Protective effects and molecular mechanisms of Litopenaeus vannamei treated with l-arginine/l-lysine against myofibrillar proteins oxidation and quality degradation during freeze-thaw cycles.

The storage and processing of Litopenaeus vannamei are often challenged by the freeze-thaw (F-T) cycle phenomenon. This study delved into the influence of pretreatment with l-arginine (Arg) and l-lysine (Lys) on the myofibrillar proteins oxidation and quality of shrimp subjected to F-T cycles. Arg and Lys pretreatment notably improved water-holding capacity (WHC), textural integrity as well as the myofibrillar structure of the shrimps. A lesser reduction in the amounts of immobile and bound water was found in the amino acid-treated groups, and the oxidation of lipids and proteins were both decelerated. Molecular simulation results indicated that Arg and Lys could form hydrogen and salt-bridge bonds with myosin, enhancing the stability of Litopenaeus vannamei. The study concludes that Arg and Lys are effective in alleviating the adverse effects of F-T cycles on the quality of Litopenaeus vannamei, and provides a new solution for the quality maintenance during storage and processing.

Network pharmacology and molecular docking approach to elucidate the mechanisms of safflower, phellodendron, scutellaria baicalensis, coptis, and gardenia in hand-foot syndrome.

Background: Safflower, phellodendron, scutellaria baicalensis, coptis, and gardenia (SPSCG) are medicinal plants with a wide range of anti-inflammatory and antioxidant effects. However, the related mechanism of SPSCG against hand-foot syndrome (HFS) has yet to be revealed. Objective: To investigate the mechanisms of SPSCG in the treatment of HFS using the Network Pharmacology. Methods: Active ingredients and targets of SPSCG for HFS were screened by the Chinese Medicine Systems Pharmacology (TCMSP) and Swiss Target Prediction databases. Potential therapeutic targets were collected from the GeneCards and OMIM databases. Subsequently, protein-protein interactions (PPI), Gene Ontology (GO) annotations, and pathways from the Kyoto Encyclopedia of Genes and Genomes (KEGG) were performed to investigate the potential mechanism of the SPSCG in HFS. Then, molecular docking and molecular dynamics simulations were performed to predict the binding interactions between the active compound and the core target. Finally, vitro experiments were used to verify the repair effect of key ingredients of SPSCG on cell damage caused by 5-Fluorouracil. Results: Quercetin, kaempferol, ß-sitosterol, and stigmasterol were identified as the major active components of SPSCG. GO analysis showed a total of 1,127 biological processes, 42 terms cellular components, and 57 molecular functions. KEGG analysis showed that the MAPK, TNF, and IL-17 signaling pathways were significantly enriched. The PPI analysis discovered that EGFR, CASP3, AKT1, CCND1, and CTNNB1 shared the highest centrality among all target genes. The experimental results confirmed that these SPSCG active ingredients could treat HFS by reducing inflammation reaction and promoting cell damage repair. Conclusion: SPSCG may alleviate HFS by exerting antioxidative effects and suppressing inflammatory responses.

Pyroptosis in lung cancer: The emerging role of non-coding RNAs.

Lung cancer remains an intractable malignancy worldwide, prompting novel therapeutic modalities. Pyroptosis, a lethal form of programmed cell death featured by inflammation, has been involved in cancer progression and treatment response. Simultaneously, non-coding RNA has been shown to have important roles in coordinating pattern formation and oncogenic pathways, including long non-coding RNA (lncRNAs), microRNA (miRNAs), circular RNA (circRNAs), and small interfering RNA (siRNAs). Recent studies have revealed that ncRNAs can promote or inhibit pyroptosis by interacting with key molecular players such as NLRP3, GSDMD, and various transcription factors. This dual role of ncRNAs offers a unique therapeutic potential to manipulate pyroptosis pathways, providing opportunities for innovative cancer treatments. In this review, we integrate current research findings to propose novel strategies for leveraging ncRNA-mediated pyroptosis as a therapeutic intervention in lung cancer. We explore the potential of ncRNAs as biomarkers for predicting patient response to treatment and as targets for overcoming resistance to conventional therapies.

Network pharmacology study and in vitro experimental validation of Xiaojianzhong decoction against gastric cancer.

