Breast cancer (BC) heterogeneity, particularly in triple-negative (TNBC) and HER2-positive subtypes, underpins therapeutic challenges and cancer-related mortality worldwide. Here, we identify the transmembrane oxidoreductase CYB561 as a pivotal oncoprotein that drives BC malignancy by coordinating lipid metabolic reprogramming and oncogenic signaling. CYB561 was significantly overexpressed in BC tissues, especially in HER2-positive (70%) and TNBC (60%) cases, and its expression correlated with advanced T stage, metastasis, and poor patient survival. Functionally, CYB561 potently promoted proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and tumor growth in vitro and in vivo. Mechanistically, CYB561 directly bound IRE1, triggering the IRE1-XBP1-SREBF1 axis to induce lipogenic enzyme expression and lipid droplet accumulation. Concurrently, it activated the FAK-ERK signaling pathway. Crucially, IRE1 knockdown abolished CYB561-induced lipogenesis and malignant phenotypes, while ERK inhibition partially attenuated these effects, revealing a synergistic crosstalk between metabolic and signaling axes. Our findings establish CYB561 as a master regulator of BC progression and nominate it as a promising therapeutic target for aggressive breast cancers.

Graft-versus-host disease (GVHD) remains the most severe complications following allogeneic hematopoietic cell transplantation (allo-HCT). Mesenchymal stromal cells (MSCs) have shown therapeutic potential in GVHD due to their immunomodulatory properties. However, their clinical application is constrained by safety concerns, including ectopic engraftment, microvascular obstruction, rejected by host, and potential tumor-supportive effects. Increasing evidence suggests that MSC-derived exosomes (MSC-Exos), as cell-free mediators, retain many of the beneficial effects of MSCs while exhibiting improved safety and stability profiles. MSC-Exos carry diverse bioactive cargo, including nucleic acids, lipids, and proteins, and can modulate immune responses, promote tissue repair, and restore barrier integrity. In this review, we place particular emphasis on both immunoregulation and tissue barrier protection as dual mechanisms underlying MSC-Exos efficacy in GVHD. We further discuss emerging preclinical and clinical evidence, as well as key challenges in translation.

Objective: Sonic Hedgehog (Shh)-Gli1 signaling and osteopontin (OPN) play vital roles in pancreatic cancer. However, the precise mechanisms of both signals have not been fully clarified, and whether there is a correlation between them in pancreatic ductal adenocarcinoma (PDAC) is unknown. This study aims to confirm the effect of OPN on human PDAC and assess whether Hh signaling affects pancreatic cancer cells through upregulation of OPN.Materials and Methods: OPN expression in human PDAC tissues and cell lines was investigated. Proliferation, apoptosis, migration, and invasion of OPN-knockdown BxPC-3 cells were observed. We analyzed the correlation between Shh or Gli1 and OPN expression in human PDAC. Hh signaling inhibitors and shRNA against Gli1 were used to confirm if OPN expression in BxPC-3 cells was regulated by Hh canonical or noncanonical pathway. We also evaluated the proliferation, apoptosis, migration, and invasion of Gli1-knockdown BxPC-3 cells.Results: OPN is highly expressed in human PDAC tissues and cell lines. The proliferation, migration, and invasion of BxPC-3 cell lines were decreased, whereas apoptosis was increased when OPN was knocked down. Correlation analysis showed that Gli1, but not Shh, was associated with OPN expression in human PDAC, and Gli1 regulated OPN production in BxPC-3 cells through a noncanonical pathway because Gli but not Smo inhibitor reduced OPN expression. Similar to above, the proliferation, migration, and invasion of BxPC-3 cells were decreased, whereas the apoptosis was increased when Gli1 was knocked down. Supplement of exogenous OPN protein could partially reverse the effect of both OPN knockdown and Gli1 knockdown on the bio-behavior of BxPC-3 cells.Conclusion: Hh signaling promotes proliferation, migration, and invasion but inhibits apoptosis of pancreatic cancer cells through upregulation of OPN in a noncanonical pathway.

