Aims and objectives To explore barriers to hepatocellular carcinoma screening among patients with hepatitis B. Background Hepatitis B‐related hepatocellular carcinoma is a major cause of cancer‐related mortality globally. A preventive strategy for screening is needed to improve early tumour detection and overall survival. However, utilisation remains suboptimal and barriers are understudied and largely focused on clinical factors. Design A qualitative study based on the preventive health model using phenomenological hermeneutical approach. Methods Face‐to‐face semi‐structured interviews were conducted with 23 hepatitis B patients from November 2020 to February 2021. Interpretative phenomenological analysis was used. The COREQ checklist was followed. Results Four themes were identified: (i) miscognition, (ii) cultural stigma and taboo, (iii) social norms of enduring hardship and (iv) social barriers at the community, health system and policy levels. Patients had misconceptions about inactive carriers, asymptomatic nature of chronic hepatitis B, hepatocellular carcinoma risks and screening recommendations. Influenced by the taboo of hepatocellular carcinoma, stigma against hepatitis B and enduring hardship norms, they perceived screening as divination, avoided utilisation to hide disease status and endured symptoms until they were intolerable. Insufficient community support, a lack of shared decision‐making in health systems, and inadequate rural reimbursement policy and hepatocellular carcinoma detection capacity further precluded utilisation. Conclusions Cognitive and sociocultural barriers precluded individuals’ intention, utilisation and persistence of hepatocellular carcinoma screening. The results highlight intervention targets for miscognition, stigma, taboo and social norms; propose family‐focused, community‐based education programs; suggest health systems to introduce decision aids; and inform policymaking and upskilling of physicians in rural areas. Relevance to clinical practice Collaborative efforts are needed to improve real‐world hepatocellular carcinoma screening, including education to address knowledge deficiencies, psychological counselling to reduce stigma and taboo beliefs, support for shared decision‐making and reimbursement policies.

Daunorubicin (Dnr) is at the forefront of acute myeloid leukemia (AML) therapy, but drug resistance poses a major threat to treatment success. MicroRNA (miR)-9 has been shown to have a pivotal role in AML development. However, little is known about the role of miR-9 in Dnr resistance in AML. We explored the potential role of miR-9 in Dnr resistance in AML cells and its mechanism of action. AML cell lines with high half-maximal inhibitory concentration to Dnr in vivo had significantly low miR-9 expression. miR-9 overexpresssion sensitized AML cells to Dnr, inhibited cell proliferation, and enhanced the ability of Dnr to induce apoptosis; miR-9 knockdown had the opposite effects. Mechanistic studies demonstrated that eukaryotic translation initiation factor 5A-2 (EIF5A2) was a putative target of miR-9, which was inversely correlated with the expression and role of miR-9 in AML cells. miR-9 improved the anti-tumor effects of Dnr by inhibiting myeloid cell leukemia-1 (MCL-1) expression, which was dependent on downregulation of EIF5A2 expression. These results suggest that miR-9 has an essential role in Dnr resistance in AML cells through inhibition of the EIF5A2/MCL-1 axis in AML cells. Our data highlight the potential application of miR-9 in chemotherapy for AML patients.

In this study, we aimed to study the effect of miR‐33b in regulating sensitivity to daunorubicin (DNR) in acute myelocytic leukemia (AML). We used quantitative real‐time polymerase chain reaction and Cell Counting Kit‐8 assay to detect the level of miR‐33b and cell viability. Cell apoptosis and the expression of eIF5A‐2 and MCL‐1 protein were detected by flow cytometry analysis and Western Blot analysis, respectively. MiR‐33b mimic increased sensitivity of AML cells against DNR, while miR‐33b inhibitor had the opposite effect. Furthermore, the results showed that the eIF5A‐2 gene was a direct target of miR‐33b, and miR‐33b regulated eIF5A‐2 mRNA and protein expression. Silencing of eIF5A‐2 by RNA interference increased the sensitivity of AML cells against DNR. We also found that MCL‐1 contributed to the regulation of DNR sensitivity, which was dependent on downregulation of eIF5A‐2. Finally, knockdown of eIF5A‐2 eliminated the effects of miRNA‐33b mimic or inhibitor on DNR sensitivity. These findings indicate that miR‐33b maybe as a new therapeutic target in AML cells.