This study demonstrates the important role of CDK5 in the pathogenesis, viability, prognosis and resistance to bortezomib of MM, laying a solid theoretical foundation for further clinical use of CDK5 inhibitors.To improve the complete response rate (CRR) and reduce the recurrence rate of newly diagnosed non‑elderly acute myeloid leukemia (AML), the present study compared the clinical efficacy of decitabine with cytarabine (A) and daunorubicin (D)‑based remission induction therapy with D + A‑based remission induction therapy. A total of 81 patients with newly diagnosed non‑elderly AML (non‑M3) were enrolled in the present study, and divided into the observation group [decitabine with D + A, demethoxydaunorubicin (I) + A or homoharringtonine (H) + A] and the control group (D + A, I + A or H + A). The observation group displayed a 91.4% CRR [95% confidence interval (CI), 81.7‑100%] and the control group displayed a 69.6% CRR (95% CI, 55.8‑83.4%). The 2‑year overall survival (OS) rate was improved in the observation group compared with the control group (P=0.008). Patients aged less then 60 years displayed a 92.9% CRR in the observational group and a 71.1% CRR in the control group (P less then 0.05). Patients with undetected methylation gene mutations displayed an improved CRR in the observation group compared with the control group (92.9 vs. 71.4%; P=0.028). Furthermore, relapse‑free survival (P=0.041) and OS (P=0.007) were significantly extended in the observation group compared with the control group.  https://www.selleckchem.com/products/PD-98059.html  The present study suggested that the administration of decitabine with DA, IA or HA as an induction therapy improved the clinical efficacy and reduced the recurrence rate in patients with AML.Human epidermal growth factor receptor 2 (HER2) is composed of an extracellular domain (ECD), a lipophilic transmembrane region and an intracellular domain (ICD). The most commonly used method to determine the status of HER2 is immunohistochemistry. However, false‑negative results are sometimes given, which causes some patients to lose the opportunity for anti‑HER2 therapy. We found that calpain‑10 may prohibit HER2‑ECD into peripheral blood resulting in a HER2‑negative result by the immunohistochemical method. We enrolled 289 patients into our experiment to assess the relationship between sHER2‑ECD and calpain‑10. The results showed that there was a positive correlation between sHER2‑ECD and calpain‑10. Moreover, we also investigated the prognostic values of sHER2‑ECD and calpain‑10 in breast cancer patients. According to the follow‑up results, positive sHER2‑ECD and tissue calpain‑10 were indicative of a poor prognosis in breast cancer patients. Subsequently, we further validated the relationship between the two molecules in in vitro experiments. In the in vitro experiments, the level of HER2‑ECD in the culture medium was increased or decreased with a decrease or increase in calpain‑10 by transfection technology, showing an inverse association. The results indicated that sHER2‑ECD and tissue calpain‑10 levels were powerful factors to assess the status of HER2. In combination with tissue HER2 detection, the occurrence of false‑negative HER2 was reduced, providing patients with additional treatment opportunities. In conclusion, sHER2‑ECD and tissue calpain‑10 may be used as new prognostic indices for breast cancer.Substantial evidence indicates that circular RNAs (circRNAs) play vital roles in several diseases, especially in cancer development. However, the functions of circRNAs in breast cancer metastasis remain to be investigated. This study aimed to identify the key circRNAs involved in epithelial mesenchymal transition (EMT) of breast cancer and evaluated their molecular function and roles in pathways that may be associated with tumor metastasis. An EMT model was constructed by treating breast cancer cells MCF‑7 and MDA‑MB‑231 with transforming growth factor‑β1. High‑throughput RNA sequencing was used to identify the differentially expressed circRNAs in EMT and blank groups of two cells, and reverse transcription‑quantitative PCR was used to validate the expression of circSCYL2 in human breast cancer tissues and cells. The effects of circSCYL2 on breast cancer cells were explored by transfecting with plasmids and the biological roles were assessed using transwell assays. EMT groups of breast cancer cells exhibited the characteristics of mesenchymal cells. Furthermore, the present study found that 7 circRNAs were significantly upregulated in both the MCF‑7 EMT and MDA‑MB‑231 EMT groups, while 16 circRNAs were significantly downregulated. The current study identified that circSCYL2 was downregulated in breast cancer tissues and cell lines, and that circSCYL2 overexpression inhibited cell migration and invasion. This study provides expression profiles of circRNAs in EMT groups of breast cancer cells. circSCYL2, which is downregulated in breast cancer tissues and cells, may play an important role in breast cancer EMT progression.A tumor contains special types of cells that have characteristics similar to stem cells that aid in tumor initiation, evasion and proliferation and are often resistant to chemotherapy. These cancer stem cells can be differentiated to eradicate their stemness and proliferative capacity by differentiating agents. This study investigated the effect of differentiation on the expression of two immune checkpoint inhibitors, human leukocyte antigen‑G (HLA‑G) and programmed death ligand‑1 (PD‑L1). Two cancer cell lines (OVCAR‑3‑NIH and KATO‑III) were treated with adipocyte and neurocyte differentiation media for 14 days. Bone‑marrow derived mesenchymal stem cells (BM‑MSCs) were used as control healthy stem cells. We found that the cancer cell lines (OVCAR‑3‑NIH and KATO‑III) when subjected to differentiation lost their proliferation ability. BM‑MSC proliferation was not halted but was decreased in the adipocyte differentiation media. There was no decrease in the CD90 stem cell marker in the BM‑MSCs; however, both cancer cell lines showed decreased CD90 stem cell marker.