Project description:We investigated the relative miRNA levels in primary prostate cancer samples from patients that had a subsequent recurrence event versus patients that did not. For one of the top miRNAs arising from this analysis, miR-33a, we carried out further investigation, including miRNA levels in normal and tumor prostate samples as well as PCa cell lines. Then, we performed a detailed functional analysis of mir-33a in LNCaP and VCaP PCa cells and evaluated proliferative, invasive and anchorage independent growth potential of cells upon overexpression and knockdown of miR-33a.
Project description:In this study, we aimed to investigate the functional roles of miR-33a in PCa.We investigated the relative miR-33a level in normal and tumor prostate samples as well as PCa cell lines. Then, we performed a detailed functional analysis of mir-33a in LNCaP and VCaP PCa cells and evaluated proliferative, invasive and anchorage independent growth potential of cells upon overexpression and knockdown of miR-33a. We next explored the potential direct targets of miR-33a in PCa cells via utilizing gene expression microarray analysis, bioinformatics search, further qRT-PCR, western blot, and luciferase assay confirmation. Our results demonstrated that miR-33a is significantly downregulated in PCa tumor samples and PCa cell lines, pointing its tumor suppressor potential in PCa. Overexpression and knockdown of miR-33a significantly altered the proliferative, invasive and anchorage independent growth potentials of cells through altering the expression of its direct target PIM1. Ectopic induction of MiR-33a expression reversed the impacts of PIM1 overexpression on cellular phenotypes associated with PCa progression. Our results suggest that mir-33a exerts its tumor suppressor potential through targeting its direct target PIM1 and carries crucial roles in PCa tumorigenesis.
Project description:To identify target genes of tumor suppressive microRNAs in human cancer, several cell lines (bladder cancer, prostate cancer, renal cell carcinoma, and head and neck squamous cell carcinoma) were subjected to Agilent whole genome microarrays. miR-517a, miR-218, miR-145, miR-1 and miR-874 function as tumor suppressors. Human cancer cell lines (BOY, T24, A498, PC3, DU145, FaDu, SAS, HSC3, IMC3) were transfected with miRNAs (miR-517a, miR-218, miR-145, miR-1, miR-874). The miRNA-transfected human cancer cell lines were compared to control cell lines.
Project description:To identify target genes of cancer-related microRNAs in human cancer, several cell lines (bladder cancer, prostate cancer, renal cell carcinoma, esophageal squamous cell carcinoma, and head and neck squamous cell carcinoma) were subjected to Agilent whole genome microarrays. Human cancer cell lines (BOY, T24, A498, 786-O, caki-1, LNCap, PC3, TE2, T.Tn, FaDu, SAS, HSC3, and IMC-3) were transfected with miRNAs (miR-375, miR-145, miR-200a, miR-200b, miR-200c, miR-141, miR-429, miR-138, miR-218, miR-874, miR-31, miR-222, miR-1285, and miR-206) or siRNAs (si-FOXA1_1, si-FOXA1_3, and si-TAGLN2). The miRNA-transfected human cancer cell lines were compared to control cell lines.
Project description:To identify target genes of oncogenic or tumor suppressive microRNAs in human cancer, several cell lines (bladder cancer, prostate cancer, renal cell carcinoma. lung squamous cell carcinoma and head and neck squamous cell carcinoma) were subject to Agilent whole genome microarray. miR-183 and miR-96 function as oncogene. miR-1, miR-133a, miR-135a, miR-145 and miR-375 function as tumor suppressor The miRNA transfected human cancer cell lines (KK47, T24, A498, PC3, DU145, FaDu, SAS, PC10 and H157) were compared to control cell lines.
Project description:This SuperSeries is composed of the following subset Series: GSE17315: mRNA expression upon reconstitution of miR-130a, miR-203 and miR-205 in prostate cancer cell line LNCaP GSE17317: miRNA expression in LNCaP, PC3, Du-145 and RWPE-1 cell lines GSE22979: Profiling of direct mRNA targets of miR-130a, miR-203 and miR-205 in prostate cancer cell line LNCaP Refer to individual Series
Project description:In this study, we used miRNA sequencing to analyze and identify possible miRNAs that can be regulated by and ELF3-AS1 in gastric cancer. The results showed that lncRNA ELF3-AS1 knockdown decreased the expression of miR-33a/b and miR-203a. Due to miR-33a/b and miR-203a were able to target SNAI2 expression, and ELF3-AS1 knockdown significantly upregulates SNAI2 expression, we speculated ELF3-AS1 may negatively regulate SNAI2 expression through positively regulating the expression of miR-33a/b and miR-203a in GC.
Project description:Lung cancer is the leading cause of cancer death worldwide. The lack of specific and sensitive methods for early diagnosis as well as inadequate targeted therapies contribute to poor outcomes. A growing body of evidences suggests different roles of microRNAs including development and progression of lung cancer. The overexpression of the DNA repair protein apurinic/apyrimidinic endonuclease 1 (APE1) is an important cause of poor chemotherapeutic and its expression is able to predict the progression-free and overall survival in patients receiving platinum-containing chemotherapy. Recently, we have demonstrated APE1 involvement in miRNA biogenesis related to cancer progression. In this article, we report the identification of miRNAs that are modulated in lung cancer cells upon APE1 silencing. We defined a miRNA signature consisting of the 13 miRNAs, which strongly correlates with APE1 expression in lung cancer: miR-1246, miR-4488, miR-24, miR-183, miR-660, miR-130b, miR-543, miR-200c, miR-376c, miR-218, miR-146a, miR-92b and miR-33a. Gene ontology annotation and pathway analysis of the miRNA signature revealed its biological significance in cancer proliferation and survival. Among the miRNAs downregulated by APE1 is miRNA-33a-5p which targets Dicer, a major miRNA biogenesis gene whose expression is found to be downregulated in several tumours. We here validated Dicer as a direct functional target of miR-33a and profiled miR-33a, DICER and APE1 expression in clinical samples. Our findings suggest that APE1 may promote lung cancer progression through modulation of Dicer expression via miR-33a regulation. Our findings reveal new mechanistic insight into how APE1 functions in tumor biology.