Astrocyte allocation during brain development is controlled by Tcf4-mediated fate restriction.

Astrocytes in the brain exhibit regional heterogeneity contributing to regional circuits involved in higher-order brain functions, yet the mechanisms controlling their distribution remain unclear. Here, we show that the precise allocation of astrocytes to specific brain regions during development is achieved through transcription factor 4 (Tcf4)-mediated fate restriction based on their embryonic origin. Loss of Tcf4 in ventral telencephalic neural progenitor cells alters the fate of oligodendrocyte precursor cells to transient intermediate astrocyte precursor cells, resulting in mislocalized astrocytes in the dorsal neocortex. These ectopic astrocytes engage with neocortical neurons and acquire features reminiscent of dorsal neocortical astrocytes. Furthermore, Tcf4 functions as a suppressor of astrocyte fate during the differentiation of oligodendrocyte precursor cells derived from the ventral telencephalon, thereby restricting the fate to the oligodendrocyte lineage in the dorsal neocortex. Together, our findings highlight a previously unappreciated role for Tcf4 in regulating astrocyte allocation, offering additional insights into the mechanisms underlying neurodevelopmental disorders linked to Tcf4 mutations.

Time Trends and Demographic Disparities in Helicobacter pylori Burden in a Large, Community-Based Population in the United States.

Background and Aims: There are minimal recent population-based data on the epidemiology of Helicobacter pylori (H. pylori) in the United States. Methods: This retrospective cohort study evaluated H. pylori positivity rates in adult members of a large, community-based US population in 2000-2019. Time trends, demographic disparities, and birth cohort effects on H. pylori test positivity rates were analyzed. Results: Among 751,322 individuals tested for H. pylori, the overall nonserological and serological test positivity rates were 18.2% (95% confidence interval [CI], 18.1%-18.4%) and 36.8% (95% CI, 36.6%-36.9%), respectively. Nonserological positivity rate (95% CI) was significantly higher among Asian (23.2% [22.8%-23.6%]), Black (25.1% [24.4%-25.8%]), and Hispanic (28.1% [27.7%-28.5%]) individuals than non-Hispanic White individuals (10.0% [9.8%-10.2%]), and was significantly higher among individuals with a non-English language preference (32.9% [32.3%-33.5%]) than those with English language preference (15.8% [15.6%-15.9%]). Patterns were similar for serological positivity, although with substantially higher rates. Serological positivity rates decreased over 2 decades but nonserological positivity rates initially decreased and then stabilized over the past decade. There was a significant decrease in both nonserological and serological positivity rates from older to younger birth cohorts. Older age, non-White race or Hispanic ethnicity, male sex, and non-English language preference were associated with high odds of H. pylori positivity. Conclusion: The burden of H. pylori decreased over 2 decades, although the rates of active infection plateaued over the past decade in a diverse, community-based US population, likely attributable to birth cohort effects and demographic changes. Asian, Black, and Hispanic individuals had 2-3-fold higher rates of active H. pylori infection than non-Hispanic White individuals. These findings should inform targeted screening and eradication of H. pylori in high-risk US populations.

Regulation of a novel circATP8B4/miR-31-5p/nestin ceRNA crosstalk in proliferation, motility, invasion and radiosensitivity of human glioma cells.

