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HOTAIR transfected Breast Cancer Cells

ABSTRACT: MDA-MB-231 Breast Cancer Cells were infected by retroviral expression with either VECTOR or HOTAIR. To test the role of polycomb in HOTAIR mediated gene expression, MDA-MB-231 HOTAIR cells were infected with short hairpin retroviral vectors targeting SUZ12 or EZH2. A genetic modification design type is where an organism(s) has had genetic material removed, rearranged, mutagenized or added, such as knock out. genetic_modification_design

ORGANISM(S): Homo sapiens

SUBMITTER: Gupta RA

PROVIDER: S-ECPF-GEOD-20435 | biostudies-other | 2010 Apr

REPOSITORIES: biostudies-other

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HOTAIR transfected Breast Cancer Cells

Project description:MDA-MB-231 Breast Cancer Cells were infected by retroviral expression with either VECTOR or HOTAIR. To test the role of polycomb in HOTAIR mediated gene expression, MDA-MB-231 HOTAIR cells were infected with short hairpin retroviral vectors targeting SUZ12 or EZH2. A genetic modification design type is where an organism(s) has had genetic material removed, rearranged, mutagenized or added, such as knock out.

2010-04-15 | GSE20435 | GEO

HOTAIR transfected Breast Cancer Cells

2010-04-15 | E-GEOD-20435 | biostudies-arrayexpress

Breast cancer MCF-7 cells and MDA-MB-231 cells: LNA-antimiR-21 transfected cells vs. LNA-control transfected cells

Project description:Transcriptional profiling of breast cancer cells comparing LNA-control transfected cells with cells transfected with LNA-antimiR-21.We searched for miR-21 targets by systematic screening of mRNA profiling of LNA-antimiR-21 transfected MCF-7 cells and MDA-MB-231 cells. Two-condition experiment, LNA-antimiR-21 Transfected vs. LNA-control Transfected MCF-7 cells. One replicate per array.

| S-ECPF-GEOD-20627 | biostudies-other

Breast cancer MCF-7 Cells and MDA-MB-435 cells: pre-miR-125b Transfected cells vs. pre-control transfected cells

Project description:Transcriptional profiling of breast cancer cells comparing pre-control transfected cells with cells transfected with pre-miR-125b. We searched for miR-125b targets by systematic screening of mRNA profiling of pre-miR-125b transfected MCF-7 cells and MDA-MB-435 cells. Two-condition experiment, pre-miR-125b Transfected vs. pre-control Transfected MCF-7 cells. One replicate per array.

| S-ECPF-GEOD-22546 | biostudies-other

Long noncoding RNA HOTAIR promotes invasion of breast cancer cells through chondroitin sulfotransferase CHST15.

Project description:The long noncoding RNA HOTAIR plays significant roles in promoting cancer metastasis. However, how it conveys an invasive advantage in cancer cells is not clear. Here we identify the chondroitin sulfotransferase CHST15 (GalNAc4S-6ST) as a novel HOX transcript antisense intergenic RNA (HOTAIR) target gene using RNA profiling and show that CHST15 is required for HOTAIR-mediated invasiveness in breast cancer cells. CHST15 catalyzes sulfation of the C6 hydroxyl group of the N-acetyl galactosamine 4-sulfate moiety in chondroitin sulfate to form the 4,6-disulfated chondroitin sulfate variant known as the CS-E isoform. We show that HOTAIR is necessary and sufficient for CHST15 transcript expression. Inhibition of CHST15 by RNA interference abolished cell invasion promoted by HOTAIR but not on HOTAIR-mediated migratory activity. Conversely, reconstitution of CHST15 expression rescued the invasive activity of HOTAIR-depleted cells. In corroboration with this mechanism, blocking cell surface chondroitin sulfate using a pan-CS antibody or an antibody specifically recognizes the CS-E isoform significantly suppressed HOTAIR-induced invasion. Inhibition of CHST15 compromised tumorigenesis and metastasis in orthotopic breast cancer xenograft models. Furthermore, the expression of HOTAIR closely correlated with the level of CHST15 protein in primary as well as metastatic tumor lesions. Our results demonstrate a novel mechanism underlying the function of HOTAIR in tumor progression through programming the context of cell surface glycosaminoglycans. Our results further establish that the invasive and migratory activities downstream of HOTAIR are distinctly regulated, whereby CHST15 preferentially controls the arm of invasiveness. Thus, the HOTAIR-CHST15 axis may provide a new avenue toward novel therapeutic strategies and prognosis biomarkers for advanced breast cancer.

| S-EPMC7263025 | biostudies-literature

Long Non-Coding RNA HOTAIR in Breast Cancer Therapy.

