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LncMAPK6 drives MAPK6 expression and liver TIC self-renewal.
Guanqun Huang1, Hui Jiang2, Yueming He2
1Department of general surgery, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangdong Sheng, China.
Summary
A novel long noncoding RNA, lncMAPK6, promotes liver tumor growth and self-renewal by activating MAPK6 signaling. This discovery offers a new therapeutic target for liver cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Liver tumor-initiating cells (TICs) possess self-renewal and differentiation capabilities, driving tumor initiation, metastasis, and drug resistance.
- Mitogen-activated protein kinase (MAPK) signaling is crucial in biological processes, but its role in liver TICs remains unexplored.
Purpose of the Study:
- To investigate the role of MAPK signaling in liver TICs.
- To identify novel regulatory mechanisms of liver TIC self-renewal and tumorigenesis.
Main Methods:
- Analysis of online datasets for unbiased screening of MAPK components.
- Characterization of liver TICs using CD133 FACS and oncosphere formation assays.
- Functional assays (loss/gain of function) for lncRNA and molecular mechanism studies (RNA pulldown, RIP, ChIP, Western blot, FISH).
Main Results:
- MAPK6 was identified as the most highly expressed MAPK component in liver cancer.
- A long noncoding RNA, lncMAPK6, was found to be overexpressed and promotes liver tumor propagation and TIC self-renewal via MAPK6 activation.
- lncMAPK6 recruits RNA polymerase II to the MAPK6 promoter, enhancing its transcription and subsequently activating MAPK signaling.
Conclusions:
- MAPK6 is highly expressed in liver cancer and TICs; lncMAPK6 transcriptionally regulates MAPK6.
- The lncMAPK6-MAPK6 pathway is critical for liver TIC self-renewal and represents a potential therapeutic target.
- This study elucidates a new regulatory layer for liver TIC self-renewal involving MAPK signaling.
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