Chemotherapy is currently the mainstay of systemic management for triple-negative breast cancer (TNBC), but chemoresistance significantly impacts patient outcomes. Our research indicates that Doxorubicin (Dox)-resistant TNBC cells exhibit increased glycolysis and ATP generation compared to their parental cells, with this metabolic shift contributing to chemoresistance. We discovered that ALKBH3, an m¹A demethylase enzyme, is crucial in regulating the enhanced glycolysis in Dox-resistant TNBC cells. Knocking down ALKBH3 reduced ATP generation, glucose consumption, and lactate production, implicating its involvement in mediating glycolysis. Further investigation revealed that aldolase A (ALDOA), a key enzyme in glycolysis, is a downstream target of ALKBH3. ALKBH3 regulates ALDOA mRNA stability through m¹A demethylation at the 3'-untranslated region (3'UTR). This methylation negatively affects ALDOA mRNA stability by recruiting the YTHDF2/PAN2-PAN3 complex, leading to mRNA degradation. The ALKBH3/ALDOA axis promotes Dox resistance both in vitro and in vivo. Clinical analysis demonstrated that ALKBH3 and ALDOA are upregulated in breast cancer tissues, and higher expression of these proteins is associated with reduced overall survival in TNBC patients. Our study highlights the role of the ALKBH3/ALDOA axis in contributing to Dox resistance in TNBC cells through regulation of ALDOA mRNA stability and glycolysis.

Objective To explore the clinical effect of Buqi Huayu prescription on chronic atrophic gastritis with intestinal metaplasia.Methods A total of 60 patients with chronic atrophic gastritis and intestinal metaplasia in the Department of Spleen and Stomach Diseases,Jinhua Hospital of Traditional Chinese Medicine Affiliated to Zhejiang Chinese Medical University from April 2019 to June 2020 were selected and randomly divided into Buqi Huayu prescription group and control group,with 30 cases in each group.Patients in Buqi Huayu prescription group were treated with Buqi Huayu prescription;Patients in control group were treated with folic acid tablets.After 6 months of treatment,the clinical comprehensive efficacy,traditional Chinese Medicine syndrome score,pathological change score,serum pepsinogen(PG)Ⅰ,PGⅡ,PGⅠ/PGⅡ(PGR)were observed before and after treatment in two groups.Results The clinical curative effect of Buqi Huayu prescription group was significantly better than that of control group(90%vs.70%,P<0.05).After treatment,traditional Chinese Medicine syndrome score and gastric mucosa pathology score of two groups were lower than before treatment(P<0.05).The intestinal metaplasia score of Buqi Huayu prescription group was significantly higher than that of control group(P<0.05).The levels of PGⅠ and PGR were higher than before treatment,while the levels of PGⅡ were lower than before treatment(P<0.05).All the indexes in Buqi Huayu prescription group were better than those in control group(P<0.05).Conclusion Buqi Huayu prescription is effective in the treatment of chronic atrophic gastritis with intestinal metaplasia.It can not only improve the pathological changes of patients,but also increase the level of serum PGⅠ and PGR,and decrease the level of PGⅡ.

Organoids can well simulate the heterogeneity of tumors,including tumor microenvironment and immune response,which helps to more accurately predict patient responses to drug and treatment effects.Organoids can be used for drug screening before drugs enter body,thus reducing the time and cost of clinical trials.However,research on tissue-organoids still faces some challenges,such as technical limitation and ethical issue.This review mainly introduces the progress in the research of breast cancer organoids,including the definition of organoids,development history,advantages and application in breast cancer research.

Objective To investigate the effect of emodin on immune suppression function of regulatory T cells in a mouse model of CT26 colon cancer. Methods Twenty-four mice were divided into the negative control group, the emodin group and the tumor group. The populations of CD8+CD3+T cells, the T cells producing IFN-γand the CD4+CD25+Tregs secreting IL-10 in different mouse tissues were detected by flow cytometry. Levels of IFN-γ, TNF- β1 and IL-10 in serum were determined by ELISA. Results Emodin could significantly increase the percent of CD8+CD3+T cells in tumor (P < 0.05) and improve the ability of IFN-γ secretion in T cells from peripheral blood and lymph nodes (P < 0.05). Emodin could reduce the levels of IFN-γ, TNF-β1 and IL-10 in the serum (P < 0.01) and inhibit IL-10 secretion in CD4+CD25+ Tregs (P < 0.01). Conclusion Emodin possesses the antitumor effect by affecting the immunosuppressive function of Tregs cells.