Deregulation of circular RNAs (circRNAs) is frequent in human glioma. Although circRNA ATPase phospholipid transporting 8B4 (circATP8B4) is highly expressed in glioma, its precise action in glioma development is still not fully understood. The relationship of microRNA (miR)-31-5p and circATP8B4 or nestin (NES) was predicted by bioinformatic analysis and confirmed by RNA pull-down and Dual-luciferase reporter assays. CircATP8B4, miR-31-5p and NES were quantified by qRT-PCR or western blot. Cell functional behaviors were assessed by EdU, wound-healing and transwell invasion assays. Xenograft model experiments were performed to define circATP8B4's activity in vivo. CircATP8B4, a true circular transcript, was upregulated in human glioma. CircATP8B4 downregulation weakened glioma cell growth, motility, and invasion and facilitated radiosensitivity. Mechanistically, circATP8B4 and NES 3'UTR harbored a shared miR-31-5p pairing site, and circATP8B4 involved the post-transcriptional NES regulation by functioning as a competing endogenous RNA (ceRNA). Furthermore, the miR-31-5p/NES axis participated in circATP8B4's activity in glioma cell proliferation, motility, invasion and radiosensitivity. Additionally, circATP8B4 loss diminished tumor growth and enhanced the anticancer effect of radiotherapy in vivo. We have uncovered an uncharacterized ceRNA cascade, circATP8B4/miR-31-5p/NES axis, underlying glioma development and radiosensitivity. Targeting the ceRNA crosstalk may have potential to improve the outcome of glioma patients.

In Situ and Rapid Toxicity Assessment of Air Pollution by Self-Assembly Passive Colonization Hydrogel.

Air pollution is a leading environmental health risk factor, and in situ toxicity assessment is urgently needed. Bacteria-based bioassays offer cost-effective and rapid toxicity assessments. However, the application of these bioassays for air toxicity assessment has been challenging, due to the instability of bacterial survival and functionality when directly exposed to air pollutants. Here, we developed an approach employing self-assembly passive colonization hydrogel (SAPCH) for in situ air toxicity assessment. The SAPCH features a core-shell structure, enabling the quantitatively immobilization of bacteria on its shell while continuously provides nutrients from its core. An antimicrobial polyelectrolyte layer between the core and shell confines bacteria to the air-liquid interface, synchronizing bacterial survival with exposure to air pollutants. The SAPCH immobilized a battery of natural and recombinant luminescent bacteria, enabling simultaneous detection of various toxicological endpoints (cytotoxicity, genotoxicity and oxidative stress) of air pollutants within 2 h. Its sensitivity was 3-5 orders of magnitude greater than that of traditional liquid-phase toxicity testing, and successfully evaluating the toxicity of volatile organic compounds and combustion smoke. This study presents a method for in situ, rapid, and economical toxicity assessment of air pollution, making a significant contribution to future air quality monitoring and control.

Ginkgolic Acid as a carbapenem synergist against KPC-2 positive Klebsiella pneumoniae.

The successful evolution of KPC-2 in bacteria has limited the clinical practice of carbapenems. This dilemma deteriorated the prognosis of associated infections and hence attracted increasing attention from researchers to explore alternative therapeutic options. Here, the enzyme inhibition assay was first performed to screen for a potent KPC-2 inhibitor. The synergistic effect of the candidate with carbapenems was further confirmed by checkboard minimum inhibitory concentration (MIC) assay, time-killing assay, disk diffusion method, and live/dead bacteria staining analysis. The mechanisms by which the candidate acts were subsequently explored through molecular dynamics (MD) simulations, etc. Our study found that Ginkgolic Acid (C13:0) (GA) exhibited effective KPC-2 inhibitory activity in both laboratory strain and clinical strain containing KPC-2. It could potentiate the killing effect of carbapenems on KPC-2-positive Klebsiella pnenmoniae (K. pnenmoniae). Further explorations revealed that GA could competitively bind to the active pocket of KPC-2 with meropenem (MEM) via residues Trp104, Gly235, and Leu166. The secondary structure and functional groups of KPC-2 were subsequently altered, which may be the main mechanism by which GA exerted its KPC-2 inhibitory effect. In addition, GA was also found to synergize with MEM to disrupt membrane integrity and increase membrane permeability, which may be another mechanism by which GA reinforced the bactericidal ability of carbapenems. Our study indicated that GA was a significant KPC-2 inhibitor that could prolong the lifespan of carbapenems and improve the prognosis of patients.

