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SLC11A1 can activate TGF-β1 signaling pathway to resist ferroptosis in colorectal cancer
DongQiang Yang1, LianMei Zhao2, Ping Shi3
1Department of Radiology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, 050000, Hebei, China.
Abstract:
High expression of Solute Carrier Family 11 Member 1(SLC11A1) leads to a poor prognosis in patients with CRC, while the specific role of SLC11A1 in CRC remains unreported. Therefore, this study mainly addressed the preliminary mechanism and specific role of SLC11A1 in CRC. The results showed that six subsequent genes were successfully screened by the line database, and the abnormal expression of SLC11A1 was the most obvious in colorectal cancer patients. Following phenotypic experiments demonstrated that SLC11A1 promoted proliferation, invasion and migration of colorectal cancer cells. SLC11A1 Is also able to downregulate Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL 4), Cyclooxygenase-2 (COX2), NADPH Oxidase 1 (NOX1) and upregulate the expression levels of Hypoxia-Inducible Factor 1 (FIH1), Glutathione Peroxidase 1 (GPX1) protein, inhibit the expression levels of MDA and Fe2+ in colorectal cancer cells, and resist ferroptosis in colorectal cancer cells. SLC11A1 Overexpression can up-regulate the protein expression level of TGFβ1 (Transforming Growth Factor Beta 1), p-Smad 2 / 3, activate TGFβ1 signaling pathway activity, and promote colorectal cancer cell progression. In conclusion, we successfully demonstrated that SLC11A1 confers resistance to ferroptosis in colorectal cancer cells, providing a potential target for the clinical treatment of colorectal cancer.
Insights
Solute Carrier Family 11 Member 1 (SLC11A1) promotes colorectal cancer progression by inhibiting ferroptosis. Targeting SLC11A1 offers a potential therapeutic strategy for colorectal cancer (CRC) treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- High expression of Solute Carrier Family 11 Member 1 (SLC11A1) is linked to poor prognosis in colorectal cancer (CRC).
- The precise function of SLC11A1 in CRC pathogenesis remains largely unelucidated.
Purpose of the Study:
- To investigate the preliminary mechanism and specific role of SLC11A1 in colorectal cancer.
- To determine SLC11A1's impact on cancer cell behavior and ferroptosis.
Main Methods:
- Gene expression analysis using a database.
- Phenotypic experiments to assess cell proliferation, invasion, and migration.
- Western blotting and biochemical assays to evaluate protein expression and cellular markers.
Main Results:
- SLC11A1 was found to be significantly overexpressed in CRC patients.
- SLC11A1 promoted CRC cell proliferation, invasion, and migration.
- SLC11A1 conferred resistance to ferroptosis by modulating key proteins and inhibiting MDA and Fe2+ levels.
- SLC11A1 activated the TGFβ1 signaling pathway, enhancing CRC progression.
Conclusions:
- SLC11A1 plays a crucial role in promoting colorectal cancer progression.
- SLC11A1 confers resistance to ferroptosis in colorectal cancer cells.
- SLC11A1 represents a potential therapeutic target for clinical intervention in CRC.
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