Background Acute myeloid leukemia (AML) is recognized as a hematological neoplasm with heterogenetic cytology and short-term outcome. HCP5 has been proven to be related with the pathogenesis of AML. However, the underlying mechanism of HCP5 in AML remains unclear. Methods Clinical profiles of AML patients were downloaded from TCGA and GTEx databases. LncBase and TargetScan online tools were utilized to predict potential targets, and dual-luciferase reporter assay was performed to verify the association between miR-1291 and HCP5 or PIK3R5. Cell Counting Kit 8 and flow cytometry tests were implemented to evaluate the effects of HCP5/miR-1291/PIK3R5 axis in AML cells. Quantitative RT-PCR and Western blot were conducted to detect the expression levels of genes. Results HCP5 and PIK3R5 were significantly increased in AML tissue samples compared with healthy controls. HCP5 facilitated AML cells viability and inhibited apoptosis. There was a positive relationship between HCP5 and PIK3R5, but miR-1291 negatively regulated PIK3R5. Overexpression of PIK3R5 enhanced the promoting effect of HCP5 in the development of AML, while weakened the suppression of miR-1291 to AML progression. Conclusion Our findings manifested that HCP5 was remarkably upregulated in AML and upregulated HCP5 promoted the malignant behaviors of AML cells by mediating miR-1291/PIK3R5 axis, which would provide a new insight for the treatment of AML.

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Purpose: The aim of the study is to determine the levels and related factors of colorectal cancer patients about stoma acceptance. Methods: This descriptive study enrolled 136 colorectal cancer outpatients follow-up at several hospitals in Shandong province. Stoma acceptance was assessed with Chinese version stoma acceptance questionnaire(SAQ). The association of stoma acceptance and colorectal cancer patients characteristics was assessed by logistic regression. Results: The total average stoma acceptance of 136 patients in this study was(37.03±4.87). General self-efficacy was(27.96±5.28). General self-efficacy was positively associated with stoma acceptance(r=0.529，P<0.001). The linear regression results showed that factors of general self-efficacy, social needs, receiving medical follow-up and education level were the factors affecting stoma acceptance in colorectal cancer patients. Conclusions: The stoma acceptance in colorectal cancer patients in grade 3 hospitals is at a medium level in China. Medical staff should pay attention to it, and improve caregiver’ supports, increase medical follow-up,meet the need for social communication. Strengthen the intervention of patients’ self-efficacy to intervene, so as to improve the stoma acceptance and improve the quality of life.

Background:It was reported that circular RNA (circRNA) circCTNNA1 plays an oncogenic role in colorectal cancer, while its rfole in mantle cell lymphoma (MCL) is unknown. This study aimed to explore the role of circCTNNA1 in MCL. Methods:Samples of B lymphocytes were collected from 56 MCL patients and 56 healthy controls. The expression of circCTNNA1 and miR-34a in these samples were determined by RT-qPCRs. The direct interaction between circCTNNA1 and miR-34a in MCL cells was detected using RNA-RNA pulldown assay. Overexpression assays were performed to study the interactions between circCTNNA1 and miR-34a. Cell proliferation was assessed with BrdU assay. Results:The results showed that circCTNNA1 was upregulated in MCL and high expression levels of circCTNNA1 predicted the poor survival of MCL patients. MiR-34a was downregulated in MCL and inversely correlated with circCTNNA1. CircCTNNA1 was predicted to interact with miR-34a, and the interaction between them was confirmed by RNA pull-down assay. Interestingly, overexpression of circCTNNA1 and miR-34a did not affect the expression of each other. Cell proliferation analysis showed that overexpression of circCTNNA1 reversed the inhibitory effects of overexpression of miR-34a on cell proliferation. Conclusion:Upregulation of circCTNNA1 in MCL predicts poor survival of patients and it may sponge miR-34a to promote cancer cell proliferation.