Project description:Breast cancer (BC) is the most common cancer type among women, and morbidity and mortality rates are still very high. Despite new innovative therapeutic approaches for all BC molecular subtypes, the discovery of new molecular biomarkers involved in tumor progression has been fundamental for the implementation of personalized treatment strategies and improvement of patient management. Many experimental studies indicate that long non-coding RNAs (lncRNAs) are strongly involved in BC initiation, metastatic progression, and drug resistance. In particular, aberrant expression of HOX transcript antisense intergenic RNA (HOTAIR) lncRNA plays an important role in BC contributing to its progression and represents a predictor of BC metastasis. For its proven prognostic value, HOTAIR could represent a potential therapeutic target in BC. In the present review, we summarize the role of HOTAIR in cancer progression and drug resistance, in particular in BC, and we illustrate the main approaches for silencing it.

| S-EPMC7281113 | biostudies-literature

Knockdown of lncRNA HOTAIR sensitizes breast cancer cells to ionizing radiation through activating miR-218.

Project description:Radiotherapy is a major therapeutic strategy for breast cancer, while cancer radioresistance remains an obstacle for the successful control of the tumor. Novel radiosensitizing targets are to be developed to overcome radioresistance. Recently, long non-coding RNAs (lncRNAs) were proved to play critical roles in cancer progression. Among all, lncRNA HOTAIR was found to participate in cancer metastasis and chemoresistance. In the present study, we aimed to investigate the radiosensitizing effects of targeting HOTAIR and the underlying mechanism. Our data showed that HOTAIR (HOX antisense intergenic RNA) was up-regulated in breast cancer cells and tissues, and the expression of HOTAIR increased following irradiation. Knockdown of HOTAIR inhibited cell survival and increased cell apoptosis in response to ionizing radiation. Moreover, compared with control group, radiation induced more DNA damage and cell cycle arrest in HOTAIR knockdown cells. Finally, we found that the radiosentizing effects of HOTAIR were related to the up-regulation of miR-218, a ceRNA of HOTAIR. In conclusion, our finding showed that HOTAIR inhibition sensitizes breast cancer cells to ionizing radiation, induced severe DNA damage and activated apoptosis pathways, suggesting a possible role of HOTAIR as a novel target for breast cancer radiosensitization.

| S-EPMC6449517 | biostudies-literature

KYSE180 cells transfected with HOTAIR compared to control cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-06-05 | GSE47639 | GEO

KYSE180 cells transfected with HOTAIR compared to control cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-06-05 | E-GEOD-47639 | biostudies-arrayexpress

Transcriptome analysis of inducible HOTAIR overexpression mouse breast cancer cells

Project description:HOTAIR is a 2.2 kb long noncoding RNA (lncRNA) whose dysregulation has been linked to oncogenesis, defects in pattern formation during early development, and irregularities during the process of epithelial-to-mesenchymal transition (EMT). However, the oncogenic transformation determined by HOTAIR in vivo and its impact on chromatin dynamics are incompletely understood. Here we generate a transgenic mouse model with doxycycline-inducible expression of human HOTAIR in the context of the MMTV-PyMT breast cancer-prone background (iHOT-PyMT mice) to systematically interrogate the cellular mechanisms by which human HOTAIR lncRNA acts to promote breast cancer progression. We isolated breast cancer cells from the primary tumors of iHOT-PyMT mice (named iHOT+ cells) and performed RNA-seq and ATAC-seq of iHOT+ cells treated with 3 conditions: Dox+, Dox- and DoxWD. We showed that HOTAIR overexpression altered both the cellular transcriptome and chromatin accessibility landscape of multiple metastasis-associated genes and promoted epithelial to mesenchymal transition. These alterations are abrogated within several cell cycles after HOTAIR expression is reverted to basal levels, indicating an erasable lncRNA-associated epigenetic memory. These results suggest that a continual role for HOTAIR in programming a metastatic gene regulatory program.

2023-01-10 | GSE201582 | GEO

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