted cell invasion and tumor progression ability. Down-regulation of CTSB in MHCC-97H showed the opposite effects. These phenotypic changes caused by CTSB knockdown or over-expression correlated with expression of the matrix metallopeptidase MMP-9. Moreover, multivariate analysis suggested that CTSB expression might be an independent prognostic indicator for the survival of HCC patients after curative surgery. Conclusions CTSB might be involved in the development and progression of HCC as an oncogene, and thereby may be a valuable prognostic marker for HCC patients. Electronic supplementary material The online version of this article (doi:10.1186/s12943-016-0503-9) contains supplementary material, which is available to authorized users.

Published
2016
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results