Exosomal Drug Delivery Systems: A Novel Therapy Targeting PD-1 in Septic-ALI.

BACKGROUND: The cytokine storm triggered by sepsis can lead to the development of acute lung injury (ALI). Human umbilical cord Mesenchymal stem cells derived exosomes (HucMSCs-EXOs) have been demonstrated to possess immunosuppressive and anti-inflammatory properties. Programmed cell death receptor 1 (PD-1) plays a crucial role in maintaining the inflammatory immune homeostasis. The aim of this study is to investigate the synergistic therapeutic effect of EXOs loaded with anti-PD-1 peptide on septic-ALI. METHODS: This study prepares a novel EXOs-based drug, named MEP, by engineering modification of HucMSCs-EXOs, which are non-immunogenic extracellular vesicles, loaded with anti-PD-1 peptide. The therapeutic effect and potential mechanism of MEP on septic-ALI are elucidated through in vivo and in vitro experiments, providing experimental evidence for the treatment of septic acute lung injury with MEP. RESULTS: We found that, compared to individual components (anti-PD-1 peptide or EXOs), MEP treatment can more effectively improve the lung injury index of septic-ALI mice, significantly reduce the expression levels of inflammatory markers CRP and PCT, as well as pro-inflammatory cytokines TNF-α and IL-1ß in serum, decrease lung cell apoptosis, and significantly increase the expression of anti-inflammatory cytokine IL-10 and CD68+ macrophages. In vitro, MEP co-culture promotes the proliferation of CD206+ macrophages, increases the M2/M1 macrophage ratio, and attenuates the inflammatory response. GEO data analysis and qRT-PCR validation show that MEP reduces the expression of inflammasome-related genes and M1 macrophage marker iNOS. CONCLUSION: In both in vitro and in vivo settings, MEP demonstrates superior therapeutic efficacy compared to individual components in the context of septic-ALI.

PM2.5-mediated cardiovascular disease in aging: Cardiometabolic risks, molecular mechanisms and potential interventions.

Air pollution, particularly fine particulate matter (PM2.5) with <2.5 µm in diameter, is a major public health concern. Studies have consistently linked PM2.5 exposure to a heightened risk of cardiovascular diseases (CVDs) such as ischemic heart disease (IHD), heart failure (HF), and cardiac arrhythmias. Notably, individuals with pre-existing age-related cardiometabolic conditions appear more susceptible. However, the specific impact of PM2.5 on CVDs susceptibility in older adults remains unclear. Therefore, this review addresses this gap by discussing the factors that make the elderly more vulnerable to PM2.5-induced CVDs. Accordingly, we focused on physiological aging, increased susceptibility, cardiometabolic risk factors, CVDs, and biological mechanisms. This review concludes by examining potential interventions to reduce exposure and the adverse health effects of PM2.5 in the elderly population. The latter includes dietary modifications, medications, and exploration of the potential benefits of supplements. By comprehensively analyzing these factors, this review aims to provide a deeper understanding of the detrimental effects of PM2.5 on cardiovascular health in older adults. This knowledge can inform future research and guide strategies to protect vulnerable populations from the adverse effects of air pollution.

Breaking through therapeutic barriers: Insights into CDK4/6 inhibition resistance in hormone receptor-positive metastatic breast cancer.

The therapeutic landscape for hormone receptor-positive (HR+) breast carcinoma has undergone a significant transformation with the advent of cyclin-dependent kinase (CDK)4/6 inhibitors, particularly in combination with endocrine therapy as the primary regimen. However, the evolution of resistance mechanisms in response to CDK4/6 inhibitors in HR+ metastatic breast cancer presents substantial challenges in managing the disease. This review explores the diverse genomic landscape underlying resistance, including disturbances in the cell cycle, deviations in oncogenic signaling pathways, deficiencies in DNA damage response (DDR) mechanisms, and changes in the tumor microenvironment (TME). Additionally, it discusses potential strategies to surmount resistance, including advancements in endocrine therapy, targeted inhibition of cell cycle components, suppression of AKT/mTOR activation, exploration of the FGFR pathway, utilization of antibody-drug conjugates (ADCs), and integration of immune checkpoint inhibitors (ICIs) with endocrine therapy and CDK4/6 inhibitors, providing pathways for enhancing patient outcomes amidst treatment challenges.