The Wnt signaling pathway is broadly categorized into two major classes: Canonical and non-canonical pathways. The canonical Wnt pathway, which is also referred to as the Wnt/β-catenin pathway, involves the nuclear translocation of β-catenin. By contrast, non-canonical Wnt pathways, including the Wnt/Ca2+ pathway and the Wnt/planar cell polarity pathway, function independently of β-catenin nuclear translocation. Among these non-canonical pathways, the Wnt/Ca2+ pathway influences cellular behavior by elevating intracellular Ca2+ concentrations. This pathway primarily regulates cytoskeletal remodeling, cell migration, polarity and immune responses, and serves a crucial role in cell proliferation, differentiation, embryonic development and tumorigenesis. Notably, Wnt/Ca2+ signaling exhibits dual functions in different tumor types, promoting tumorigenesis in certain cancers, whilst inhibiting it in others. The present review systematically summarizes research regarding the Wnt/Ca2+ signaling pathway, elucidates its mechanisms in cancer progression, and outlines current strategies for targeting the Wnt/Ca2+ signaling pathway in cancer, along with the associated challenges.

BACKGROUND:Perimenopausal women often experience physiological and psychological decline due to the effects of oestrogen fluctuations and the decline of ovarian function, leading to significantly increased depression rates, decreases in the quality of life and mental health issues. Studies have shown that the gut microbiota exerts anti-perimenopausal depression (PMD) effects via the microbiota-gut-brain (MGB) axis, the mechanisms of which may be related to inflammation. In this review, we discuss the effects and mechanisms of gut microbiota in PMD and provide new insights for future PMD treatment. METHODS:This review elaborates on the role of MGB axis in PMD from different aspects of inflammation, including gut microbiota metabolites, inflammatory signaling pathways, and clinical applications. RESULTS:Disorders of gut microbiota and decreased levels of gut microbiota metabolites (short-chain fatty acids, monoamine neurotransmitters) may cause PMD. The mechanism of intestinal microbiota-mediated inflammation may be related to TLR4/NF-κB pathway, NOD-like receptor protein 3 (NLRP3) inflammasome pathway and JAK-STAT pathway. At the same time, it was found that gut microbiota (probiotics, prebiotics, etc.) had good therapeutic potential in the treatment of PMD. CONCLUSIONS:MGB axis mediated inflammation may play an important role in PMD. The application of gut microbiota in the treatment of PMD patients has profound clinical transformation value, but a lot of efforts are still needed.

Hyperinflammatory response in early stage of sepsis was the key factor leading to multi-organ injury. Therefore, exploring an effective therapy to attenuate or reverse hyperinflammation was the priority of sepsis treatment. Previous study from our team showed that recombinant human interleukin-11 (rhIL-11) was a promising anti-inflammation cytokine in sepsis. However, the molecular mechanism was not fully elucidated. This study aims to evaluate the therapeutic potential of rhIL-11 in septic mice model and explore the underlying the molecular mechanism. A cecal ligation and puncture (CLP) model was applied to induce septic mice. Mice were separated into five groups with six animals in each group, including normal, sham, sham + rhIL-11, CLP and CLP + rhIL-11 groups. Therapeutic potential of rhIL-11 was evaluated by comparing body weight, survival time and liver damage (hematoxylin and eosin (H E) staining, pro-inflammatory cytokines and serum measurements of liver enzymes). Hepatic myeloid-derived suppressor cells (MDSC) percentage was also compared. In vitro, MDSC differentiation from bone marrow (BM) cells was induced in the presence of appropriate stimuli, followed by the proportion and subsets analysis via flow cytometer. The related signal pathways including STAT3 and mTORC1 were detected by western blotting. The effect of MDSCs inhibition by STAT3 and mTORC1 inhibitors on septic mice was evaluated by comparing survival time, liver damage and MDSCs percentage. Here, we declared that early treatment of rhIL-11 exerted a liver protective effect and caused the expansion of monocytic myeloid-derived suppressor cells (M-MDSCs) in septic mice model. The results of in vitro studies declared that rhIL-11 promoted differentiation of BM cells into M-MDSCs phenotypically and functionally via activating STAT3 signaling, which was cross-regulated by the mTORC1. Furthermore, we also elucidated that mTORC1 bound directly to STAT3 through an interaction between raptor and TOS motif in STAT3. Finally, inhibition of mTORC1 or STAT3 in vivo blocked the differentiation of M-MDSCs and attenuated liver protective effect of rhIL-11. Taken together, these results suggested that early treatment of rhIL-11 in septic mice might reverse the hepatic damage at least in part by inducing the differentiation of M-MDSCs via STAT3 signaling pathway, and STAT3 signaling is modulated by a parallel branch of mTORC1.

As the population aging, the prevalence of age-related diseases is also rising. Mitochondrial malfunction is one of the hallmarks of aging, and optic atrophy type 1 (OPA1), a protein found in the inner membrane (IM) of mitochondrial, is essential to this process. OPA1 regulates the fusion of IM and cristae structure, hence maintaining cellular energy metabolism and function. Its abnormalities may impair the multiple functions of tissues and are also closely related to various diseases. OPA1 is highly expressed in metabolically active organs, such as the brain, skeletal muscle, and heart, ensuring the normal metabolism and function of these organs. This review summarizes the physiological functions of OPA1 in these organs, along with the effect of aberrant OPA1 expression on aging related disorders. By deeply studying the mechanisms of OPA1's function in these diseases, we might achieve a more profound comprehension of the pathological processes of age-related diseases and explore potential therapeutic strategies.

The capacity of lymphocytes continuously home to lymphoid structures is remarkable for cancer immunosurveillance and immunotherapy. Lymphocyte homing and recirculation within the tumor microenvironment (TME) are now understood to be adaptive processes that are regulated by specialized cytokines and adhesion molecule signaling cascades. Restricted lymphocyte infiltration and recirculation have emerged as key mechanisms contributing to poor responses in cancer immunotherapies like chimeric antigen receptor (CAR)-T cell therapy and immune checkpoint blockades (ICBs). Uncovering the kinetics of lymphocytes in tumor infiltration and circulation is crucial for improving immunotherapies. In this review, we discuss the current insights into the adhesive and migrative molecules involved in lymphocyte homing and transmigration. The potential mechanisms within the TME that restrain lymphocyte infiltration are also summarized. Advanced on these, we outline the determinates for tertiary lymphoid structures (TLSs) formation within tumors, placing high expectations on the prognostic values of TLSs as therapeutic targets in malignancies.

Alterations in glycosylation are associated with breast tumor formation and progression. Nevertheless, the specific functions and mechanisms of the human major UDP‐galactose transporter‐encoding gene solute carrier family 35 member A2 ( SLC35A2 ) in breast invasive carcinoma (BRCA) have not been fully determined. Here, we report that SLC35A2 promotes BRCA progression by activating extracellular signal regulated kinase (ERK). SLC35A2 expression and prognosis‐predictive significance in pan‐cancer were evaluated using public databases. The upstream non‐coding RNAs (ncRNAs) of SLC35A2 were analyzed, and their expression and regulations were validated in breast tissues and cell lines by a quantitative PCR and dual‐luciferase assays. We used bioinformatic tools to assess the link between SLC35A2 expression and immune infiltration and performed immunohistochemistry for validation. Cell Counting Kit‐8, 5‐ethynyl‐2′‐deoxyuridine, transwell, flow cytometer and western blotting were used to assess the proliferation, motility, cell cycle and apoptosis of BRCA cells in vitro . The xenograft models were constructed to assess the effect of SLC35A2 on BRCA tumor growth in vivo . The results indicated that SLC35A2 expression was upregulated and linked to an unfavorable prognosis in BRCA. The most likely upstream ncRNA‐associated pathway of SLC35A2 in BRCA was the AC074117.1/hsa‐let‐7b‐5p axis. SLC35A2 expression had positive correlations with the presence of Th2 cells, regulatory T cells and immune checkpoints. Knockdown of SLC35A2 could reduce BRCA cell proliferation, motility, and cause G2/M arrest and cell apoptosis via ERK signaling. Moreover, ERK activation can rescue the inhibitory effects of knockdown SLC35A2 in BRCA. In conclusion, AC074117.1/hsa‐let‐7b‐5p axis‐mediated high expression of SLC35A2 acts as a tumor promoter in BRCA via ERK signaling, which provides a potential target for BRCA treatment.

Extracellular trap networks (neutrophil extracellular traps [NETs]) of polymorphonuclear neutrophils are mesh-like substances that prevent the spread of pathogens. They primarily consist of DNA skeletons, histones, granule components, and cytoplasmic proteins. NETs formation requires a certain environment and there are different pathways for NETs production. However, it is still not clear how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) promotes NETs. NETs exert antiinflammatory effects through immune response, while they can also lead to certain adverse outcomes, such as the development of immunothrombosis. Coronavirus disease 2019 (COVID-19) is an inflammatory reaction affecting various organs caused by SARS-CoV-2, especially the lungs. NETs production and disease severity are linked with unique neutrophil clusters by single-cell RNA sequencing. NETs might exert an anti-inflammatory role in the initial stage of lung tissue inflammation. Nevertheless, numerous studies and cases have shown that they can also result in pulmonary thrombosis. There is mounting evidence that NETs are tightly related with COVID-19 pulmonary thrombosis, and many studies on the mechanisms are involved. The role and mechanism of NETs in the development of pulmonary thrombosis will be the main topics of this manuscript. Additionally, we address the potential targeting of NETs in COVID-19 patients.

Purpose:The roles of T cell immunoreceptor with Ig and ITIM domains (TIGIT) in the diagnosis of primary breast cancer (PBC) are still unclear. This study was designed to investigate the expression of TIGIT in PBC patients, with an aim to analyze its diagnostic value in PBC.Patients and Methods:We first explore the expression of TIGIT in cancer patients based on TCGA database, and then we analyzed its correlation with clinicopathological features. Afterwards, we compared the protein and mRNA expressions of TIGIT in two BC cell lines (MCF-7 and MDA-MB-231) and normal breast epithelial cell line (MCF-10A). Subsequently, 56 PBC female patients admitted to the Taizhou People's Hospital from October 2018 to June 2021 were included in this study. Flow cytometry was used to detect TIGIT level on peripheral blood CD3+ T cells of PBC patients and healthy controls. TIGIT expression in PBC tissues was detected by immunohistochemistry (IHC) and immunofluorescence staining.Results:TCGA database showed that compared with adjacent tissues, TIGIT was significantly upregulated in tumor tissues. High TIGIT expression was positively correlated with tumor stage and negatively correlated with recurrence free survival (RFS) and overall survival (OS). TIGIT level in BC cell lines, peripheral blood and tumor tissues of PBC patients was significantly higher than that of control (P < 0.05). TIGIT level was correlated with age (P < 0.05), rather than tumor size, pathological type, lymph node metastasis, ER, PR, HER-2, and P53. ROC curve showed that the optimal critical value of peripheral blood TIGIT for BC screening was 23.38%. Postoperative TIGIT level in peripheral blood was significantly decreased compared to the preoperative TIGIT level (P < 0.05).Conclusion:TIGIT was upregulated in PBC and was correlated with age. It may be a potential target for the diagnosis and immunotherapy of PBC.

As the cell's energy factory and metabolic hub, mitochondria are critical for ATP synthesis to maintain cellular function. Mitochondria are highly dynamic organelles that continuously undergo fusion and fission to alter their size, shape, and position, with mitochondrial fusion and fission being interdependent to maintain the balance of mitochondrial morphological changes. However, in response to metabolic and functional damage, mitochondria can grow in size, resulting in a form of abnormal mitochondrial morphology known as megamitochondria. Megamitochondria are characterized by their considerably larger size, pale matrix, and marginal cristae structure and have been observed in various human diseases. In energy-intensive cells like hepatocytes or cardiomyocytes, the pathological process can lead to the growth of megamitochondria, which can further cause metabolic disorders, cell damage and aggravates the progression of the disease. Nonetheless, megamitochondria can also form in response to short-term environmental stimulation as a compensatory mechanism to support cell survival. However, extended stimulation can reverse the benefits of megamitochondria leading to adverse effects. In this review, we will focus on the findings of the different roles of megamitochondria, and their link to disease development to identify promising clinical therapeutic targets.

BackgroundRecent studies have shown that systemic inflammation responses and hyperventilation are associated with poor outcomes in patients with severe traumatic brain injury (TBI). The aim of this retrospective study was to investigate the relationships between the systemic immune inflammation index (SII = platelet × neutrophil/lymphocyte) and peripheral blood CO2 concentration at admission with the Glasgow Outcome Score (GOS) at 6 months after discharge in patients with severe TBI.MethodsWe retrospectively analyzed the clinical data for 1266 patients with severe TBI at three large medical centers from January 2016 to December 2021, and recorded the GOS 6 months after discharge. The receiver operating characteristic (ROC) curve was used to determine the best cutoff values for SII, CO2, neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), and lymphocyte to monocyte ratio (LMR), and chi-square tests were used to evaluate the relationships among SII, CO2 and the basic clinical characteristics of patients with TBI. Multivariate logistic regression analysis was used to determine the independent prognostic factors for GOS in patients with severe TBI. Finally, ROC curve, nomogram, calibration curve and decision curve analyses were used to evaluate the value of SII and coSII-CO2 in predicting the prognosis of patients with severe TBI. And we used the multifactor regression analysis method to build the CRASH model and the IMPACT model. The CRASH model included age, GCS score (GCS, Glasgow Coma Scale) and Pupillary reflex to light: one, both, none. The IMPACT model includes age, motor score and Pupillary reflex to light: one, both, none.ResultsThe ROC curves indicated that the best cutoff values of SII, CO2, PLR, NLR and LMR were 2651.43×109, 22.15mmol/L, 190.98×109, 9.66×109 and 1.5×109, respectively. The GOS at 6 months after discharge of patients with high SII and low CO2 were significantly poorer than those with low SII and high CO2. Multivariate logistic regression analysis revealed that age, systolic blood pressure (SBP), pupil size, subarachnoid hemorrhage (SAH), SII, PLR, serum potassium concentration [K+], serum calcium concentration [Ca2+], international normalized ratio (INR), C-reactive protein (CRP) and co-systemic immune inflammation index combined with carbon dioxide (coSII-CO2) (P < 0.001) were independent prognostic factors for GOS in patients with severe TBI. In the training group, the C-index was 0.837 with SII and 0.860 with coSII-CO2. In the external validation group, the C-index was 0.907 with SII and 0.916 with coSII-CO2. Decision curve analysis confirmed a superior net clinical benefit with coSII-CO2 rather than SII in most cases. Furthermore, the calibration curve for the probability of GOS 6 months after discharge showed better agreement with the observed results when based on the coSII-CO2 rather than the SII nomogram. According to machine learning, coSII-CO2 ranked first in importance and was followed by pupil size, then SII.ConclusionsSII and CO2 have better predictive performance than NLR, PLR and LMR. SII and CO2 can be used as new, accurate and objective clinical predictors, and coSII-CO2, based on combining SII with CO2, can be used to improve the accuracy of GOS prediction in patients with TBI 6 months after discharge.

The error-proneness in the preanalytical and postanalytical stages is higher than that in the analytical stage of the total testing process. However, preanalytical and postanalytical quality management has not received enough attention in medical laboratory education and tests in clinical biochemistry courses. Clinical biochemistry teaching program aim to improve students’ awareness and ability of quality management according to international organization for standardization 15,189 requirements. We designed a student-centred laboratory training program, according to case-based learning that included 4 stages: “establish an overall testing process based on the patient’s clinical indicator, clarify principles, improve operational skills, and review process and continuous improvement”. The program was implemented in our college during the winter semesters of 2019 and 2020. A total of 185 undergraduate students majoring in medical laboratory science participated in the program as a test group, and the other 172 students were set up as the control group and adopted the conventional method. The participants were asked to finish an online survey to evaluate the class at the end. The test group had significantly better examination scores not only in experimental operational skills (89.27 ± 7.16 vs. 77.51 ± 4.72, p < 0.05 in 2019 grade, 90.31 ± 5.35 vs. 72.87 ± 8.41 in 2020 grade) but also in total examination (83.47 ± 6.16 vs. 68.90 ± 5.86 in 2019 grade, 82.42 ± 5.72 vs. 69.55 ± 7.54 in 2020 grade) than the control group. The results of the questionnaire survey revealed that the students in the test group better achieved classroom goals than those in the control group (all p < 0.05). The new student-centred laboratory training program based on case-based learning in clinical biochemistry is an effective and acceptable strategy compared with the conventional training program.

类风湿性关节炎(rheumatoid arthritis,RA)是一种慢性全身性自身免疫性疾病,以滑膜炎导致的软骨、骨、关节的破坏和重塑导致畸形为特征.程序性死亡受体 1(programmed cell death protein 1,PD-1)表达于各种活化的免疫细胞表面,参与调控免疫细胞的活化、增殖、存活和免疫应答的转归,介导机体免疫耐受和免疫稳态的维持等生理过程.近年来,研究发现PD-1/PD-L1 信号参与了RA的病程进展,因此,深入探讨该信号途径对 RA的诊疗具有重要的临床意义.该文从 PD-1 表达及PD-1/PD-L1对T、B细胞的功能调节角度阐述了PD-1/PD-L1 信号在RA发病中的作用机制及其临床检测技术进展.

