Targeting claudin-3 suppresses stem cell-like phenotype in nonsquamous non-small-cell lung carcinoma.

Aim: To determine the role of claudin-3 in cancer stemness in nonsquamous non-small-cell lung carcinoma (NSCLC).

Materials & Methods: extreme limiting dilution analysis and the side population assay were used to investigate the role of claudin-3 in regulating cancer stemness in nonsquamous NSCLC.

Results & Conclusion: Claudin-3 depletion decreased the formation rates of spheres and tumors and increased cisplatin sensitivity.

Identification of a novel splice variant of the human musashi-1 gene.

Musashi-1 (Msi1) is an evolutionarily conserved RNA-binding protein that has been reported to be the key regulator in malignancies and with involvement in cancer stemness. In the present study, a novel Msi1 transcript variant generated by alternative splicing was identified and termed Msi1 variant 2. This variant was observed to be ubiquitously expressed in cancerous and non-cancerous cells compared with its wild-type variant, which is preferentially expressed in cancer cells.

Suppression of cancer stemness by upregulating Ligand-of-Numb protein X1 in colorectal carcinoma.

Cancer stem-like cells (CSCs) have been reported to play major roles in tumorigenesis, tumor relapse, and metastasis after therapy against colorectal carcinoma (CRC). Therefore, identification of colorectal CSC regulators could provide promising targets for CRC. Ligand-of-Numb protein X1 (LNX1) is one E3 ubiquitin ligase which mediates the ubiquitination and degradation of Numb.