Colorectal cancer (CRC) continues to be one of the most malignant cancers with a high mortality rate to date. Promoting the radio‐responsiveness of CRC is of great importance for local control and prognosis. In this study, we examined the roles of exosomal microRNA‐19b (miR‐19b) in CRC radioresistance. The regulatory role of miR‐19b in CRC stem cells and radiotherapy‐resistant cells was determined using miRNA microarray analysis, and its prognostic value was probed using the TCGA database. It was found that miR‐19b was overexpressed in CRC tissues, which indicated a poor prognosis. CRC‐derived exosomes (EXOs) enhanced the radio‐resistance and stemness properties of CRC cells via delivery of miR‐19b in vitro and in vivo. FBXW7 was identified as a putative target of miR‐19b. On the contrary, reintroduction of FBXW7 reversed the effects of miR‐19b on radioresistance and stemness properties. Furthermore, the Wnt/β‐catenin pathway activity was elevated in CRC cells upon EXOs treatment, decreased after miR‐19b downregulation, and increased again after FBXW7 downregulation. These results suggest that miR‐19b inhibition could enhance the efficacy of radiotherapy while reducing the stemness properties, thus presenting a promising strategy for sensitizing CRC cells to radiotherapy.

Radiotherapy represents the most effective nonsurgical therapy, whereas acquired radioresistance remains a major challenge in glioma treatment. Deregulation of long noncoding RNAs (lncRNAs) is frequently involved in tumorigenesis. This study investigates the role of LINC01123 in radioresistance in glioma with molecules involved. LINC01123 was identified as the most upregulated gene in a glioma gene expression dataset GSE103227. LINC01123 was highly expressed in the radioresistant glioma tissues radioresistant glioma U251 (U251R) cells. Downregulation of LINC01123 reduced cell proliferation and colony formation abilities, as well as resistance to apoptosis of the U251R cells after 4 Gy X‐ray irradiation. The micro(mi)RNA‐151a gene (miR‐151a) was a poorly expressed miRNA in glioma, and it was a target of LINC01123. The centromere protein B gene (CENPB) mRNA was a direct target of miR‐151a and demonstrated a positive correlation with LINC01123 in glioma tissues and cells. Further inhibition of miR‐151a or overexpression of CENPB restored radioresistance of glioma cells. In addition, silencing of LINC01123 suppressed growth of xenograft tumors formed by U251R cells in nude mice. To conclude, the present study demonstrates that LINC01123 serves as a sponge for miR‐151a and upregulates CENPB expression to increase the radioresistance of glioma cells in vitro and in vivo.