Distribution and Determinants of Anterior Chamber Angle and Anterior Chamber Volume in Young Chinese Adults.

PURPOSE: Current study aimed to understand the distribution and determinants of anterior chamber angle (ACA) and anterior chamber volume (ACV) in Chinese young adults, which can help fill current data gaps and aid in early detection and intervention for high-risk population of primary angle closure glaucoma. METHODS: This cross-sectional study utilized data from 2014 participants who completed questionnaire and eye examination in September 2021. ACV and ACA were measured using a Pentacam tomographer. Spherical equivalent (SE) was evaluated by autorefractor without cycloplegia. Central corneal thickness (CCT) and biomechanically corrected intraocular pressure (bIOP) were evaluated using Corvis-ST. Axial length (AL), corneal radius (CR), anterior chamber depth (ACD), and white to white were assessed using the IOL Master. RESULTS: A total of 1635 students were included in the analysis. The mean ACV and AVA were 194.74 ± 32.30 µL and 38.81 ± 4.84°, respectively. Males have a larger ACV and wider ACA than females. ACV was positively correlated with ACA (r = 0.24, p < 0.001), and the correlation was stronger for non-myopic students than for myopic students. Multivariable linear regression model showed that AL (ß = 2.41), CR (ß = -4.12), CCT (ß = -0.11), ACD (ß = 97.93), and bIOP (ß = 0.40) were associated with ACV, and CCT (ß = -0.01), CR (ß = 0.38), and ACD (ß = 7.41) were associated with ACA (all p < 0.05). Random forest model indicated that ACD was the most critical predictor of both ACV and ACA. CONCLUSIONS: This study reported the distribution and determinants of ACA and ACV. Deeper ACD was associated with larger ACV and wider ACA.

circE2F1-encoded peptide inhibits circadian machinery essential for nucleotide biosynthesis and tumor progression via repressing SPIB/E2F1 axis.

Circadian clock dominates a variety of biological activities, while its roles and regulatory mechanisms in neuroblastoma (NB), a pediatric extracranial malignancy, still remain largely elusive. Herein, through comprehensive analyses of public datasets, E2F transcription factor 1 (E2F1) and its circular RNA (circE2F1)-encoded 99-amino acid peptide (E2F1-99aa) were identified as vital regulators of circadian machinery essential for purine and pyrimidine biosynthesis during NB progression. Mechanistically, through interaction with Spi-B transcription factor (SPIB), E2F1 was transactivated to up-regulate circadian machinery genes (CRY1 and TIMELESS), resulting in relief of CLOCK/BMAL1-repressed transcription of enzymes (DHODH, PAICS, or PPAT) essential for de novo purine and pyrimidine biosynthesis. The biogenesis of circE2F1 was repressed by eukaryotic translation initiation factor 4A3 (EIF4A3), while E2F1-99aa or its truncated peptide competitively bound to SPIB, leading to decrease in SPIB-E2F1 interaction, circadian machinery and nucleotide biosynthetic gene expression, purine or pyrimidine biosynthesis, tumorigenesis, and aggresiveness of NB cells. In clinical NB cases, high EIF4A3, E2F1 or SPIB levels were correlated with low survival possibility of patients, while lower circE2F1 or E2F1-99aa levels were associated with advanced stages and tumor progression. These results indicate that circE2F1-encoded peptide inhibits circadian machinery essential for nucleotide biosynthesis and tumor progression via repressing SPIB/E2F1 axis.

