Publications by authors named "Bang-Yin Li"
[Effect of overexpression of Smad7 gene on cell proliferation].
Zhonghua Zhong Liu Za Zhi
September 2004
Objective: To study the effect of overexpression of Smad7 gene on cell proliferation in human bronchial epithelial cell lines.
Methods: Human bronchial epithelial cell lines, BEP2D and BERP35T2 cells, were cotransfected with the mammalian expression vectors PCISmad7.neo and pMyc-SEAP, the latter was ac-myc cis-acting enhancer element fused with alkaline phosphatase (SEAP) reporter gene.
Objective: To investigate the change of expression of methylthioadenosine phosphorylase (MTAP) gene in patients with non-small cell lung cancer and its clinical significance.
Methods: Thirty fresh samples of cancer with adjacent tissues were collected from 15 patients with lung cancer, 12 males and 8 females, aged 53.6 (38 approximately 72), 8 with squamous cell carcinoma and 7 with adenocarcinoma.
Background & Objective: Maspin, a serepin inhibitor, plays a key role in tumor growth and metastasis. The aim of this study was to identify the differential expression of Maspin in malignant transformation process of bronchial epithelial cells by proteomics.
Methods: Functional proteomics analysis of Maspin on bronchial epithelial immortalized cells and malignant transformation cells was carried out using immobilized pH gradient (IPG) two-dimensional electrophoresis, peptide mass fingerprinting (PMF), and post source decay (PSD) of bio-mass spectrometry.
Article Synopsis
- Research suggests that the ability of cancer cells to escape the growth-inhibiting effects of TGF-beta may contribute to tumor development, with Smad7 playing a critical role in this process.
- The study involved analyzing Smad7 mRNA expression and its regulation by TGF-beta 1 in BEP2D cells, using various laboratory methods like RNA extraction and protein analysis.
- Results indicated that Smad7 expression increased in BEP2D cells upon TGF-beta 1 stimulation, while BERP35T-2 cells showed lesser changes, pointing to a potential mechanism behind radiation-induced lung cancer.