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Published on: October 27, 2020
FLOT2 promotes nasopharyngeal carcinoma progression through suppression of TGF-β pathway via facilitating CD109
Hongjuan Xu1,2,3, Yuze Yin1,2,4, Yihan Li1,2,4
1NHC Key Laboratory of Carcinogenesis, NHC Key Laboratory of Nanobiological Technology, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Abstract:
In nasopharyngeal carcinoma (NPC), the TGF-β/Smad pathway genes are altered with inactive TGF-β signal, but the mechanisms remain unclear. RNA-sequencing results showed that FLOT2 negatively regulated the TGF-β signaling pathway via up-regulating CD109 expression. qRT-PCR, western blot, ChIP, and dual-luciferase assays were used to identify whether STAT3 is the activating transcription factor of CD109. Co-IP immunofluorescence staining assays were used to demonstrate the connection between FLOT2 and STAT3. In vitro and in vivo experiments were used to detect whether CD109 could rescue the functional changes of NPC cells resulting from FLOT2 alteration. IHC and Spearman correlation coefficients were used to assay the correlation between FLOT2 and CD109 expression in NPC tissues. Our results found that FLOT2 promotes the development of NPC by inhibiting TGF-β signaling pathway via stimulating the expression of CD109 by stabilizing STAT3, which provides a potential therapeutic strategy for NPC treatment.
Insights
FLOT2 promotes nasopharyngeal carcinoma (NPC) by inhibiting the TGF-β pathway through upregulating CD109 expression. This involves stabilizing STAT3, offering a potential therapeutic target for NPC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cell Signaling
Background:
- Nasopharyngeal carcinoma (NPC) exhibits altered TGF-β/Smad pathway signaling, but the underlying mechanisms are not fully understood.
- Identifying key regulators of this pathway in NPC is crucial for therapeutic development.
Purpose of the Study:
- To elucidate the role of FLOT2 in NPC pathogenesis.
- To investigate the molecular mechanism by which FLOT2 influences TGF-β signaling.
- To explore the potential of targeting the FLOT2/CD109/STAT3 axis in NPC.
Main Methods:
- RNA-sequencing to identify gene expression changes.
- Quantitative reverse transcription PCR (qRT-PCR) and Western blot for gene and protein expression analysis.
- Chromatin immunoprecipitation (ChIP) and dual-luciferase assays to determine transcription factor activity.
- Co-immunoprecipitation (Co-IP) and immunofluorescence staining to assess protein interactions.
- In vitro and in vivo experiments to evaluate cellular and tumor development.
- Immunohistochemistry (IHC) and Spearman correlation to analyze tissue expression.
Main Results:
- FLOT2 negatively regulates TGF-β signaling by upregulating CD109 expression.
- STAT3 acts as the activating transcription factor for CD109.
- FLOT2 interacts with STAT3, stabilizing it.
- CD109 can rescue functional changes in NPC cells caused by FLOT2 alteration.
- FLOT2 and CD109 expression are positively correlated in NPC tissues.
Conclusions:
- FLOT2 promotes NPC development by inhibiting the TGF-β signaling pathway via STAT3-mediated CD109 expression.
- The FLOT2/STAT3/CD109 axis represents a potential therapeutic target for nasopharyngeal carcinoma.
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