Mesoporous metal-organic framework NH2-MIL-101(Cr) as an efficient photocatalyst for the epoxidation of styrene.

Oxidation of styrene is a key reaction in the synthesis of pharmaceuticals and fine chemicals, and therefore oxidizing styrene with selective, efficient, and recyclable heterogeneous catalysts is significant from an environmental and economic standpoint. In this study, we report the transition Cr-based metal-organic framework [NH2-MIL-101(Cr)] as a heterogeneous photocatalyst, which efficiently promotes styrene epoxidation using H2O2 as a green oxidant, achieving high conversion efficiency (98%) and excellent selectivity (82%) under ambient conditions. Radical detection and quenching experiments reveal that the superoxide radical anion (O2˙-) acts as an active oxygen species, selectively promoting the oxidation of styrene to its oxidized form. This work provides insight into the development of a sustainable and cost-effective method for producing styrene oxide.

Three-Supercenter Two-Electron Bonds in C16H10: Two-Dimensional Analogue of Halogen-Bridge Bonding.

Three-center two-electron bridging bonding plays a vital role in rationalizing structures and stabilities of certain molecules. Herein, the π electron rule of pyrene (C16H10) was unraveled based on a newly proposed two-dimensional (2D) superatomic-molecule theory, where the superatomic sextet rule was regarded as a π electron counting target. C16H10 can be taken as a ◊N2◊F2 superatomic molecule, where ◊N and ◊F denote 2D superatoms bearing 3π and 5π electrons, respectively. Interestingly, it represents the first 2D superatomic halogen-bridge molecule, which realizes π electronic shell-closure via two three-supercenter two-electron bridging bonds. Additionally, a N-doped nanoporous graphene with a wide band gap (1.22 eV) was designed based on C16H10, which can be considered as a periodic aggregate of 2D superatomic wires composed of 2π-◊C and bridging ◊F superatoms. This work enriches the 2D superatomic-molecule chemistry and provides a practicable bottom-up assemble approach to obtain 2D functional materials with tunable band gaps.

Elevated concentrations of amyloid-ß oligomers and their proapoptotic effects on age-related cataract.

Recently, amyloid-ß oligomers (AßOs) have been studied as the primary pathogenic substances in Alzheimer's disease (AD). Our previous study revealed that the Aß expression level is closely related to ARC progression. Here, we demonstrated that the accumulation of AßOs in the lens epithelium of age-related cataract (ARC) patients increased during ARC progression and that this alteration was consistent with the changes in mitochondrial function, oxidative stress, and cellular apoptosis. In vitro, human lens epithelial cells (HLECs) treated with AßOs exhibited Ca2+ dyshomeostasis, impaired mitochondrial function, elevated oxidative stress levels, and increased apoptosis. Moreover, the proapoptotic effect of AßOs was alleviated after the uptake of mitochondrial Ca2+ was inhibited. These results establish that AßOs may promote HLEC apoptosis by inducing mitochondrial Ca2+ overload, thus preliminarily revealing the possible association between the accumulation of AßOs and other pathological processes in ARC.

Primary coexisting adenocarcinoma of the colon and neuroendocrine tumor of the duodenum: A case report and review of the literature.

BACKGROUND: Neuroendocrine tumors (NETs) arise from the body's diffuse endocrine system. Coexisting primary adenocarcinoma of the colon and NETs of the duodenum (D-NETs) is a rare occurrence in clinical practice. The classification and treatment criteria for D-NETs combined with a second primary cancer have not yet been determined. CASE SUMMARY: We report the details of a case involving female patient with coexisting primary adenocarcinoma of the colon and a D-NET diagnosed by imaging and surgical specimens. The tumors were treated by surgery and four courses of chemotherapy. The patient achieved a favorable clinical prognosis. CONCLUSION: Coexisting primary adenocarcinoma of the colon and D-NET were diagnosed by imaging, laboratory indicators, and surgical specimens. Surgical resection combined with chemotherapy was a safe, clinically effective, and cost-effective treatment.

