ArticleMolecular therapy. Nucleic acids2021
lncRNA LOC102724169 plus cisplatin exhibit the synergistic anti-tumor effect in ovarian cancer with chronic stress.
Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Article
- ESM1 suppresses LncRNA GAS5/miR-23a-3p/PTEN axis to promote the cisplatin-chemotherapy resistance of ovarian cancer cells via activating the PI3K/AKT pathway.Discover oncology · 2025Article
- Long non-coding RNAs in cancer: multifaceted roles and potential targets for immunotherapy.Molecular and cellular biochemistry · 2024Review
- Emerging role of MYB transcription factors in cancer drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Review
- Identification of a Novel Immune-Related lncRNA CTD-2288O8.1 Regulating Cisplatin Resistance in Ovarian Cancer Based on Integrated Analysis.Frontiers in genetics · 2022Article
- Intricate crosstalk between MYB and noncoding RNAs in cancer.Cancer cell international · 2021Review
- HOTTIP-miR-205-ZEB2 Axis Confers Cisplatin Resistance to Ovarian Cancer Cells.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic stress has been proven to accelerate the development and progression of ovarian cancer, but the underlying molecular mechanisms have not been fully elucidated. In a combination survey of ovarian cancer with chronic stress (OCCS) mouse models and high-throughput sequencing, a key lncRNA named LOC102724169 on chromosome 6q27 has been identified, which functions as a dominant tumor suppressor in OCCS. Transcriptionally regulated by CCAAT enhancer binding protein (CEBP) beta (CEBPB), LOC102724169 shows low expression and correlates with poor progression-free survival (PFS) in OCCS patients. LOC102724169 is an instructive molecular inhibitor of malignancy of ovarian cancer cells, which is necessary to improve the curative effect of cisplatin therapy on ovarian cancer. This function stems from the inactivation of molecules in phosphatidylinositol 3-kinase (PI3K)/AKT signaling, repressing MYB expression and retaining the responsiveness of cancer cells to cisplatin. These findings provide a mechanistic understanding of the synergistic anti-tumor purpose of LOC102724169 as a bona fide tumor suppressor, enhancing the therapeutic effect of cisplatin. The new regulatory model of "lncRNA-MYB" provides new perspectives for LOC102724169 as a chronic stress-related molecule and also provides mechanistic insight into exploring the cancer-promoting mechanism of MYB in OCCS, which may be a promising therapeutic strategy for ovarian cancer.
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