CASC19 expression was also positively associated with tumor diameter and pathological grade. Additionally, its high expression was closely associated with tumor MRI signal heterogeneity and peritumoral edema. CASC19 upregulation promoted glioma cell proliferation and metastasis, while CASC19‑knockdown demonstrated the opposite effect. CASC19 sponged miR‑454‑3p, which indirectly increased RAB5A expression. The results demonstrated that the CASC19/miR‑454‑3p/RAB5A axis is involved in the promotion of glioma progression.Multiple studies have demonstrated chemoresistance in multiple types of tumor, which limits the effectiveness of cancer treatments. Chemoresistance often contributes to cancer relapse. Non‑coding RNAs, are a group of regulatory RNAs, that are involved in tumor drug resistance. Exosomes, membranous vesicles secreted by cells, are reported to mediate cell‑to‑cell communication, including in cancer. Furthermore, exosomal non‑coding RNAs have been reported to mediate chemoresistance via exchange of biological information. In the present review, the main roles of exosomal non‑coding RNAs, including micro(mi) RNAs, long non‑coding (lnc) RNAs, and circular (circ) RNAs in cancer are described and their potential roles in chemoresistance in various types of cancer are also discussed.Oncogenic Bcr‑Abl kinase mimics pre‑B cell receptor (pre‑BCR) survival signals in BCR‑ABL1‑positive B‑cell acute lymphoblastic leukemia (BCR‑ABL1+ B‑ALL), driving B‑cell progenitor malignant transformation; thus, defining a particularly unfavorable prognosis for patients. During B‑cell development, pre‑BCR differentiation signaling components terminate proliferative expansion and promote B‑cell maturation. 2-APQC activator To study whether pre‑BCR differentiation signaling components regulate the initiation and development of BCR‑ABL1+ B‑ALL, the tumor suppression mechanism of differentiation‑related signaling molecules in BCR‑ABL1‑transformed pro‑B cells were analyzed. The results demonstrated that Bcr‑Abl kinase activated the PI3K/Akt pathway, promoting cell growth, and upregulated Aid expression, increasing genomic instability in pro‑B cells. These findings suggest that Bcr‑Abl kinase mediates pro‑B cell malignant transformation. Furthermore, the present data revealed that BCR‑ABL1 oncogenic stress triggered enhanced expression of B‑cell differentiation components B‑cell linker (Blnk) and forkhead box protein O1 (Foxo1) in BCR‑ABL1 transformed pro‑B cells. Using the CRISPR/Cas9‑mediated Blnk or Foxo1 knockout BCR‑ABL1‑transformed pro‑B cells, it was identified that, in BCR‑ABL1‑transformed pro‑B cells, Blnk and Foxo1 reduced Bcr‑Abl kinase activity to induce cell cycle arrest and decrease genomic instability. In addition, Blnk suppressed the PI3K/Akt pathway to reduce Foxo1 phosphorylation and heighten the Foxo1 activity, indicating that, in BCR‑ABL1‑transformed pro‑B cells, Foxo1 participated in the regulation of Bcr‑Abl kinase by Blnk. The present data highlighted the antitumor mechanisms of Blnk and Foxo1 in the regulation of Bcr‑Abl kinase, and thus, may offer an alternative therapeutic strategy to Bcr‑Abl kinase regulation in BCR‑ABL1+ B‑ALL.The oncogenic role of Erb‑B2 Receptor Tyrosine Kinase 2 (ERBB2) has been identified in several types of cancer, but less is known on its function and mechanism of action in cervical cancer cells. The present study employed a multipronged approach to investigate the role of ERBB2 in cervical cancer. ERBB2 and microRNA (miR)‑3184‑5p expression was assessed in patient‑derived cervical cancer biopsy tissues, revealing that higher levels of ERBB2 and lower levels of miR‑3184‑5p were associated with clinicopathological indicators of cervical cancer progression. Furthermore, ERBB2 stimulated proliferation, migration and sphere‑formation of cervical cancer cells in vitro. This effect was mediated by enhanced phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit α activity. Additionally, it was revealed that miR‑3184‑5p directly suppressed ERBB2 in cervical cancer cells. The p53 activator Mithramycin A stimulated p53 and miR‑3184‑5p expression, thereby lowering the levels of ERBB2 and attenuating proliferation, migration and sphere‑formation of cervical cancer cells. In conclusion, the findings of the present study suggested ERBB2 as an oncogenic protein that may promote invasiveness in cervical cancer cells. Treatment of cervical cancer cells with the p53 activator Mithramycin A restored the levels of the endogenous ERBB2 inhibitor miR‑3184‑5p and may represent a novel treatment strategy for cervical cancer.Currently, the prognosis of acute myeloid leukemia (AML) is poor. In the AML microenvironment, bone marrow (BM) mesenchymal stem cells (BMMSCs) serve an important role in protecting AML cells from chemotherapy‑induced apoptosis. The present study aimed to evaluate the expression of fibroblast activation protein α (FAPα) in BMMSCs and BM biopsy samples via flow cytometry, reverse transcription‑quantitative PCR and immunohistochemistry, as well as to identify the correlation between the expression of FAPα in BM with clinical parameters and survival of newly diagnosed patients with AML. Subsequently, the protective effect of FAPα on Cytosine arabinoside (Ara‑C)‑induced apoptosis in Kasumi‑1 cells was investigated via small interfering (si)RNA, and its underlying mechanism was examined by western blotting. The results demonstrated significant differences in FAPα expression in BMMSCs and BM biopsy samples between patients with AML and healthy donors. Furthermore, BMMSCs protected Ara‑C‑induced Kasumi‑1 cells from apoptosis, and knockdown of FAPα using siRNA decreased this protection. It was found that Kasumi‑1 cells expressed β‑catenin, which could be inhibited by Ara‑C, and β‑catenin expression was significantly activated when co‑cultured with BMMSCs, even in the presence of Ara‑C. Knockdown of FAPα with siRNA significantly suppressed the expression of β‑catenin. The present results indicated that FAPα serves an important role in the AML BM microenvironment, and that increased expression of FAPα in BM may be a poor prognostic factor in patients with AML. Moreover, the current findings demonstrated that BMMSCs protected AML cells from apoptosis, which was in part contributed by FAPα, and may occur via the β‑catenin signaling pathway.