Machine Learning and Imputation to Characterize Human Norovirus Genotype Susceptibility to Sodium Hypochlorite.

Human norovirus (HuNoV) is the leading cause of foodborne illness in the developed world and a major contributor to gastroenteritis globally. Its low infectious dose and environmental persistence necessitate effective disinfection protocols. Sodium hypochlorite (NaOCl) bleach is a widely used disinfectant for controlling HuNoV transmission via contaminated fomites. This study aimed to evaluate the susceptibility of HuNoV genotypes (n = 11) from genogroups I, II, and IV to NaOCl in suspension. HuNoV was incubated for 1 and 5 min in diethyl pyrocarbonate (DEPC) treated water containing 50 ppm, 100 ppm, or 150 ppm NaOCl, buffered to maintain a pH between 7.0 and 7.5. Neutralization was achieved by a tenfold dilution into 100% fetal bovine serum. RNase pre-treatment followed by RT-qPCR was used to distinguish between infectious and non-infectious HuNoV. Statistical methods, including imputation, machine learning, and generalized linear models, were applied to process and analyze the data. Results showed that NaOCl reduced viral loads across all genotypes, though efficacy varied. Genotypes GI.1, GII.4 New Orleans, and GII.4 Sydney were the least susceptible, while GII.6 and GII.13 were the most susceptible. All NaOCl concentrations above 0 ppm were statistically indistinguishable, and exposure duration did not significantly affect HuNoV reduction, suggesting rapid inactivation at effective concentrations. For instance, some genotypes were completely inactivated within 1 min, rendering extended exposure unnecessary, while other genotypes maintained the initial concentration at both 1 and 5 min, indicating a need for longer contact times. These findings underscore the critical role of HuNoV genotype selection in testing disinfection protocols and optimizing NaOCl concentrations. Understanding HuNoV susceptibility to NaOCl bleach informs better disinfection strategies, aiding public health and food safety authorities in reducing HuNoV transmission and outbreaks.

Reaction-Modulated Surface-Enhanced Raman Scattering Strategy for Stereoselective Differentiation and Identification of Amino Acids.

Surface-enhanced Raman scattering (SERS) sensing of racemates is a remarkably fascinating yet very sophisticated objective because of similar physicochemical features of enantiomers. Inspired by the enantiomeric selectivity of nucleophilic addition reaction (NAR) toward amino acids, we herein propose highly effective, robust SERS discrimination of d- and l-valine by synergizing asymmetric gold nanorods-embedded ZIF-8 nanoparticles (AGNZ) with NAR to engender stereoselective molecular fingerprint. Experimental and chemometric analyses disclose that enantioselectivity lies in dual aspects: (i) abundant interfacial cavities and 3D hot-spots in AGNZ offer necessary confined asymmetrical surroundings to trigger enantiospecific molecular adsorption and interaction affinity, and (ii) the specified NAR drags the racemates adjacent to the interfacial area of AGNZ for maximum analytes-substrate interaction. This strategy is universal and can be utilized for the recognition of different amino acid enantiomers. Importantly, multiple quantifications of the racemic ratio can be realized with superior prognostic performances. This synergizing strategy therefore provides a significant paradigm shift from traditional methods to realize highly effective SERS discrimination of racemates.

Echinatin alleviates sepsis severity through modulation of the NF-κB and MEK/ERK signaling pathways.

