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LUCAT1 Mediates MYC-Targeted Suppression of Squamous Cell Carcinoma
Yifan Wen1,2, Shuo Liu1,2, Zhen Qin1,2
1Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, Beijing, China.
Abstract:
Small-molecule MYC inhibitors that directly target MYC are considered attractive cancer therapeutics. Here, we demonstrate that LUCAT1, a long noncoding RNA, serves as a critical mediator of MYC-driven signaling in head and neck squamous cell carcinoma (HNSCC). The LUCAT1 expression is significantly downregulated in HNSCC cells following treatment with the MYC inhibitor MYCi975. Mechanically, MYC transcriptionally activates LUCAT1 through direct promoter binding, facilitating oncogenic functions. Clinically, elevated LUCAT1 is linked to cervical lymph node involvement in HNSCC and is associated with unfavorable patient outcomes. Functional studies in vitro demonstrated that LUCAT1 knockdown inhibits proliferation, migratory capacity, and invasive activity of HNSCC cells. This suppression also extends to the in vivo growth of tumors. Importantly, LUCAT1 overexpression attenuates the MYCi975 anti-tumor effects on HNSCC, confirming its role in therapeutic resistance. These results establish LUCAT1 as both a biomarker of aggressive disease and a mediator of MYC-driven oncogenesis, proposing LUCAT1 as a candidate synergistic therapeutic target in the treatment of HNSCC with MYC inhibition.
Insights
LUCAT1, a long noncoding RNA, drives head and neck cancer (HNSCC) by mediating MYC signaling. Inhibiting LUCAT1 may overcome resistance to MYC-targeted therapies in HNSCC patients.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- MYC is a key oncogene in various cancers, including head and neck squamous cell carcinoma (HNSCC).
- Direct MYC inhibitors are promising cancer therapeutics, but resistance mechanisms need elucidation.
- Long noncoding RNAs (lncRNAs) play crucial roles in cancer development and progression.
Purpose of the Study:
- To investigate the role of LUCAT1, a lncRNA, in MYC-driven HNSCC.
- To determine if LUCAT1 mediates therapeutic resistance to MYC inhibitors.
- To evaluate LUCAT1 as a potential biomarker and therapeutic target in HNSCC.
Main Methods:
- Analysis of LUCAT1 expression in HNSCC cells and patient samples.
- Investigating the transcriptional regulation of LUCAT1 by MYC.
- In vitro and in vivo functional assays (e.g., knockdown, overexpression) to assess LUCAT1's impact on HNSCC cell behavior and tumor growth.
- Evaluating the effect of LUCAT1 on MYC inhibitor (MYCi975) efficacy.
Main Results:
- MYC directly activates LUCAT1 transcription in HNSCC.
- LUCAT1 expression is downregulated by MYC inhibitor MYCi975.
- Elevated LUCAT1 correlates with cervical lymph node metastasis and poor outcomes in HNSCC patients.
- LUCAT1 knockdown inhibits HNSCC cell proliferation, migration, and invasion, and suppresses tumor growth in vivo.
- LUCAT1 overexpression confers resistance to MYCi975 anti-tumor effects.
Conclusions:
- LUCAT1 is a critical mediator of MYC oncogenic signaling in HNSCC.
- LUCAT1 acts as a biomarker for aggressive HNSCC and predicts unfavorable outcomes.
- LUCAT1 contributes to therapeutic resistance against MYC inhibitors.
- Targeting LUCAT1 in combination with MYC inhibitors represents a potential synergistic therapeutic strategy for HNSCC.
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