Profiling of SORBS2-bound RNAs
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE100323 | GEO | 2018/02/20
REPOSITORIES: GEO
Similar Datasets
Project description:In this study, we examined the differential RNA profile of alpha amanitin-treated SORBS2-depleted ovarian cancer cells compared with control-treated SORBS2-depleted cells
2018-02-20 | GSE101595 | GEO
Project description:In this study, we examined the differential RNA profile of SORBS2-depleted ovarian cancer cells compared with control cells
2018-02-20 | GSE101594 | GEO
Project description:We purified all RNAs in direct interaction with biotinylated versions of miR-491-5p or a control miRNA in the cytoplasmic compartment (see protocol) of IGROV1-R10 chemoresistant human ovarian cancer cell line. Input and purified RNA were deep-sequenced in order to calculate an enrichment score able to identify which transcripts were bound in cellulo by miR-491-5p
2020-10-28 | GSE160213 | GEO
Project description:Epithelial ovarian cancer (EOC) constitutes a major gynecological malignancy, with a reported incidence rate of 3-12/100 000 woman annually. As early symptoms of ovarian cancer are often clinically atypical or absent, the majority of ovarian cancer patients are diagnosed at a late stage, when the five-year survival rate is extremely low. This condition underscores the urgency of early detection of these patients and establishment of new therapeutic targets for successful intervention. Considering that the predominant biological characteristic that differentiates malignant from benign tumors is the ability to metastasize, it is necessary to identify novel metastasis-related molecules for ovarian cancer. In this study, we found that CAFs could significantly increase the metastatic potential of ovarian cancer cells compared with non-cancer associated fibroblasts(NAFs), which is associated with over-expression of CXCL14 in CAFs. We examined the impact of CAF-secreted CXCL14 on the lncRNA expression profiles in ovarian cancer during metastasis. We treated A2780s ovarian cancer cell line with recombinant CXCL14 protein and control respectively and subjected them to Arraystar Human LncRNA microarray v3.0 to profile differential lncRNAs in ovarian cancer upon treatment of CXCL14
2016-06-01 | E-GEOD-82059 | biostudies-arrayexpress
Project description:In order to identify specific events that are causatively involved in the metastatic process, we analyzed matched samples from 3 high grade serous ovarian cancer patients by RNA-seq. For each patient we examined samples representing the three cancer states: 1) primary tumor; 2) omentum metastasis (solid metastasis); 3) effusion metastasis. We identified genes differentially expressed between the various states. One of the genes found to be expressed in the primary tumor but not in the omentum or effusion metastasis is FOXL2, a transcription factor known to play a role in ovarian development and function. This change was successfully validated by RT-PCR in both the patients' samples as well as in a set of 27 independent patient samples representing the three cancer states. Knock-down of FOXL2 in patient-derived immortal fallopian tube cells lead to increased proliferation and survival. RNA-seq of the immortal fallopian tube cells after FOXL2 knock-down revealed a pro-metastatic gene expression signature. Our results suggest that FOXL2 is an important tumor suppressor and an inhibitor of ovarian cancer progression.
2021-06-01 | GSE115573 | GEO
Project description:In order to identify specific events that are causatively involved in the metastatic process, we analyzed matched samples from 3 high grade serous ovarian cancer patients by RNA-seq. For each patient we examined samples representing the three cancer states: 1) primary tumor; 2) omentum metastasis (solid metastasis); 3) effusion metastasis. We identified genes differentially expressed between the various states. One of the genes found to be expressed in the primary tumor but not in the omentum or effusion metastasis is FOXL2, a transcription factor known to play a role in ovarian development and function. This change was successfully validated by RT-PCR in both the patients' samples as well as in a set of 27 independent patient samples representing the three cancer states. Knock-down of FOXL2 in patient-derived immortal fallopian tube cells lead to increased proliferation and survival. RNA-seq of the immortal fallopian tube cells after FOXL2 knock-down revealed a pro-metastatic gene expression signature. Our results suggest that FOXL2 is an important tumor suppressor and an inhibitor of ovarian cancer progression.
2021-06-01 | GSE115446 | GEO
Project description:Epithelial ovarian cancer (EOC) constitutes a major gynecological malignancy, with a reported incidence rate of 3-12/100 000 woman annually. As early symptoms of ovarian cancer are often clinically atypical or absent, the majority of ovarian cancer patients are diagnosed at a late stage, when the five-year survival rate is extremely low. This condition underscores the urgency of early detection of these patients and establishment of new therapeutic targets for successful intervention. Considering that the predominant biological characteristic that differentiates malignant from benign tumors is the ability to metastasize, it is necessary to identify novel metastasis-related molecules for ovarian cancer. In this study, we found that CAFs could significantly increase the metastatic potential of ovarian cancer cells compared with non-cancer associated fibroblasts(NAFs), which is associated with over-expression of CXCL14 in CAFs. We examined the impact of CAF-secreted CXCL14 on the lncRNA expression profiles in ovarian cancer during metastasis.
2016-06-01 | GSE82059 | GEO
Project description:Ovarian cancer is the most frequent cause of cancer death in women and the leading cause of death related to gynecological cancer, accounting for 5% of estimated cancer deaths. Due to its asymptomatic nature at early stages, most ovarian cancers were diagnosed at an advanced stage, with distant metastasis in the abdominal cavity. Cancer metastasis is the primary cause of morbidity, and contributes to 95% of cancer-related deaths. Metastatic ovarian cancer is closely related with recurrence and drug resistance, rendering metastasis as the major challenge in the course of ovarian cancer treatment. Thorough understanding of ovarian cancer metastasis is believed to contribute to improve cancer cure rates, while it is still not well elucidated. One important aspect of ovarian cancer metastasis research is the identification of driver molecular. To identify proteins required for ovarian cancer metastasis, we carried out unbiased high-throughput screening by comparing the expression profile of ovarian cancer primary and metastasis tissues.
2023-01-20 | GSE222982 | GEO
Project description:Abstract:
Accumulating experimental and clinical evidence suggest that the immune response to cancer is not exclusively anti-tumor. Indeed, the pro-tumor roles of the immune system - as suppliers of growth and pro-angiogenic factors or defenses against cytotoxic immune attacks, for example - have been long appreciated, but relatively few theoretical works have considered their effects. Inspired by the recently proposed "immune-mediated" theory of metastasis, we develop a mathematical model for tumor-immune interactions at two anatomically distant sites, which includes both anti- and pro-tumor immune effects, and the experimentally observed tumor-induced phenotypic plasticity of immune cells (tumor "education" of the immune cells). Upon confrontation of our model to experimental data, we use it to evaluate the implications of the immune-mediated theory of metastasis. We find that tumor education of immune cells may explain the relatively poor performance of immunotherapies, and that many metastatic phenomena, including metastatic blow-up, dormancy, and metastasis to sites of injury, can be explained by the immune-mediated theory of metastasis. Our results suggest that further work is warranted to fully elucidate the pro-tumor effects of the immune system in metastatic cancer.
2024-09-02 | BIOMD0000000926 | BioModels