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Updated: Jan 6, 2026
Lung Tumor Cell Recruitment Assay
Published on: February 26, 2019
DIAPH3 promotes the tumorigenesis of lung adenocarcinoma
Guo Xiang1, He Weiwei1, Gao Erji2
1The First Affiliated Hospital of Soochow University, Suzhou, 215006, China; Department of Thoracic Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Abstract:
Aberrant activation of MEKK-MEK-ERK signaling is frequently observed in lung cancer. Several inhibitors, which target this pathway, have shown clinical potential for the lung cancer treatment. Better understanding the regulation of this pathway would help the development of treatment strategies. In this study, we have identified the DIAPH3 as an up-regulated gene in lung adenocarcinoma. DIAPH3 promoted the growth of lung cancer cells both in the liquid culture and in the soft agar, and knockdown DIAPH3 inhibited the tumorigenesis both in the nude mice and in the de novo mouse model. In the molecular mechanism study, DIAPH3 was identified as the binding protein of STK38, impaired the interaction between STK38 and MEKK, and activated ERK signaling. Taken together, this study demonstrated the oncogenic roles of DIAPH3 in the tumorigenesis of lung cancer by interacting with STK38.
Insights
DIAPH3 promotes lung cancer growth by activating the MEKK-MEK-ERK pathway. This study reveals DIAPH3 as a potential therapeutic target for lung adenocarcinoma, highlighting its oncogenic role.
Area of Science:
- Oncology
- Molecular Biology
- Cell Signaling
Background:
- Aberrant MEKK-MEK-ERK signaling is common in lung cancer.
- Targeting this pathway shows clinical promise for lung cancer treatment.
- Understanding pathway regulation is crucial for developing effective strategies.
Purpose of the Study:
- Identify novel genes involved in lung adenocarcinoma.
- Investigate the role of DIAPH3 in lung cancer progression.
- Elucidate the molecular mechanism by which DIAPH3 influences tumorigenesis.
Main Methods:
- Gene expression analysis to identify up-regulated genes.
- Cell culture and soft agar assays to assess cell growth.
- In vivo studies using mouse models (nude and de novo) to evaluate tumorigenesis.
- Co-immunoprecipitation assays to determine protein interactions.
Main Results:
- DIAPH3 was identified as an up-regulated gene in lung adenocarcinoma.
- DIAPH3 overexpression promoted lung cancer cell growth in vitro.
- Knockdown of DIAPH3 inhibited tumor formation in vivo.
- DIAPH3 binds to STK38, disrupting STK38-MEKK interaction and activating ERK signaling.
Conclusions:
- DIAPH3 plays a significant oncogenic role in lung cancer.
- DIAPH3 promotes lung cancer tumorigenesis by modulating the MEKK-MEK-ERK pathway via STK38 interaction.
- DIAPH3 represents a potential therapeutic target for lung adenocarcinoma treatment.
