Project description:To investigate cisplatin chemo-sensitivity in established KYSE 150/510 cell lines in which each target gene has been knocked out by CRISPR-Cas9. We performed gene expression profiling analysis using data obtained from RNA-seq of 8 different cells by three biological replicate.
Project description:Esophageal cancer is one of the most serious health problems globally because of its high incidence and mortality rate. Cisplatin (CDDP) is the primary treatment but limited by the drug resistance. However, the mechanism of cisplatin resistance remains unclear. Herein, the CDDP-resistant cell line TE-1/CDDP was established to compared with TE-1, the expression profiles of circRNAs mRNA and lncRNA were compared between TE-1/CDDP and TE-1 using microarray analysis, and used this as a basis for exploring possible mechanisms of drug resistance in genes such as HDAC9.
Project description:To investigate mRNA expression difference in cisplatin chemo-sensitivity in esophageal squamous carcinoma patients. We performed gene expression profiling analysis using data obtained from RNA-seq of 6 different patients.
Project description:Salvia chinensia Benth. (Shijianchuan in Chinese, SJC) has been used as a traditional anti-cancer herb. SJC showed good anti-esophageal cancer efficacy based on our clinical application. However, the current research on SJC is minimal, and its anti-cancer effect lacks scientific certification. This study aims to clarify the inhibitory effect of SJC on esophageal cancer and explore its underlying mechanism. Q-Orbitrap high-resolution LC/MS was used to identify the primary chemical constituents in SJC. Cell proliferation and colony formation assays showed that SJC could effectively inhibit the growth of esophageal tumor cells in vitro. To clarify its mechanism of action, proteomic and bioinformatic analyses were carried out by combining tandem mass labeling and two-dimensional liquid chromatography-mass spectrometry (LC-MS). The results indicated that SJC could activate AMPK signaling pathway and effectively promote autophagy in esophageal cancer cells. Therefore, we further used WB to confirm that SJC activated autophagy in esophageal cancer cells through the AMPK / ULK1 signaling pathway. The results showed that P-AMPK and P-ULK1 were significantly up-regulated after the treatment with SJC. The ratio of autophagosomes marker proteins LC3II/I was significantly increased. In addition, the expression of the autophagy substrate protein P62 decreased with the degradation of autophagosomes. Using lentiviral transfection of fluorescent label SensGFP-StubRFP-LC3 protein and revalidation of LC3 expression before and after administration by laser confocal microscopy. Compared with the control group, the fluorescence expression of the SJC group was significantly enhanced, indicating that it promoted autophagy in esophageal cancer cells. Cell morphology and the formation of autophagosomes were observed by transmission electron microscopy. Our study shows that the tumor suppressor effect of SJC is related to promoting autophagy in esophageal tumor cells via the AMPK/ULK1 signaling pathway.
Project description:Cisplatin is used in chemotherapy of prostate, ovary and other cancer types but unfortunately the efficiency of cisplatin treatment is frequently hampered by acquired resistance. The cytotoxic effect of cisplatin has been attributed to its binding to DNA. HMGB1 is able to bind to cisplatin-DNA adducts with high affinity and its expression levels are associated with cisplatin resistance. This study reports the interactome of HMGB1 in prostate and ovarian cancer cells treated with cisplatin.
Project description:We konckout PARK2 in Esophageal Squamous Cell Cancer Cell Line EC9706 and then detected differentially expressed genes We konckout PARK2 in Esophageal Squamous Cell Cancer Cell Line EC9706 and then detected differentially expressed genes