BACKGROUND: Cancer is one of the most serious threats to human health worldwide. Conventional treatments such as surgery and chemotherapy are associated with some drawbacks. In recent years, traditional Chinese medicine treatment has been increasingly advocated by patients and attracted attention from clinicians, and has become an indispensable part of the comprehensive treatment for gastric cancer. AIM: To investigate the mechanism of Xiaojianzhong decoction (XJZ) in the treatment of gastric cancer (GC) by utilizing network pharmacology and experimental validation, so as to provide a theoretical basis for later experimental research. METHODS: We analyzed the mechanism and targets of XJZ in the treatment of GC through network pharmacology and bioinformatics. Subsequently, we verified the impact of XJZ treatment on the proliferative ability of GC cells through CCK-8, apoptosis, cell cycle, and clone formation assays. Additionally, we performed Western blot analysis and real-time quantitative PCR to assess the protein and mRNA expression of the core proteins. RESULTS: XJZ mainly regulates IL6, PTGS2, CCL2, MMP9, MMP2, HMOX1, and other target genes and pathways in cancer to treat GC. The inhibition of cell viability, the increase of apoptosis, the blockage of the cell cycle at the G0/G1 phase, and the inhibition of the ability of cell clone formation were observed in AGS and HGC-27 cells after XJZ treatment. In addition, XJZ induced a decrease in the mRNA expression of IL6, PTGS2, MMP9, MMP2, and CCL2, and an increase in the mRNA expression of HOMX1. XJZ significantly inhibited the expression of IL6, PTGS2, MMP9, MMP2, and CCL2 proteins and promoted the expression of the heme oxygenase-1 protein. CONCLUSION: XJZ exerts therapeutic effects against GC through multiple components, multiple targets, and multiple pathways. Our findings provide a new idea and scientific basis for further research on the molecular mechanisms underlying the therapeutic effects of XJZ in the treatment of GC.

Recent advancements in understanding of biological role of homeobox C9 in human cancers.

Homeobox (HOX) C9, a member of the HOX family, is an important transcription factor, and it plays a significant role in various biological processes. This family of genes is highly valued for their essential roles in establishing and maintaining the body axis during embryonic development and adult tissues. Further, HOXC9 plays a central role in neuronal differentiation, angiogenesis, and adipose distribution, which are essential for the development of the nervous system, maturation of tissues and organs, and maintenance of energy balance and metabolic health. Recent research has found that abnormal HOXC9 expression is closely associated with the development and progression of various tumor types. The HOXC9 expression level can be an indicator of tumor prognosis. Therefore, elucidating the association between HOXC9 expression and its regulatory mechanisms and tumorigenesis can provide novel insights on the diagnosis and treatment of patients with cancer.

Circadian gene signatures in the progression of obesity based on machine learning and Mendelian randomization analysis.

Objective: Obesity, a global health concern, is associated with a spectrum of chronic diseases and cancers. Our research sheds light on the regulatory role of circadian genes in obesity progression, providing insight into the immune landscape of obese patients, and introducing new avenues for therapeutic interventions. Methods: Expression files of multiple datasets were retrieved from the GEO database. By 80 machine-learning algorithm combinations and Mendelian randomization analysis, we discovered the key circadian genes contributing to and protecting against obesity. Subsequently, an immune infiltration analysis was conducted to examine the alterations in immune cell types and their abundance in the body and to investigate the relationships between circadian genes and immune cells. Furthermore, we delved into the molecular mechanisms of key genes implicated in obesity. Results: Our study identified three key circadian genes (BHLHE40, PPP1CB, and CSNK1E) associated with obesity. BHLHE40 was found to promote obesity through various pathways, while PPP1CB and CSNK1E counteracted lipid metabolism disorders, and modulated cytokines, immune receptors, T cells, and monocytes. Conclusion: In conclusion, the key circadian genes (BHLHE40, CSNK1E, and PPP1CB) may serve as novel biomarkers for understanding obesity pathogenesis and have significant correlations with infiltrating immune cells, thus providing potential new targets for obese prevention and treatment.

Biomarkers and Novel Therapies of Diabetic Neuropathy: An Updated Review.

Diabetic neuropathy is a persistent consequence of the biochemical condition known as diabetes mellitus. As of now, the identification and management of diabetic neuropathy continue to be problematic due to problems related to the safety and efficacy of existing therapies. This study examines biomarkers, molecular and cellular events associated with the advancement of diabetic neuropathy, as well as the existing pharmacological and non-pharmacological treatments employed. Furthermore, a holistic and mechanism-centric drug repurposing approach, antioxidant therapy, Gene and Cell therapies, Capsaicin and other spinal cord stimulators and lifestyle interventions are pursued for the identification, treatment and management of diabetic neuropathy. An extensive literature survey was done on databases like PubMed, Elsevier, Science Direct and Springer using the keywords "Diabetic Neuropathy", "Biomarkers", "Cellular and Molecular Mechanisms", and "Novel Therapeutic Targets".Thus, we may conclude that non-pharmacological therapies along with palliative treatment, may prove to be crucial in halting the onset of neuropathic symptoms and in lessening those symptoms once they have occurred.

Mechanism of Polygala-Acorus in Treating Autism Spectrum Disorder Based on Network Pharmacology and Molecular Docking.

BACKGROUND: Recent epidemic survey data have revealed a globally increasing prevalence of autism spectrum disorders (ASDs). Currently, while Western medicine mostly uses a combination of comprehensive intervention and rehabilitative treatment, patient outcomes remain unsatisfactory. Polygala-Acorus, used as a pair drug, positively affects the brain and kidneys, and can improve intelligence, wisdom, and awareness; however, the underlying mechanism of action is unclear. OBJECTIVES: We performed network pharmacology analysis of the mechanism of Polygala-Acorus in treating ASD and its potential therapeutic effects to provide a scientific basis for the pharmaceutical's clinical application. METHODS: The chemical compositions and targets corresponding to Polygala-Acorus were obtained using the Traditional Chinese Medicine Systematic Pharmacology Database and Analysis Platform, Chemical Source Website, and PharmMapper database. Disease targets in ASD were screened using the DisGeNET, DrugBank, and GeneCards databases. Gene Ontology functional analysis and metabolic pathway analysis (Kyoto Encyclopedia of Genes and Genomes) were performed using the Metascape database and validated via molecular docking using AutoDock Vina and PyMOL software. RESULTS: Molecular docking analysis showed that the key active components of Polygala- Acorus interacted with the following key targets: EGFR, SRC, MAPK1, and ALB. Thus, the key active components of Polygala-Acorus (sibiricaxanthone A, sibiricaxanthone B tenuifolin, polygalic acid, cycloartenol, and 8-isopentenyl-kaempferol) have been found to bind to EGFR, SRC, MAPK1, and ALB. CONCLUSION: This study has preliminarily revealed the active ingredients and underlying mechanism of Polygala-Acorus in the treatment of ASD, and our predictions need to be proven by further experimentation.

Soybean gene GmMLP34 regulates Arabidopsis negative response to high temperature stress.

The functions of major latex proteins (MLPs) in plant defense and stress responses have been widely documented; however, their roles in HT stress response in soybeans have not been elucidated. This study investigated the role of GmMLP34, a member of the major latex protein (MLP) family, in the response of soybeans to HT stress. Transcriptome analysis of HT-resistant (JD21) and HT-sensitive (HD14) soybean leaves under HT stress (43.40 ± 1.70 °C) and field conditions revealed differential expression of GmMLP34. Further examination across different HT-resistant varieties showed that GmMLP34 was down-regulated in the leaves of 6 HT-resistant varieties (85.7 %) and up-regulated in the leaves of 6 HT-sensitive varieties (85.7 %) under the HT treatment (45 °C for 3 h). The results of this study indicate that ectopic expression of the GmMLP34 gene in Arabidopsis led to a significant decrease in the survival rate of seedling when compared to the wild type (WT) under HT stress conditions of 37/28 °C (day/night) for 5 d, Moreover, the results indicated a significant decrease in primary root length and lateral root number under 45 °C/3 h HT stress followed by 12 h room temperature recovery. Additionally, the levels of abscisic acid (ABA), and flavonoids, and the activity of the peroxidase (POD) enzyme in the antioxidant system was decreased, while the activity of the superoxide dismutase (SOD) enzyme increased in GmMLP34-overexpressing transgenic Arabidopsis thaliana. The expression levels of the HT-response genes AtCHS1 and AtCHI2-A, were significantly down-regulated, whereas that of AtGBP1 was significantly up-regulated. These results suggest that GmMLP34 negatively regulates the response of Arabidopsis thaliana to HT stress by modulating flavonoid synthesis, hormone synthesis, and the antioxidant enzyme system. These findings provide theoretical information for the genetic improvement of HT tolerance in soybean and contribute to the understanding of the molecular mechanisms underlying plant responses to abiotic stress.

Treating chronic pulmonary heart disease with traditional Chinese medicine: Systematic evaluation and mechanistic insights into the resolving phlegm and activating blood approach.

BACKGROUND: Chronic Pulmonary Heart Disease (CPHD) significantly impacts global health, especially among middle-aged and older adults. In China, the Traditional Chinese Medicine (TCM) technique of Resolving Phlegm and Activating Blood (RPAB) is widely used to treat CPHD, although high-quality evidence supporting its efficacy remains limited. OBJECTIVES: The purpose of this study was to rigorously assess the clinical efficacy of RPAB for CPHD and elucidate the mechanisms underlying its primary herbal components. METHODS: Through a detailed search of literature in both Chinese and English and strict inclusion and exclusion criteria, 18 randomized controlled trials (RCTs) were selected for meta-analysis. We identified RPAB's core herbal combinations using association rule analysis. This method statistically analyzes the frequency and correlation of herbal medicine usage. We then analyzed the chemical components of these combinations and investigated their potential intervention mechanisms on CPHD through network pharmacology. RESULTS: The combination of RPAB with Western medicine was superior to Western medicine alone in improving blood gas analysis and pulmonary function and reducing plasma viscosity in CPHD patients. The core herbal combination identified was Astragalus membranaceus (Fisch.) Bunge, Ligusticum chuanxiong Hort. ex S. H. Qiu & al., and Stellaria alsine Grimm (ALS). This combination targeted 588 therapeutic and 27 core targets. It influenced ten core compounds across 34 pathways, primarily through the chemokine signaling pathway and the JAK-STAT signaling pathway. CONCLUSION: RPAB with Western medicine significantly improves CPHD treatment outcomes. The study highlights the therapeutic potential of the ALS combination, which operates through multiple pathways to remodel pulmonary arteries, decrease inflammation, and lessen oxidative stress. These insights support the clinical application of RPAB in CPHD treatment and open new avenues for research and therapeutic development.

Unravelling the Mechanism of Arsenic Resistance and Bioremediation in Stenotrophomonas maltophilia: A Molecular Approach.

The mechanism of arsenic resistance in bacteria is under studied and still lacks a clear understanding despite of wide research work. The advanced technologies can help in analysing the arsenic bioremediating bacteria at a molecular level. With this line of idea, highly efficient arsenic bioremediating S. maltophilia was subjected to extensive analysis to understand the mechanism of arsenic resistance and bioremediation. The cell surface analysis revealed that S. maltophilia induces only slight changes in cell surface in the presence of arsenic. Whereas, TEM analysis has indicated the bioaccumulation of arsenic in S. maltophilia. Also, arsenic was found to generate ROS in a concentration dependant manner, and in response, S. maltophilia activated SOD, catalase, thioredoxin reductase etc. to manage oxidative stress which is very much crucial in managing arsenic toxicity. S. maltophilia was found to possess genes such as arsC, aoxB, aoxC and aioA. These genes are involved in arsenic reduction and oxidation. Transcriptomics and proteomics analysis have shown that S. maltophilia detoxifies arsenic by upregulating ars operon, arsH, BetB etc. which are responsible for arsenic reduction, efflux methylation, oxidation etc. A detailed molecular mechanism of arsenic bioremediation in S. maltophilia was put forth.

Refined egoist: the toxin-antitoxin immune system of T6SS.

The Type VI secretory system (T6SS) is a key regulatory network in the bacterial system, which plays an important role in host-pathogen interactions and maintains cell homeostasis by regulating the release of effector proteins in specific competition. T6SS causes cell lysis or competitive inhibition by delivering effector molecules, such as toxic proteins and nucleic acids, directly from donor bacterial cells to eukaryotic or prokaryotic targets. Additionally, it orchestrates synthesis of immune effectors that counteract toxins thus preventing self-intoxication or antagonistic actions by competing microbes. Even so, the mechanism of toxin-antitoxin regulation in bacteria remains unclear. In response, this review discusses the bacterial T6SS's structure and function and the mechanism behind toxin-antitoxin secretion and the T6SS's expression in order to guide the further exploration of the pathogenic mechanism of the T6SS and the development of novel preparations for reducing and replacing toxins and antitoxins.

Therapeutic potential of Astragalus membranaceus-Pueraria lobata decoction for the treatment of chemotherapy bowel injury.

