AI Article Synopsis
- SALL4 is highly expressed in EGFR-mutated lung tumors compared to non-tumor tissue, and patients with higher levels of SALL4 have worse surgical outcomes.
- The activation of EGFR increases SALL4 expression through the ERK1/2 signaling pathway, and reducing SALL4 can inhibit key cancer behaviors like spheroid formation and migration.
- Targeting SALL4 may enhance the effectiveness of Erlotinib, making it a promising new approach for treating lung cancer.
Article Abstract
The transcriptional factor SALL4, an important stem cell regulator, is expressed in hematopoietic stem cells and various malignancies, but its role in EGFR-mutated NSCLCs has not been studied yet. Here, we report that the expression of Sal-like protein 4 (SALL4), was significantly higher in EGFR mutated lung tumors than in non-tumor tissue. SALL4-high lung cancer patients had poorer prognosis after surgery than SALL4-low patients. The expression of SALL4 could be induced by the activation of EGFR through the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. The knockdown of SALL4 expression could suppress spheroid formation and the expression of lung cancer stem cell marker CD44. More interestingly, the knockdown of SALL4 expression could suppress the migration, invasion, and metastasis of the lung cancer cells and significantly increase the sensitivity of EGFR mutated cells to Erlotinib. These results suggest that SALL4 may be a novel potential therapeutic target for the diagnosis and treatment of lung cancer.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5915399 | PMC |
| http://dx.doi.org/10.1038/s41389-018-0045-7 | DOI Listing |
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