Project description:Colorectal cancer (CRC) is the third most common cancer in the world and the second leading cause of cancer-related deaths. However, there are few effective therapeutic targets for colorectal cancer. Here, we report that Capping Actin Protein, Gelsolin Like (CAPG), a protein involved in actin related movement, is significantly overexpressed in human CRC tissues, and that expression levels are inversely correlated with overall survival. CAPG knockdown CRC cell lines inhibited cell proliferation, blocked cell cycle in G1 phase, increased apoptosis rate and promoted the occurrence of ferroptosis. RNA-seq data suggested that CAPG silencing promotes cell cycle arrest, apoptosis, and ferroptosis by activating the P53 pathway. Therefore, CAPG has potential to serve as a prognostic marker as well as a cancer therapy target in the future.
Project description:We discovered, through mining TCGA data and conducting CRISPR screens, that DUSP18 expression within tumor cells significantly influences the immune microenvironment of colorectal cancer.To explore the role of DUSP18 in regulating the immune microenvironment of colorectal cancer (CRC), we established MC38 and HCT116 cell lines with targeted gene knockdown via shRNA and performed RNA-Seq.
Project description:The purpose of this study is to identify miRNAs involved in the pathology of colorectal cancer (CRC) liver metastasis and investigate their underlying mechanisms. A total of 39 miRNAs were identified to be differentially expressed between 16 primary CRC tissues with liver metastases and 16 CRC tissues without liver metastases from 32 patients by Affymetric miRNA microarrays. 16 coloretcal cancer tissues with liver metastasis and 16 colorectal cancer tissues without liver metastasis were included in this study for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify the differentially expressed miRNAs between colorectal cancer tissues with and without liver metastasis.
Project description:Loss of the p53-inducible LINC01021 in p53-proficient CRC cell lines results in increased sensitivity to DNA-damaging chemotherapeutics. Here, we comprehensively analyzed how LINC01021 affects the p53-induced transcriptional program. Using a CRISPR/Cas9-approach we deleted the p53 binding site in the LINC01021 promoter of SW480 colorectal cancer cells and subjected them to RNA-Seq analysis after activation of ectopic p53. RNA affinity purification followed by mass spectrometry was used identify proteins associated with LINC01021.
Project description:We ortho-topically implanted 16 human colorectal cancer (CRC) cell lines onto the cecal walls of nude mice . To identify the genes possibly involved in EMT of CRC, we analyze the EMT related changes with the orthotopic implantation method in vivo in combination with that of gene expression profiles using a cDNA microarray in vitro. We analyzed 16 human colorectal cancer cell lines. For each cell line, the experiments were carried out twice.
Project description:To investigate the presence and abundance of piRNAs in Colorectal Cancer (CRC), we performed deep-sequencing of the small RNA transcriptome of eight human CRC cell lines (HT-115, Caco-2, SW-1417, SW 403, COLO 205, HT-29, HCT 116 and RKO).
Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.
