Project description:Cbx7 knockdown resulted in increase of genes related with apoptosis and inflammation. Expression microarray was performed using RNA extracted from 2 ovarian clear cell adenocarcinoma cell lines, namely, KOC-7C and TOV21G, either trancduced by Cbx7 siRNA or control.
Project description:We conduct an experiment where CBX7 is knocked down in 4 different cell lines: A549, H1299, K562 and THP-1. After culturing these cell lines for three days with or without knockdown of CBX7, we then perform RNA sequencing (RNA-seq) to assess the impact.
Project description:In lung adenocarcinoma (LUAD), metastasis is a leading cause of mortality and notably tends to occur at an early stage of the disease. CBX7, a component of canonical Polycomb Repressive Complex 1 (PRC1) which mediates transcriptional repression, exhibits complex and context-dependent functions across different types of cancer. However, the roles of CBX7 in LUAD metastasis remain largely uncharacterized. Here we report that overexpression of CBX7 promotes, whereas its knockdown suppresses, LUAD cell migration and invasion in vitro. In vivo studies further confirm the pro-metastatic role of CBX7 in LUAD. Mechanistically, CBX7 suppresses the expression of SOCS3, which has been reported to be involved in cancer cell migration and invasion. At the molecular level, CBX7 binds to SOCS3 transcription start site (TSS) downstream region to establish monoubiquitination of histone H2A at lysine 119 (H2AK119ub), leading to transcriptional repression of SOCS3. Furthermore, knockdown of SOCS3 rescues the reduced migration and invasion caused by CBX7 depletion in LUAD cells. Together, our findings identify CBX7 as a positive regulator of LUAD metastasis and suggest its potential as a therapeutic target for LUAD treatment.
Project description:ARID1A, which encodes a component of the SWI/SNF chromatin-remodeling complex, is commonly mutated in ovarian clear cell carcinoma and many other cancer types. We used label-free LC-MS/MS to identify ARID1A-dependent proteome changes in ovarian clear cell carcinoma cell lines. In our first analysis, we compared ARID1A-wildtype ovarian clear cell carcinoma cell line OVCA429 with or without ARID1A CRISPR knockout. In a complementary analysis, we compared ARID1A-mutated ovarian clear cell carcinoma cell line OVISE with or without ARID1A overexpression using a tet-inducible promoter.