Sepsis, a frequently fatal condition, emerges from an exaggerated inflammatory response to infection, resulting in multi-organ dysfunction and alarmingly high mortality rates. Despite the urgent need for effective treatments, current therapeutic options remain limited to antibiotics, with no other efficacious alternatives available. Echinatin (Ecn), a potent bioactive compound extracted from the roots and rhizomes of licorice, has gained significant attention for its broad pharmacological properties, particularly its ability to combat oxidative stress. Recent research highlights the crucial role that oxidative stress plays in the onset and progression of sepsis further emphasizing the potential therapeutic value of Ecn in this context. In this study, we explored the protective effects of Ecn in a murine model of sepsis induced by cecal ligation and puncture (CLP). Ecn demonstrated a significant reduction in the levels of inflammatory cytokines and reactive oxygen species (ROS) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Network pharmacology analysis identified 41 targets and top 15 pathways involved in the Ecn-mediated signaling network, revealing that Ecn might exert its effects through key targets including the NF-κB and MAPK signaling pathways. Molecular docking studies suggested a strong affinity between Ecn and MEK, with kinetic simulations and binding energy calculations confirming a stable interaction. Mechanistically, Ecn treatment inhibited NF-κB and the MEK/ERK signaling pathway, as evidenced by decreased phosphorylation of IκBα and nuclear p65, along with reduced phosphorylation of MEK and ERK in both LPS-stimulated RAW 264.7 macrophages and septic mice. Furthermore, the administration of MEK signaling agonists reversed the anti-inflammatory effects of Ecn, indicating the involvement of this signaling pathway in Ecn's protective mechanism. Notably, our investigation revealed that Ecn did not affect bacterial proliferation either in vivo or in vitro, underscoring its specific immunomodulatory effects rather than direct antimicrobial activity. In summation, our findings underscored the potential of Ecn as an innovative therapeutic remedy for sepsis-induced injury, particularly through the regulation of the NF-κB and MEK/ERK signaling pathway. This exploration unveiled a promising therapeutic approach for treating sepsis, supplementing existing interventions and addressing their constraints.

The role of the miR-30a-5p/BCL2L11 pathway in rosmarinic acid-induced apoptosis in MDA-MB-231-derived breast cancer stem-like cells.

Background: Rosmarinic acid (RA), a natural phenolic acid, exhibits promising anti-cancer properties. The abnormal expression of microRNA (miRNA) regulates the gene expression and plays a role as an oncogenic or tumor suppressor in TNBC. However, the biological role of RA in miR-30a-5p on BCL2L11 during MDA-MB-231 induced breast cancer stem-like cells (BCSCs) progression and its regulatory mechanism have not been elucidated. Objective: To investigate whether RA inhibited the silencing effect of miR-30a-5p on the BCL2L11 gene and promoted apoptosis in BCSCs. Materials and Methods: We assessed the migration, colony formation, proliferation, cell cycle, and apoptosis of BCSCs after RA treatment using the wound-healing assay, colony formation assay, CCK-8 assay, and flow cytometry, respectively. The expression of mRNA and protein levels of BCL-2, Bax, BCL2L11, and P53 genes in BCSCs after RA treatment was obtained by real-time polymerase chain reaction and Western blot. Differential miRNA expression in BCSCs was analyzed by high-throughput sequencing. Targetscan was utilized to predict the targets of miR-30a-5p. The dual luciferase reporter system was used for validation of the miR-30a-5p target. Results: Wound-healing assay, colony formation assay, CCK-8 assay, and cell cycle assay results showed that RA inhibited migration, colony formation and viability of BCSCs, and cell cycle arrest in the G0-G1 phase. At the highest dose of RA, we noticed cell atrophy, while the arrest rate at 100 µg/mL RA surpassed that at 200 µg/mL RA. Apoptotic cells appeared early (Membrane Associated Protein V FITC+, PI-) or late (Membrane Associated Protein V FITC+, PI+) upon administration of 200 µg/mL RA, Using high-throughput sequencing to compare the differences in miRNA expression, we detected downregulation of miR-30a-5p expression, and the results of dual luciferase reporter gene analysis indicated that BCL2L11 was a direct target of miR-30a-5p. Conclusion: RA inhibited the silencing effect of miR-30a-5p on the BCL2L11 gene and enhanced apoptosis in BCSCs.