MALINC1 a Novel Oncogenic Long Non-Coding RNA Associated with Early Stage Breast Cancer Progression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA799319 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17690867.fastq.gz | Fastqsanger.gz | |||
| SRR17690867_1.fastq.gz | Fastqsanger.gz | |||
| SRR17690867_2.fastq.gz | Fastqsanger.gz | |||
| SRR17690868.fastq.gz | Fastqsanger.gz | |||
| SRR17690868_1.fastq.gz | Fastqsanger.gz |
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Project description:The long-non-coding MALINC1 intergenic RNA (also known as LINC001024) was identified as significantly upregulated in breast ductal carcinoma in situ (DCIS). The aim of this study was to characterize the MALINC1 expression and localization, their phenotypic and molecular effects in non-invasive and invasive breast cancer models. We determined that MALINC1 is a E2-ER modulated lncRNA enriched in the cytoplasmic fraction of luminal A/B breast cancer cells that is associated with worse overall survival in patients with primary invasive breast carcinomas (p=0.027). Transcriptomic studies (RNA-seq) in normal and DCIS cells identified the main signaling pathways modulated by MALINC1 which include bioprocesses related to extracellular matrix remodeling, epithelial cell migration, adhesion, proliferation, and activation of AP1 signaling pathway. We conclude that MALINC1 over-expression behaves as an oncogenic lncRNA both in normal and DCIS breast cells involved with early-stage breast cancer progression.
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Project description:The long-non-coding HOX transcript antisense intergenic RNA (HOTAIR) was identified as significantly upregulated in breast ductal carcinoma in situ (DCIS). The aim of this study was to characterize the phenotypic effects and signaling pathways modulated by HOTAIR in early-stage breast cancer progression. We determined that HOTAIR induces premalignant phenotypic changes by increasing cell proliferation, migration, invasion and in vivo growth in normal and DCIS breast cell lines. Transcriptomic studies (RNA-seq) identified the main signaling pathways modulated by HOTAIR which include bioprocesses related to cell migration, epithelial to mesenchymal transition, extracellular matrix remodeling and activation of HIF1A, AP1 and FGFR signaling pathways among others. Similar pathways were identified as activated in primary invasive breast carcinomas with HOTAIR over-expression. We conclude that HOTAIR over-expression behaves as a positive regulator of cell growth and migration both in normal and DCIS breast cells involved with early-stage breast cancer progression.
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Project description:Multiple myeloma (MM) ranks the second most prevalent haematological malignancy globally. Despite advancements in managing MM, it remains incurable due to the high genetic heterogeneity leading to treatment resistance and disease severity. One key drug resistance associated signalling pathway often hyperactivated in MM patients is the non-canonical NF- κB/p52 pathway. Additionally, dysregulated expression of various oncogenic long non-coding RNAs (lncRNAs) have been observed in MM. This study aims to examine the potential link between ncNF-κB activation and dysregulated lncRNA expression controlling the chemoresistance and oncogenic progression of MM. Using mutant MM cell lines as model system and omics data from MM patients, we identified a novel p52 regulated lncRNA enriched in high-risk MM patients. The lncRNA termed PLUM (PRC2 associated LncRNA regulating UPR in MM) is found to interact directly with PRC2 complex to mediate myeloma progression and chemoresistance. RACE (Rapid amplification of cDNA ends) analysis revealed PLUM exists in three main isoforms in drug resistant multiple myeloma cell lines (MMCLs), comprising 8 exons without coding potential. Functionally, PLUM exerts its oncogenic and drug resistance properties in vivo and in vitro via the activation of unfolded protein response (UPR) pathway. This is consistent with its elevated expression in VRd (Bortezomib- Lenalidomide-Dexamethasone) non-responsive MM patients. PLUM localizes predominantly in the nucleus where it interacts directly with the disordered region of EZH2 (489-494 aa residues) to facilitate formation of the PRC2 complex and EZH2 activity. Disruption of this interaction using steric antisense oligonucleotides (ASOs) re-sensitized MMCLs to drug treatment in vitro and in vivo, correlating with the loss of EZH2 H3K27 trimethylation activity and PRC2 complex stability. Finally, we demonstrate that PLUM-EZH2 regulates the expression of tumour suppressor genes, FOXO3 and ZFP36, to activate the UPR pathway and promote chemoresistance in MM. These findings indicate that ncNF-κB pathway regulated lncRNA PLUM is oncogenic, acting through the PRC2/FOXO3/ZFP36 axis to confer chemoresistance in MM.
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Project description:Long non-coding RNAs are increasingly being recognized as cancer biomarkers in various malignancies, acting as either tumor suppressors or oncogenes. The long non-coding MALINC1 intergenic RNA was identified as significantly upregulated in breast ductal carcinoma in situ. The aim of this study was to characterize MALINC1 expression, localization, and phenotypic and molecular effects in non-invasive and invasive breast cancer cells. We determined that MALINC1 is an estrogen-estrogen receptor-modulated lncRNA enriched in the cytoplasmic fraction of luminal A/B breast cancer cells that is associated with worse overall survival in patients with primary invasive breast carcinomas. Transcriptomic studies in normal and DCIS cells identified the main signaling pathways modulated by MALINC1, which mainly involve bioprocesses related to innate and adaptive immune responses, extracellular matrix remodeling, cell adhesion, and activation of AP-1 signaling pathway. We determined that MALINC1 induces premalignant phenotypic changes by increasing cell migration in normal breast cells. Moreover, high MALINC1 expression in invasive carcinomas was associated with a pro-tumorigenic immune environment and a favorable predicted response to immunotherapy both in luminal and basal-like subtypes compared with low-MALINC1-expression tumors. We conclude that MALINC1 behaves as an oncogenic and immune-related lncRNA involved with early-stage breast cancer progression.
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