Regulation of Cancer Stem Cells and Epithelial-Mesenchymal Transition by CTNNAL1 in Lung Cancer and Glioblastoma

CTNNAL1 is a protein known to be involved in cell-cell adhesion and cell adhesion. Alterations in the expression or function of CTNNAL1 have been reported to contribute to the development and progression of various types of cancer. In breast cancer, CTNNAL1 has been reported as a cancer suppressor gene, and in melanoma and lung cancer, it has been reported as a cancer driver gene. However, due to a lack of research, its function remains unclear. In this study, it is shown that CTNNAL1 regulates cancer stem cells (CSCs) in lung cancer and glioblastoma and modulates their migration and invasion abilities. CSCs are known to play an important role in the malignant transformation of cancer. They have the ability to resist chemotherapeutic drugs and irradiation, which is a known obstacle to cancer treatment. We found that CTNNAL1 regulates the ability to resist irradiation. In addition, we observed that CTNNAL1 regulates the ability of cells to migrate and invade, a key feature of the epithelial to mesenchymal transition phenomenon associated with cancer metastasis. CTNNAL1 was also involved in the secretion of C-C motif chemokine ligand 2 (CCL2), one of the chemokines. CCL2 plays a role in the recruitment of immune cells to the tumor microenvironment, but in cancer, it is known to influence malignancy and metastasis. CTNNAL1 may be a novel target for treating lung CSCs and glioma stem cells and may be used as a marker of malignancy.

Automated summary

CTNNAL1 is a protein involved in cell-cell adhesion and has been found to have various roles in cancer development and progression. It acts as a cancer suppressor gene in breast cancer, but as a cancer driver gene in melanoma and lung cancer. This study reveals that CTNNAL1 regulates cancer stem cells (CSCs) in lung cancer and glioblastoma, affecting their ability to migrate, invade, and resist treatments like irradiation. Furthermore, CTNNAL1 is also involved in the secretion of CCL2, a chemokine known to influence malignancy and metastasis in cancer. These findings suggest that CTNNAL1 may serve as a potential target for treating lung CSCs and glioma stem cells, as well as a marker of malignancy.