Project description:The study aims to elucidate the effect of histone methyltransferase SMYD3 on gene expression in MCF-7 breast cancer cell line. Knockdown luciferase control v.s. knockdown SMYD3 in MCF-7 breast cancer cell line were conducted. Results identify a large proportion of cell cycle-related genes regulated by SMYD3.
Project description:RNA-sequencing analysis of control and SMYD3-overexpressed MCF7 cell lines. SMYD3 (also known as KMT3E), a hisone H3 lysine K4 methyltransferase, is highly expressed in several human cancers, including colorectal and breast carcinomas. Results provide insight into the transcriptional regulation of SMYD3 in breast cancer.
Project description:SET (Su) and MYND (myeloid-Nervy-DEAF-1) domain-containing protein (SMYD) is a methyltransferase family, including five members of which SMYD1, SMYD2, SMYD3 and SMYD4, has been found to play critical roles in human carcinogenesis. It has been demonstrated that the altered expression of SMYD3 is associated with the progression of several solid tumors, including bladder cancer, glioma, gastric cancer, prostate cancer and colorectal cancer. Several trials have explored the effects of SMYD3 overexpression on proliferation, viability, cancer cells migration and invasion. The series of elegant experiments suggested that SMYD3 could serve as a potential biomarker for clinically aggressive disease and an attractive therapeutic target. In our previous study (PMID: 26980013), we found SMYD3 expression is frequently upregulated in human esophageal squamous cell carcinoma (ESCC) clinical tissues, correlating with overall survival of ESCC patients. RNAi-mediated knockdown of SMYD3 suppressed ESCC cell proliferation, migration and invasion in vitro, and inhibited local tumor invasion in vivo. To identify genes and biological pathways associated with SMYD3 functions and mechanism, SMYD3 was knockdowned bypGLV3/H1/GFP/+Puro Vector in ESCC cell line KYSE150 with an empty plasmid as a control, these two cells were applied for mRNA expression profile analyses to find the differentially expressed genes using GeneChip® PrimeView⢠Human Gene Expression Array. shRNA sequences targeting SMYD3 was ligated into the pGLV3/H1/GFP/+Puro Vector and transfected into ESCC cell line KYSE150 with an empty plasmid as a control. The mRNA expression profiles of SMYD3 knockdown was analyzed by GeneChip® PrimeViewâ¢Â Human Gene Expression Array (Affymetrix, USA). The knockdown of SMYD3 was confirmed by QRT-PCR and Western blot. Total RNAs from SMYD3 knockdown cells and control cells were extracted for GeneChip® PrimeView⢠Human Gene Expression Array.
Project description:RNA-sequencing analysis of control and SMYD3-knockdown MDA-MB-231 tumors from the mammary glands of orthotopic xenograft NOD/SCID mice. SMYD3 (also known as KMT3E), a hisone H3 lysine K4 methyltransferase, is highly expressed in several human cancers, including colorectal and breast carcinomas. Results provide insight into the transcriptional regulation of SMYD3 in breast cancer.
Project description:The goal of this study is to identify ERalpha-target genes affected by knocking down of the histone arginine methyltransferase CARM1 in MCF7 breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 knockingdown MCF7 cell line where CARM1 is decreased to 20% of endogeneous level to determine the created a Dox-inducible CARM1shRNA overexpressing MCF7 cells for evaluation of the global effects of CARM1 on ERalpha-target gene expression.
Project description:The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression.
Project description:The goal of this study is to identify ERalpha-target genes affected by knocking down of the histone arginine methyltransferase CARM1 in MCF7 breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 knockingdown MCF7 cell line where CARM1 is decreased to 20% of endogeneous level to determine the created a Dox-inducible CARM1shRNA overexpressing MCF7 cells for evaluation of the global effects of CARM1 on ERalpha-target gene expression. MCF7-tet-on-CARM1shRNA clone 1 were treated under 4 conditions: DMSO; Dox; E2 (10nM); Dox+E2. In Dox+E2 condition, cells were pre-treated with Dox for 5 days before treating with E2 for 4 hours. 3 biological replicates were included and total of 12 samples were analyzed.
Project description:The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression. MCF7-tet-on-CARM1 clone 13 were treated under 4 conditions: DMSO; Dox; E2 (10nM); Dox+E2. In Dox+E2 condition, cells were pre-treated with Dox for 5 days before treating with E2 for 4 hours. 3 biological replicates were included and total of 12 samples were analyzed.
Project description:SET (Su) and MYND (myeloid-Nervy-DEAF-1) domain-containing protein (SMYD) is a methyltransferase family, including five members of which SMYD1, SMYD2, SMYD3 and SMYD4, has been found to play critical roles in human carcinogenesis. It has been demonstrated that the altered expression of SMYD3 is associated with the progression of several solid tumors, including bladder cancer, glioma, gastric cancer, prostate cancer and colorectal cancer. Several trials have explored the effects of SMYD3 overexpression on proliferation, viability, cancer cells migration and invasion. The series of elegant experiments suggested that SMYD3 could serve as a potential biomarker for clinically aggressive disease and an attractive therapeutic target. In our previous study (PMID: 26980013), we found SMYD3 expression is frequently upregulated in human esophageal squamous cell carcinoma (ESCC) clinical tissues, correlating with overall survival of ESCC patients. RNAi-mediated knockdown of SMYD3 suppressed ESCC cell proliferation, migration and invasion in vitro, and inhibited local tumor invasion in vivo. To identify genes and biological pathways associated with SMYD3 functions and mechanism, SMYD3 was knockdowned bypGLV3/H1/GFP/+Puro Vector in ESCC cell line KYSE150 with an empty plasmid as a control, these two cells were applied for mRNA expression profile analyses to find the differentially expressed genes using GeneChip® PrimeView™ Human Gene Expression Array.
Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC).