A ferroptosis-related signature predicts the clinical diagnosis and prognosis, and associates with the immune microenvironment of lung cancer.

Targeting ferroptosis-related pathway is a potential strategy for treatment of lung cancer (LC). Consequently, exploration of ferroptosis-related markers is important for treating LC. We collected LC clinical data and mRNA expression profiles from TCGA and GEO database. Ferroptosis-related genes (FRGs) were obtained through FerrDB database. Expression analysis was performed to obtain differentially expressed FRGs. Diagnostic and prognostic models were constructed based on FRGs by LASSO regression, univariate, and multivariate Cox regression analysis, respectively. External verification cohorts GSE72094 and GSE157011 were used for validation. The interrelationship between prognostic risk scores based on FRGs and the tumor immune microenvironment was analyzed. Immunocytochemistry, Western blotting, and RT-qPCR detected the FRGs level. Eighteen FRGs were used for diagnostic models, 8 FRGs were used for prognostic models. The diagnostic model distinguished well between LC and normal samples in training and validation cohorts of TCGA. The prognostic models for TCGA, GSE72094, and GSE157011 cohorts significantly confirmed lower overall survival (OS) in high-risk group, which demonstrated excellent predictive properties of the survival model. Multivariate Cox regression analysis further confirmed risk score was an independent risk factor related with OS. Immunoassays revealed that in high-risk group, a significantly higher proportion of Macrophages_M0, Neutrophils, resting Natural killer cells and activated Mast cells and the level of B7H3, CD112, CD155, B7H5, and ICOSL were increased. In conclusion, diagnostic and prognostic models provided superior diagnostic and predictive power for LC and revealed a potential link between ferroptosis and TIME.

Mulberry and Hippophae-based solid beverage promotes weight loss in rats by antagonizing white adipose tissue PPARγ and FGFR1 signaling.

Obesity, a multifactorial disease with many complications, has become a global epidemic. Weight management, including dietary supplementation, has been confirmed to provide relevant health benefits. However, experimental evidence and mechanistic elucidation of dietary supplements in this regard are limited. Here, the weight loss efficacy of MHP, a commercial solid beverage consisting of mulberry leaf aqueous extract and Hippophae protein peptides, was evaluated in a high-fat high-fructose (HFF) diet-induced rat model of obesity. Body component analysis and histopathologic examination confirmed that MHP was effective to facilitate weight loss and adiposity decrease. Pathway enrichment analysis with differential metabolites generated by serum metabolomic profiling suggests that PPAR signal pathway was significantly altered when the rats were challenged by HFF diet but it was rectified after MHP intervention. RNA-Seq based transcriptome data also indicates that MHP intervention rectified the alterations of white adipose tissue mRNA expressions in HFF-induced obese rats. Integrated omics reveals that the efficacy of MHP against obesogenic adipogenesis was potentially associated with its regulation of PPARγ and FGFR1 signaling pathway. Collectively, our findings suggest that MHP could improve obesity, providing an insight into the use of MHP in body weight management.

CAPN2 correlates with insulin resistance states in PCOS as evidenced by multi-dataset analysis.

OBJECTIVE: IR emerges as a feature in the pathophysiology of PCOS, precipitating ovulatory anomalies and endometrial dysfunctions that contribute to the infertility challenges characteristic of this condition. Despite its clinical significance, a consensus on the precise mechanisms by which IR exacerbates PCOS is still lacking. This study aims to harness bioinformatics tools to unearth key IR-associated genes in PCOS patients, providing a platform for future therapeutic research and potential intervention strategies. METHODS: We retrieved 4 datasets detailing PCOS from the GEO, and sourced IRGs from the MSigDB. We applied WGCNA to identify gene modules linked to insulin resistance, utilizing IR scores as a phenotypic marker. Gene refinement was executed through the LASSO, SVM, and Boruta feature selection algorithms. qPCR was carried out on selected samples to confirm findings. We predicted both miRNA and lncRNA targets using the ENCORI database, which facilitated the construction of a ceRNA network. Lastly, a drug-target network was derived from the CTD. RESULTS: Thirteen genes related to insulin resistance in PCOS were identified via WGCNA analysis. LASSO, SVM, and Boruta algorithms further isolated CAPN2 as a notably upregulated gene, corroborated by biological verification. The ceRNA network involving lncRNA XIST and hsa-miR-433-3p indicated a possible regulatory link with CAPN2, supported by ENCORI database. Drug prediction analysis uncovered seven pharmacological agents, most being significant regulators of the endocrine system, as potential candidates for addressing insulin resistance in PCOS. CONCLUSIONS: This study highlights the pivotal role of CAPN2 in insulin resistance within the context of PCOS, emphasizing its importance as both a critical biomarker and a potential therapeutic target. By identifying CAPN2, our research contributes to the expanding evidence surrounding the CAPN family, particularly CAPN10, in insulin resistance studies beyond PCOS. This work enriches our understanding of the mechanisms underlying insulin resistance, offering insights that bridge gaps in the current scientific landscape.

Integrated proteomics reveals autophagy landscape and an autophagy receptor controlling PKA-RI complex homeostasis in neurons.

Autophagy is a conserved, catabolic process essential for maintaining cellular homeostasis. Malfunctional autophagy contributes to neurodevelopmental and neurodegenerative diseases. However, the exact role and targets of autophagy in human neurons remain elusive. Here we report a systematic investigation of neuronal autophagy targets through integrated proteomics. Deep proteomic profiling of multiple autophagy-deficient lines of human induced neurons, mouse brains, and brain LC3-interactome reveals roles of neuronal autophagy in targeting proteins of multiple cellular organelles/pathways, including endoplasmic reticulum (ER), mitochondria, endosome, Golgi apparatus, synaptic vesicle (SV) for degradation. By combining phosphoproteomics and functional analysis in human and mouse neurons, we uncovered a function of neuronal autophagy in controlling cAMP-PKA and c-FOS-mediated neuronal activity through selective degradation of the protein kinase A - cAMP-binding regulatory (R)-subunit I (PKA-RI) complex. Lack of AKAP11 causes accumulation of the PKA-RI complex in the soma and neurites, demonstrating a constant clearance of PKA-RI complex through AKAP11-mediated degradation in neurons. Our study thus reveals the landscape of autophagy degradation in human neurons and identifies a physiological function of autophagy in controlling homeostasis of PKA-RI complex and specific PKA activity in neurons.

An oligopeptide permease, OppABCD, requires an iron-sulfur cluster domain for functionality.

Oligopeptide permease, OppABCD, belongs to the type I ABC transporter family. Its role is to import oligopeptides into bacteria for nutrient uptake and to modulate the host immune response. OppABCD consists of a cluster C substrate-binding protein (SBP), OppA, membrane-spanning OppB and OppC subunits, and an ATPase, OppD, that contains two nucleotide-binding domains (NBDs). Here, using cryo-electron microscopy, we determined the high-resolution structures of Mycobacterium tuberculosis OppABCD in the resting state, oligopeptide-bound pre-translocation state, AMPPNP-bound pre-catalytic intermediate state and ATP-bound catalytic intermediate state. The structures show an assembly of a cluster C SBP with its ABC translocator and a functionally required [4Fe-4S] cluster-binding domain in OppD. Moreover, the ATP-bound OppABCD structure has an outward-occluded conformation, although no substrate was observed in the transmembrane cavity. Here, we reveal an oligopeptide recognition and translocation mechanism of OppABCD, which provides a perspective on how this and other type I ABC importers facilitate bulk substrate transfer across the lipid bilayer.

Transcriptomic insights into the lipotoxicity of high-fat high-fructose diet in rat and mouse.

Along with the increasing prevalence of obesity worldwide, the deleterious effects of high-calorie diet are gradually recognized through more and more epidemiological studies. However, the concealed and chronic causality whitewashes its unhealthy character. Given an ingenious mechanism orchestrates the metabolic adaptation to high-fat high-fructose (HFF) diet and connive its lipotoxicity, in this study, an experimental rat/mouse model of obesity was induced and a comparative transcriptomic analysis was performed to probe the mystery. Our results demonstrated that HFF diet consumption altered the transcriptomic pattern as well as different high-calorie diet fed rat/mouse manifested distinct hepatic transcriptome. Validation with RT-qPCR and Western blotting confirmed that SREBP1-FASN involved in de novo lipogenesis partly mediated metabolic self-adaption. Moreover, hepatic ACSL1-CPT1A-CPT2 pathway involved in fatty acids ß-oxidation, played a key role in the metabolic adaption to HFF. Collectively, our findings enrich the knowledge of the chronic adaptation mechanisms and also shed light on future investigations. Meanwhile, our results also suggest that efforts to restore the fatty acids metabolic fate could be a promising avenue to fight against obesity and associated steatosis and insulin resistance challenged by HFF diet.

Calcium Carbonate-Based Nanoplatforms for Cancer Therapeutics: Current State of Art and Future Breakthroughs.

With the rapid development of nanotechnology, nanomaterials have shown immense potential for antitumor applications. Nanosized calcium carbonate (CaCO3) materials exhibit excellent biocompatibility and degradability, and have been utilized to develop platform technologies for cancer therapy. These materials can be engineered to carry anticancer drugs and functional groups that specifically target cancer cells and tissues, thereby enhancing therapeutic efficacy. Additionally, their physicochemical properties can be tailored to enable stimuli-responsive therapy and precision drug delivery. This Review consolidates recent literatures focusing on the synthesis, physicochemical properties, and multimodal antitumor therapies of CaCO3-based nanoplatforms (CBN). We also explore the current challenges and potential breakthroughs in the development of CBN for antitumor applications, providing a valuable reference for researchers in the field.

The effect and mechanism of low-molecular-weight heparin on the decidualization of stromal cells in early pregnancy.

OBJECTIVE: This study aimed to analyze the effect of low-molecular-weight heparin (LMWH) on the decidualization of stromal cells in early pregnancy and explore the effect of LMWH on pregnancy outcomes. METHODS: Recurrent spontaneous abortion (RSA) mouse model (CBA/J × DBA/2) and normal pregnant mouse model (CBA/J × BALB/c) were established. The female mice were checked for a mucus plug twice daily to identify a potential pregnancy. When a mucus plug was found, conception was considered to have occurred 12 h previously. The pregnant mice were divided randomly into a normal pregnancy control group, an RSA model group, and an RSA + LMWH experimental group (n = 10 mice in each group). Halfway through the 12th day of pregnancy, the embryonic loss of the mice was observed; a real-time quantitative polymerase chain reaction was used to detect the messenger ribonucleic acid (mRNA) expressions of prolactin (PRL) and insulin-like growth factor-binding protein 1 (IGFBP1) in the decidua of the mice. Additionally, the decidual tissues of patients with RSA and those of normal women in early pregnancy who required artificial abortion were collected and divided into an RSA group and a control group. Decidual stromal cells were isolated and cultured to compare cell proliferation between the two groups, and cellular migration and invasion were detected by membrane stromal cells. Western blotting was used to detect the protein expressions of proliferating cell nuclear antigen (PCNA), cyclin D1, matrix metalloproteinase- (MMP) 2, and MMP-7 in stromal cells treated with LMWH. RESULTS: Compared with the RSA group, LMWH significantly reduced the pregnancy loss rate in the RSA mice (p < 0.05). Compared with the RSA group, the LMWH + RSA group had significantly higher expression levels of PRL and IGFBP1 mRNA (p < 0.01). LMWH promoted the proliferation, migration, and invasion of human decidual stromal cells; compared with the control group, the expression levels of MMP-2, MMP-7, cyclin D1, and PCNA proteins in the decidual stromal cells of the LMWH group increased (p < 0.05). CONCLUSIONS: The use of LMWH can improve pregnancy outcomes by enhancing the proliferation and migration of stromal cells in early pregnancy and the decidualization of stromal cells.

A Novel Ultrafiltrate Extract of Propolis Exerts Anti-inflammatory Activity through Metabolic Rewiring.

Thousands of years ago, humans started to use propolis because of its medicinal properties, and modern science has successfully identified several bioactive molecules within this resinous bee product. However, a natural propolis extract which has been removed the adhesive glue and preserved propolis bioactive compounds is urgently needed to maximise the therapeutic opportunities. In this study, a novel ultrafiltrate fraction from Brazilian green propolis, termed P30K, was demonstrated with anti-inflammatory properties, both in vitro and in vivo. Total flavonoids and total phenolic acids content in P30K were 244.6 mg/g and 275.8 mg/g respectively, while the IC50 value of inhibition of cyclooxygenase-2 (COX-2) was 8.30 µg/mL. The anti-inflammatory activity of P30K was furtherly corroborated in experimental models of lipopolysaccharides (LPS)-induced acute liver and lung injury. Mechanistically, integrated GC-MS and LC-MS based serum metabolomics analysis revealed that P30K modulated citrate cycle (TCA), pyruvate, glyoxylate and dicarboxylate metabolism pathways to inhibit secretion of pro-inflammatory cytokines. Results of network pharmacology and molecular docking suggested that P30K targeted catechol-O-methyltransferases (COMT), 11ß-hydroxysteroid dehydrogenases (HSD11B1), and monoamine oxidases (MAOA and MAOB) to promote cellular metabolomic rewiring. Collectively, our work reveals P30K as an efficient therapeutic agent against inflammatory conditions and its efficacy is related to metabolic rewiring.

Update on clinical characteristics and molecular insights for uterine intravenous leiomyomatosis (Review).

Intravenous leiomyomatosis (IVL) is a rare benign disease, which typically develops along vascular vessels and extends to the inferior vena cava and right atrium of the heart. In the early stages of the disease, the clinical manifestations and the results of imaging examinations are not uniform among patients. Thus, a high rate of misdiagnosis and missed diagnosis is common. When the tumor extends along the venous system to the pelvic floor vein or through the inferior vena cava involving the right atrium of the heart or the pulmonary artery, severe symptoms occur, such as ascites, dyspnea, heart failure and even sudden mortality. Improving the understanding of IVL to identify and evaluate this disease in its early stages is important. Complete tumor resection remains the primary treatment option for IVL. The recurrence rate of the disease varies depending on multiple factors, such as type of surgical procedure performed. Therefore, long-term follow-up is necessary for patients with IVL. The review of recent findings on the molecular and clinicopathological characterization of IVL is important to understand the pathogenesis of IVL. In the present study, the clinical manifestations, pathogenesis, differential diagnosis, treatment and prognosis of IVL are summarized in order to provide a single source of insightful information on IVL.

STING promotes invasion and migration of uveal melanoma through p38­MAPK signaling.

Uveal melanoma (UM) is the most common intraocular malignant tumor in adults, with a lack of effective treatment for metastasis and a poor prognosis. Stimulator of interferon genes (STING, also known as TMEM173) plays an important role in tumor development by regulating cell proliferation, metastasis and other cellular processes. However, the function of STING in UM remains unclear and requires further investigation. The present study analyzed the expression status of STING to elucidate the mechanisms underlying UM. The correlation between STING and the prognosis of UM was evaluated based on UM RNA­seq data and clinical information extracted from The Cancer Genome Atlas database. Quantification of STING in UM cell lines and tissues was performed using the Wes Separation protein immunoassay. The effects of STING on the proliferation, migration and invasion of UM cells were investigated using Cell Counting Kit­8, Transwell and wound healing experiments. Survival analysis demonstrated that high levels of STING in UM tissues indicated a poor prognosis. The expression of STING in UM tissues was higher than that in the choroid membranes. Furthermore, it was found that downregulation of STING expression in UM cells suppressed migration and invasion, whereas overexpression of STING significantly promoted migration and invasion. Notably, STING had no significant effect on UM cell proliferation. It was also identified that STING positively upregulated the phosphorylation of p38 mitogen­activated protein kinase (p38­MAPK) in UM cells, enhancing cell migration and invasion, which the p38­MAPK inhibitor SB203580 reversed. Finally, the results of the present study demonstrated that high STING expression in UM indicates a poor prognosis. STING was revealed to promote the migration and invasion of UM cells through p38­MAPK signaling.

The intestinal microbiota exerts a sex-specific influence on neuroinflammation in a Parkinson's disease mouse model.

Parkinson's disease (PD) is a neurodegenerative disorder characterised by chronic and progressive symptoms; it is more prevalent in men than in women. The sex-specific influence of the intestinal microbiota has been associated with some neurodegenerative diseases, but the relationship with PD is currently unclear. In this study, we treated mice with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to establish a PD mouse model, and we utilised an antibiotic cocktail (Abx) to deplete the intestinal microbiota to evaluate the influence of the intestinal microbiota on male and female PD mice. MPTP treatment obviously caused bradykinesia and low mobility in female and male mice. Meanwhile, Abx treatment exerted a greater effect on male mice than female mice. Western blotting and immunofluorescence revealed that male mice treated with MPTP had higher expression of α-synuclein and proteins related to neuroinflammation and intestinal inflammation based on activation of glial cells and the TLR4-MyD88 signalling pathway. The sex-specific differences could be due to the different composition of the intestinal microbiota. Specifically, female mice had significantly higher abundance of Allobaculum, Turicibacter and Ruminococcus than male mice. Moreover, the abundance of the probiotic genus Bifidobacterium showed opposite trends in male and female mice. Our results indicate that the intestinal microbiota has an important effect on PD mice, especially male mice, by influencing neuroinflammation through the microbiota-gut-brain axis. In the future, there should be a focus on providing more reliable evidence for the pathogenesis and precise treatment of PD.

Physiological, anatomical and quality indexes of root tuber formation and development in chayote (Sechium edule).

BACKGROUND: Chayote is an underutilized species of Cucurbitaceae. It is rich in nutrients such as protein, minerals, phenols and its extracts have anti-cardiovascular and anti-cancer effects, making it a versatile plant for both medicinal and culinary purposes. Although research on its root tuber is limited, they are rich in starch and have a structure similar to that of potatoes, cassava, and sweet potatoes. Therefore, they can serve as potential substitutes for potatoes and offer promising prospects as agricultural and industrial resources. However, the physiological and cellular mechanisms of chayote root tuber formation and development are still unclear. RESULTS: In this study, we observed the growth habit of 'Tuershao' (high yield of root tuber). The results revealed that the tuber enlargement period of 'Tuershao' lasts approximately 120 days, with the early enlargement phase occurring during 0-30 days, rapid enlargement phase during 30-90 days, and maturation phase during 90-120 days. Physiological indicators demonstrated a gradual increase in starch content as the tuber developed. The activities of sucrose synthase (SUS) and invertase (VIN) showed a consistent trend, reaching the highest level in the rapid expansion period, which was the key enzyme affecting tuber expansion. Moreover, the special petal like structure formed by the secondary phloem and secondary xylem of the tuber resulted in its enlargement, facilitating the accumulation of abundant starch within the thin-walled cells of this structure. Principal component analysis further confirmed that starch content, SUS and VIN activities, as well as the concentrations of calcium (Ca), iron (Fe), and selenium (Se), were the major factors influencing tuber development. Moreover, the low temperature environment not only promoted the growth of 'Tuershao' tubers but also enhanced the accumulation of nutritional substances. CONCLUSIONS: These findings contribute to a deeper understanding of the formation and developmental mechanisms of 'Tuershao' tubers, providing valuable guidance for cultivation practices aimed at improving crop yield.

Extralesional triamcinolone acetonide injection in the treatment of small chalazion.

Purpose: To evaluate the effect of extralesional triamcinolone acetonide (TA) injection in the treatment of small chalazion (diameter ≤ 5 mm). Methods: Prospective interventional clinal study that included patients diagnosed as chalazion of small size not responding to conservative management for at least 2 weeks. All patients were treated with extralesional TA injection (4 mg). Successful resolution of a chalazion was defined as a decrease in size to 1 mm or smaller. Results: Thirty-eight patients were included in the study. The resolution was achieved in 33 (87%) patients. Nineteen (50%) patients had complete resolution after the first injection, and 13 (34.2%) patients had complete resolution after the second injection. Chalazion near the lower punctum needed more times of injections than those elsewhere (P = 0.02). Conclusions: Extralesional TA injection is effective in the treatment of both primary and recurred small chalazia. It is a simple and cost-saving procedure and can be considered an alternative first-line treatment for small chalazion.

Structural insights into trehalose capture and translocation by mycobacterial LpqY-SugABC.

The human pathogen, Mycobacterium tuberculosis (Mtb) relies heavily on trehalose for both survival and pathogenicity. The type I ATP-binding cassette (ABC) transporter LpqY-SugABC is the only trehalose import pathway in Mtb. Conformational dynamics of ABC transporters is an important feature to explain how they operate, but experimental structures are determined in a static environment. Therefore, a detailed transport mechanism cannot be elucidated because there is a lack of intermediate structures. Here, we used single-particle cryo-electron microscopy (cryo-EM) to determine the structure of the Mycobacterium smegmatis (M. smegmatis) trehalose-specific importer LpqY-SugABC complex in five different conformations. These structures have been classified and reconstructed from a single cryo-EM dataset. This study allows a comprehensive understanding of the trehalose recycling mechanism in Mycobacteria and also demonstrates the potential of single-particle cryo-EM to explore the dynamic structures of other ABC transporters and molecular machines.

Intracellular hydrogelation of macrophage conjugated probiotics for hitchhiking delivery and combined treatment of colitis.

Immune cell membrane coated nanomedicine was developed to neutralize cytokines via receptor-ligand interaction, which showed potential for the treatment of inflammatory bowel disease (IBD). However, cell membrane isolation and re-assembly process involved protein loss and spatial disorder, which reduced the sequestration efficiency towards cytokines. In addition, oral administration of probiotics was accepted for IBD treatment via gut microbiota modulation, but most probiotics showed weak adhesion to intestine mucosa and were quickly expelled from gastrointestinal tract. Herein, an intracellular hydrogelation technology was proposed to construct gelated peritoneal macrophage (GPM) with intact membrane structure, resulting from the avoidance of membrane isolation and re-assembly process. GPM efficiently neutralized multiple cytokines in vitro and in vivo to ameliorate inflammatory Caco-2 â€‹cells and colitis rats by regulating oxidative stress, inflammation level and intestinal barrier repair. Moreover, the probiotics (Nissle1917, EcN) were easily attached on GPM surface through specific recognition, to construct GPM-EcN conjugate for GPM hitchhiking delivery to colitis tissue. Conjugation process of GPM and EcN showed no damage on bacterial physiological function. Due to the chemical attachment on inflammatory cells, GPM carried the attached EcN hand-in-hand to accumulate in the colitis tissue of IBD rat, and enhanced intestine retention time of EcN in comparison to free EcN, which improved bacterial diversity, and shifted the microbiota community and acid metabolites to an anti-inflammatory phenotype. This study transferred the hydrogel synthesis from in vitro to intracellular cytoplasm, and came to a new insight of conjugating strategy of GPM and probiotics for hitchhiking delivery and combined anti-IBD treatment.

Molecular mechanisms of ROS-modulated cancer chemoresistance and therapeutic strategies.

Drug resistance is the main obstacle to achieving a cure in many cancer patients. Reactive oxygen species (ROS) are master regulators of cancer development that act through complex mechanisms. Remarkably, ROS levels and antioxidant content are typically higher in drug-resistant cancer cells than in non-resistant and normal cells, and have been shown to play a central role in modulating drug resistance. Therefore, determining the underlying functions of ROS in the modulation of drug resistance will contribute to develop therapies that sensitize cancer resistant cells by leveraging ROS modulation. In this review, we summarize the notable literature on the sources and regulation of ROS production and highlight the complex roles of ROS in cancer chemoresistance, encompassing transcription factor-mediated chemoresistance, maintenance of cancer stem cells, and their impact on the tumor microenvironment. We also discuss the potential of ROS-targeted therapies in overcoming tumor therapeutic resistance.

Structure of the human respiratory complex II.

Human complex II is a key protein complex that links two essential energy-producing processes: the tricarboxylic acid cycle and oxidative phosphorylation. Deficiencies due to mutagenesis have been shown to cause mitochondrial disease and some types of cancers. However, the structure of this complex is yet to be resolved, hindering a comprehensive understanding of the functional aspects of this molecular machine. Here, we have determined the structure of human complex II in the presence of ubiquinone at 2.86 Å resolution by cryoelectron microscopy, showing it comprises two water-soluble subunits, SDHA and SDHB, and two membrane-spanning subunits, SDHC and SDHD. This structure allows us to propose a route for electron transfer. In addition, clinically relevant mutations are mapped onto the structure. This mapping provides a molecular understanding to explain why these variants have the potential to produce disease.

Genome-Wide Identification of the MADS-Box Gene Family during Male and Female Flower Development in Chayote (Sechium edule).

The MADS-box gene plays an important role in plant growth and development. As an important vegetable of Cucurbitaceae, chayote has great edible and medicinal value. So far, there is little molecular research on chayote, and there are no reports on the MADS-box transcription factor of chayote. In this study, the MADS-box gene family of chayote was analyzed for the first time, and a total of 70 MADS-box genes were identified, including 14 type I and 56 type II MICK MADS genes. They were randomly distributed on 13 chromosomes except for chromosome 11. The light response element, hormone response element and abiotic stress response element were found in the promoter region of 70 MADS genes, indicating that the MADS gene can regulate the growth and development of chayote, resist abiotic stress, and participate in hormone response; GO and KEGG enrichment analysis also found that SeMADS genes were mainly enriched in biological regulation and signal regulation, which further proved the important role of MADS-box gene in plant growth and development. The results of collinearity showed that segmental duplication was the main driving force of MADS gene expansion in chayote. RNA-seq showed that the expression levels of SeMADS06, SeMADS13, SeMADS26, SeMADS28, SeMADS36 and SeMADS37 gradually increased with the growth of chayote, indicating that these genes may be related to the development of root tubers of 'Tuershao'. The gene expression patterns showed that 12 SeMADS genes were specifically expressed in the male flower in 'Tuershao' and chayote. In addition, SeMADS03 and SeMADS52 may be involved in regulating the maturation of male flowers of 'Tuershao' and chayote. SeMADS21 may be the crucial gene in the development stage of the female flower of 'Tuershao'. This study laid a theoretical foundation for the further study of the function of the MADS gene in chayote in the future.