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Updated: Feb 24, 2026

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos
Published on: December 13, 2018
STAT3-induced long noncoding RNAs in multiple myeloma cells display different properties in cancer
Stefanie Binder1,2,3, Nadine Hösler4,5,6, Diana Riedel4,5
1Institute of Clinical Immunology, Faculty of Medicine, University of Leipzig, Leipzig, Germany. stefanie.binder@medizin.uni-leipzig.de.
Abstract:
Interleukin-6 (IL-6)-activated Signal Transducer and Activator of Transcription 3 (STAT3) facilitates survival in the multiple myeloma cell line INA-6 and therefore represents an oncogenic key player. However, the biological mechanisms are still not fully understood. In previous studies we identified microRNA-21 as a STAT3 target gene with strong anti-apoptotic potential, suggesting that noncoding RNAs have an impact on the pathogenesis of human multiple myeloma. Here, we describe five long noncoding RNAs (lncRNAs) induced by IL-6-activated STAT3, which we named STAiRs. While STAiRs 1, 2 and 6 remain unprocessed in the nucleus and show myeloma-specific expression, STAiRs 15 and 18 are spliced and broadly expressed. Especially STAiR2 and STAiR18 are promising candidates. STAiR2 originates from the first intron of a tumor suppressor gene. Our data support a mutually exclusive expression of either STAiR2 or the functional tumor suppressor in INA-6 cells and thus a contribution of STAiR2 to tumorigenesis. Furthermore, STAiR18 was shown to be overexpressed in every tested tumor entity, indicating its global role in tumor pathogenesis. Taken together, our study reveals a number of STAT3-induced lncRNAs suggesting that the interplay between the coding and noncoding worlds represents a fundamental principle of STAT3-driven cancer development in multiple myeloma and beyond.
Insights
Signal Transducer and Activator of Transcription 3 (STAT3) drives multiple myeloma by inducing long noncoding RNAs (lncRNAs), termed STAiRs. These STAiRs, including STAiR2 and STAiR18, contribute to cancer development and progression.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Interleukin-6 (IL-6)-activated Signal Transducer and Activator of Transcription 3 (STAT3) is crucial for multiple myeloma cell survival.
- The precise oncogenic mechanisms of STAT3 in multiple myeloma are not fully elucidated.
- Noncoding RNAs, such as microRNA-21, have been implicated in multiple myeloma pathogenesis.
Purpose of the Study:
- To identify and characterize novel long noncoding RNAs (lncRNAs) induced by IL-6-activated STAT3.
- To investigate the role of these STAT3-induced lncRNAs in multiple myeloma development and other cancers.
Main Methods:
- Analysis of STAT3 target genes in the INA-6 multiple myeloma cell line.
- Identification and characterization of five novel lncRNAs, named STAiRs.
- Assessment of STAiR expression patterns in different cell lines and tumor entities.
Main Results:
- Five STAT3-induced lncRNAs (STAiRs) were identified.
- STAiR2 exhibits mutually exclusive expression with a tumor suppressor gene in INA-6 cells, suggesting a role in tumorigenesis.
- STAiR18 is overexpressed across various tumor types, indicating a broader role in cancer pathogenesis.
- STAiRs 1, 2, and 6 are primarily nuclear and myeloma-specific, while STAiRs 15 and 18 are spliced and broadly expressed.
Conclusions:
- STAT3 induces a set of lncRNAs (STAiRs) that contribute to multiple myeloma pathogenesis.
- The interaction between coding and noncoding RNAs is a fundamental aspect of STAT3-driven oncogenesis.
- STAiR2 and STAiR18 are particularly promising candidates for further investigation in cancer research.
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lncRNA - Long Non-coding RNAs
lncRNA - Long Non-coding RNAs
RNA Splicing
MicroRNAs
MicroRNAs
Non-LTR Retrotransposons