The fundamental principle of immune checkpoint blockade (ICB) is to protect tumor-infiltrating T cells from being exhausted. Despite the remarkable success achieved by ICB treatment, only a small group of patients benefit from it. Characterized by a hypofunctional state with the expression of multiple inhibitory receptors, exhausted T (Tex) cells are a major obstacle in improving ICB. T cell exhaustion is a progressive process which adapts to persistent antigen stimulation in chronic infections and cancers. In this review, we elucidate the heterogeneity of Tex cells and offer new insights into the hierarchical transcriptional regulation of T cell exhaustion. Factors and signaling pathways that induce and promote exhaustion are also summarized. Moreover, we review the epigenetic and metabolic alterations of Tex cells and discuss how PD-1 signaling affects the balance between T cell activation and exhaustion, aiming to provide more therapeutic targets for applications of combinational immunotherapies.

Objective: This research was aimed to preliminarily explore the clinical roles and potential molecular mechanisms of MIR99AHG and its significant transcripts in breast cancer (BRCA). Methods: Public databases were utilized to analyze the expression and prognostic roles of MIR99AHG and its transcripts. Relationships between MIR99AHG expression and immune cells infiltration were analyzed in Xiantao platform. In addition, co-expressed genes and interacting proteins of MIR99AHG were predicted. CancerSEA analyzed its relationship with functional states. Next, CNV status, DNA methylation, interacting transcription factors (TFs) and ceRNA network were analyzed to explore its possible mechanisms. Then, RNA ISH and FISH assays were used to detect its expression and location in BRCA tissues and cell lines, respectively. Finally, qRT-PCR was utilized to investigate MIR99AHG expression in cell lines.Results: Compared with the corresponding normal tissues, MIR99AHG expression levels were lower in all BRCA subtypes, and luminal B's was the lowest one. And MIR99AHG expression was negatively related to the tumor stage. In addition, 4 transcripts (ENST00000619222.4, ENST00000418813.6, ENST00000602901.5 and ENST00000453910.5) of MIR99AHG showed significant differences in the expression. Databases also suggested that the high MIR99AHG expression levels indicated good prognosis, especially in patients without lymph node metastasis. Xiantao found that MIR99AHG was positively related to 17 immune cells and negatively linked with 2 immune cells. CancerSEA analysis showed no relationships between MIR99AHG and functional states. From GEPIA and BCIP databases, 19 co-expressed genes were highly related to these four significant transcripts of MIR99AHG. StarBase, RNAct and HDOCK showed that several tumor-associated proteins, including U2AF65, hnRNPC, AEBP2, CHIC1 and so on, might interact with MIR99AHG. Genetically, BRCA had a higher proportion of MIR99AHG CNV loss than CNV gain, and the high level of DNA methylation indicated a good prognosis. Furthermore, 19 TFswere predicted to combine with the promoter of MIR99AHG. Then, we screened out 10 miRNAs potentially interacting with the significant transcripts of MIR99AHG, and five were significantly increased in breast tumors compared to normal tissues, including miR-194-5p, miR-320 b and so on, which could combine 14 mRNAs. Through ISH and FISH assays, we verified that MIR99AHG was down-regulated in BRCA samples and cell lines in comparison to non-tumor tissues and mammary epithelial cell line (MCF10A), and MIR99AHG was located both in cytoplasm and nucleus. qRT-PCR assay also showed the lower expression of MIR99AHG in breast cancer cells than that in MCF10A.Conclusion: These results indicate that MIR99AHG can be a favorable prognostic indicator for BRCA. ENST00000619222.4, ENST00000418813.6, ENST00000602901.5 and ENST00000453910.5 are significant transcripts and their down-regulation may play crucial roles in the progression of BRCA.

近年来,生殖泌尿系统肿瘤的发病率与死亡率逐年上升,临床上迫切需要新的生物学标志物以进行早期的诊断和治疗.目前N-甲基腺苷(m6 A)修饰受到基础医学和临床研究者的高度关注,它能够加快mRNA在细胞中的运转和出核速度.许多生殖泌尿系统疾病的发生、发展都受m6 A的修饰调控.m6 A修饰不仅作用于RNA,也调控非编码RNA(non-coding RNA,ncRNA).该文就m6 A修饰调控ncRNA作用以及在生殖泌尿系统肿瘤中的研究进展作一综述.