Background: To understand the carcinogenesis caused by accumulated genetic and epigenetic alterations and seek novel biomarkers for various cancers, studying differentially expressed genes between cancerous and normal tissues is crucial. In the study, two cDNA libraries of lung cancer were constructed and screened for identification of differentially expressed genes. Methods: Two cDNA libraries of differentially expressed genes were constructed using lung adenocarcinoma tissue and adjacent nonmalignant lung tissue by suppression subtractive hybridization. The data of the cDNA libraries were then analyzed and compared using bioinformatics analysis. Levels of mRNA and protein were measured by quantitative real-time polymerase chain reaction (q-RT-PCR) and western blot respectively, as well as expression and localization of proteins were determined by immunostaining. Gene functions were investigated using proliferation and migration assays after gene silencing and gene over-expression. Results: Two libraries of differentially expressed genes were obtained. The forward-subtracted library (FSL) and the reverse-subtracted library (RSL) contained 177 and 59 genes, respectively. Bioinformatic analysis demonstrated that these genes were involved in a wide range of cellular functions. The vast majority of these genes were newly identified to be abnormally expressed in lung cancer. In the first stage of the screening for 16 genes, we compared lung cancer tissues with their adjacent non-malignant tissues at the mRNA level, and found six genes (ERGIC3, DDR1, HSP90B1, SDC1, RPSA, and LPCAT1) from the FSL were significantly up-regulated while two genes (GPX3 and TIMP3) from the RSL were significantly down-regulated (P < 0.05). The ERGIC3 protein was also over-expressed in lung cancer tissues and cultured cells, and expression of ERGIC3 was correlated with the differentiated degree and histological type of lung cancer. The up-regulation of ERGIC3 could promote cellular migration and proliferation in vitro.

Cisplatin (cis-dichlorodiamine platinum, CDDP) is a potent antitumor agent. However, its clinical application is limited by its side effects and the development of drug resistance. Tannic acid (TA) has previously been reported to suppress tumor growth in different types of cancer. The present study evaluated the anticancer efficacy of TA in combination with CDDP on the liver cancer cell line HepG2, and investigated the associated underlying molecular mechanisms. The results revealed that treatment with TA or CDDP alone inhibited HepG2 cell growth, with a half maximal inhibitory concentration of 360 µM and 1.8 µg/ml, respectively. The combination of TA and CDDP induced mitochondria-mediated apoptosis in HepG2 cells and significantly enhanced the growth inhibitory effect compared with TA or CDDP treatment alone. The results obtained from the present study suggest that the combination of TA and CDDP may exert synergistic anticancer effects and may be a novel adjuvant treatment for liver cancer.