Project description:LncRNA ENO1-IT1 has been found to be mainly located in the nucleus of colorectal mucosa epithelial cells, which indicates that this lncRNA may be responsible for regulating the expression of target gene. To address whether ENO1-IT1 modulates epigenetic changes genome-wide, we performed chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) in HCT116 cells
Project description:Background: Long noncoding RNAs (lncRNAs) have emerged recently as a new class of genes regulating cellular processes, such as cell growth and apoptosis. The SPRY4 intronic transcript 1 (SPRY4-IT1) is a 708-bp lncRNA on chromosome 5 with a potential functional role in tumorigenesis. The clinical significance of SPRY4-IT1 and the effect of SPRY4-IT1 on cancer progression are unclear. Methods: Quantitative reverse transcriptase PCR (qRT-PCR) was performed to investigate the expression of SPRY4-IT1 in 48 breast cancer tissues and four breast cancer cell lines. Gain and loss of function approaches were used to investigate the biological role of SPRY4-IT1 in vitro. Microarray bioinformatics analysis was performed to identify the putative targets of SPRY4-IT1, which were further verified by rescue experiments, as well as by western blotting and qRT-PCR. Results: SPRY4-IT1 expression was significantly upregulated in 48 breast cancer tumor tissues compared to normal tissues. Additionally, increased SPRY4-IT1 expression was associated with larger tumor size and an advanced pathological stage in breast cancer patients. Knockdown of SPRY4-IT1 significantly suppressed proliferation and caused apoptosis of breast cancer cells in vitro. Furthermore, we discovered ZNF703 was a direct target of SPRY4-IT1 and was downregulated by SPRY4-IT1 knockdown. Moreover, we demonstrated for the first time that ZNF703 is a genetic driver in ER (-) breast carcinoma cells. Conclusions: SPRY4-IT1 is a novel prognostic biomarker and a potential therapeutic candidate for breast cancer. Five samples are analyzed, including three control groups and two small interfering RNA groups
Project description:The functional analysis of RUNX1-IT1 in tumors is relatively lacking, and its role and mechanism in pancreatic have not been reported. RUNX1-IT1 is transcribed from the intron of the RUNX1 gene, which plays an important role in solid tumors, and its abnormal expression is closely associated with cancer progression. However, due to the lack of systematic research, the regulatory mechanism and important downstream targets of RUNX1-IT1 and RUNX1 in PC are unclear. To investigate the downstream pathway of RUNX1-IT1 and RUNX1, we performed RNA-seq using two PANC-1 cell groups: RUNX1-IT1 knockdown and control, and RUNX1 knockdown and control.
Project description:To investigate the function of RUNX1-IT1 in ovarian cancer progression, we constructed ES2 cell lines with knockdown of RUNX1-IT1 and the control group. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.
Project description:Background: Long noncoding RNAs (lncRNAs) have emerged recently as a new class of genes regulating cellular processes, such as cell growth and apoptosis. The SPRY4 intronic transcript 1 (SPRY4-IT1) is a 708-bp lncRNA on chromosome 5 with a potential functional role in tumorigenesis. The clinical significance of SPRY4-IT1 and the effect of SPRY4-IT1 on cancer progression are unclear. Methods: Quantitative reverse transcriptase PCR (qRT-PCR) was performed to investigate the expression of SPRY4-IT1 in 48 breast cancer tissues and four breast cancer cell lines. Gain and loss of function approaches were used to investigate the biological role of SPRY4-IT1 in vitro. Microarray bioinformatics analysis was performed to identify the putative targets of SPRY4-IT1, which were further verified by rescue experiments, as well as by western blotting and qRT-PCR. Results: SPRY4-IT1 expression was significantly upregulated in 48 breast cancer tumor tissues compared to normal tissues. Additionally, increased SPRY4-IT1 expression was associated with larger tumor size and an advanced pathological stage in breast cancer patients. Knockdown of SPRY4-IT1 significantly suppressed proliferation and caused apoptosis of breast cancer cells in vitro. Furthermore, we discovered ZNF703 was a direct target of SPRY4-IT1 and was downregulated by SPRY4-IT1 knockdown. Moreover, we demonstrated for the first time that ZNF703 is a genetic driver in ER (-) breast carcinoma cells. Conclusions: SPRY4-IT1 is a novel prognostic biomarker and a potential therapeutic candidate for breast cancer.