Exploring the Effect of Fidgetin-Like 1 on Colorectal Cancer Through Tissue Chip and In Vitro Experiments
- Yunxing Xu 1, Yucheng Shen 1, Chen Zhang 1, Liangfeng Zheng 1, Feiyue Ji 1, Jin Chen 1, Shouliang Cheng 1, Yu Zheng 1
- Yunxing Xu 1, Yucheng Shen 1, Chen Zhang 1
- 1Clinic of Central Laboratory, Hai’an City People’s Hospital of Jiangsu Province, Hai’an Hospital Affiliated to Nantong University, Nantong, China
- 0Clinic of Central Laboratory, Hai’an City People’s Hospital of Jiangsu Province, Hai’an Hospital Affiliated to Nantong University, Nantong, China
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View abstract on PubMed
Summary
This summary is machine-generated.Fidgetin-like 1 (FIGNL1) promotes colorectal cancer (CRC) cell growth and spread. Inhibiting FIGNL1 may offer a new strategy for treating CRC patients.
Area Of Science
- Oncology
- Molecular Biology
- Cancer Research
Background
- Fidgetin-like 1 (FIGNL1) is overexpressed in various cancers, linked to poor prognosis in renal clear-cell carcinoma, gliomas, and hepatocellular carcinoma.
- Its role in colorectal cancer (CRC) remains largely uncharacterized.
Purpose Of The Study
- To investigate the function of FIGNL1 in colorectal cancer (CRC).
Main Methods
- Utilized TCGA database and immunohistochemistry to assess FIGNL1 expression in CRC tissues.
- Employed cell viability, migration, and invasion assays to evaluate FIGNL1's functional impact.
- Used siRNA and lentivirus for FIGNL1 knockdown and overexpression, respectively, and STRING database for protein interaction prediction.
Main Results
- FIGNL1 is upregulated in CRC tissues and correlates with advanced TNM stages and lymph node metastasis.
- Silencing FIGNL1 inhibited CRC cell proliferation, migration, and invasion.
- Overexpression of FIGNL1 promoted CRC cell proliferation, migration, and invasion through P38 signaling pathway activation, dependent on SPIDR interaction.
Conclusions
- FIGNL1 plays a significant role in CRC progression.
- FIGNL1 represents a potential therapeutic target for colorectal cancer treatment.
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