Intestinal mucositis (IM) is one of the most serious side effects of the chemotherapeutic agent irinotecan (CPT-11). Astragalus membranaceus-Pueraria lobata decoction is from the ancient medical book Zhengzhihuibu, has been reported to be used for the treatment of diabetes and hypertension. However, the beneficial effect and mechanism of AP on chemotherapy intestinal mucositis (CIM) remain largely unknown. This study aimed to investigate the efficacy and mechanism of Astragalus membranaceus-Pueraria lobata decoction (AP) in treating CIM. The beneficial effect and mechanism of AP on chemotherapy intestinal mucositis (CIM) were detected using Drosophila model, and combination with RT qPCR, transcriptomics. AP supplementation could significantly alleviate the CPT-11-induced body injury in Drosophila, such as increasing the survival rate, recovering the impaired digestion, improving the movement, and repairing the reproduction and developmental processes. Administration of AP remarkably alleviated the IM caused by CPT-11, including inhibiting the excretion, repairing the intestinal atrophy, improving the acid-base homeostasis imbalance, and inhibiting the disruption of intestinal structure. Mechanistic studies revealed that the protective role of AP against CPT-11 induced intestinal injury was regulated mainly by inhibiting immune-related Toll and Imd pathways, and enhancing the antioxidant capacity. Taken together, these results suggest that AP may be a novel agent to relieve CIM.

Brain Specific RagA Overexpression Triggers Depressive-Like Behaviors in Mice via Activating ADORA2A Signaling Pathway.

Neuroinflammation hallmarks the pathology of depression although the etiological complexity has not yet been resolved. Previous studies demonstrate that bacterial lipopolysaccharide induces depressive-like behaviors by activating RagA-mTOR-p70S6K signaling pathway. The current project aims to investigate whether and how brain-specific RagA overexpression triggers depressive-like behaviors in mice. Full-length RagA cDNA is cloned into the mammalian expression vector under the control of brain specific promoter, and subsequently overexpressed in the brain of mouse embryos. Indeed, RagA transgenic mice exhibit depressive-like behaviors and memory impairments. RNA-seq profiling of the prefrontal cortex (PFC) transcriptome highlights adenosine A2a receptor (ADORA2A) as a key differentially expressed gene (DEG). Western blotting confirms that ADORA2A and phospho-p70S6K are markedly elevated in RagA transgenic mice. Behavioral assessments demonstrate that ADORA2A inhibitor istradefylline markedly attenuates depressive-like behaviors. Further metabolomics reveals that N-acetylserotonin and several depression-related metabolites are downregulated while proteomic profiling showed that OLIG1 and other proteins are significantly regulated in RagA transgenic mice. Collectively, RagA overexpression alters the expression patterns of signaling proteins and the metabolism of depression-associated metabolites. RagA may cause depressive-like behaviors in mice via activating p70S6K/ADORA2A signaling pathway. Thus, RagA-p70S6K-ADORA2A signaling pathway may be a target for the development of new antidepressant therapies.

Significantly enhanced specific activity of Bacillus subtilis (2,3)-butanediol dehydrogenase through computer-aided refinement of its substrate-binding pocket.

(2,3)-Butanediol dehydrogenases (BDHs) are widely utilized for the stereoselective interconversion between α-hydroxy ketones and vicinal diols to produce various functional building blocks. In this study, to enhance the specific activity towards (R)-phenyl-1,2-ethanediol (1a) for 2-hydroxyacetophenone (1b), the substrate-binding pocket of a Bacillus subtilis BDH (BsBDHA) was refined through site-directed mutagenesis. Based on molecular docking simulations, 14 residues were identified and subjected to alanine scanning mutagenesis. After screening, two residues, His42 and Gly292, were singled out for partial site-saturation mutagenesis. The results revealed that BsBDHAH42A and BsBDHAG292A displayed high activities of 3.21 and 1.97 U/mg, respectively. Employing combinatorial mutagenesis, a superior mutant, BsBDHAI49L/V266L/G292A, was developed, exhibiting significantly enhanced specific activity and catalytic efficiency towards (R)-1a, achieving 14.81 U/mg and 4.47 mM-1 s-1, respectively, which were 27.4- and 55.9-fold higher than those of BsBDHA. Further substrate spectrum analysis revealed that the superior mutant displayed increased specific activities for (R)-2a-6a by 1.4- to 10.3-fold. The integration of BsBDHAI49L/V266L/G292A into a three-enzymatic cascade for the synthesis of 1b effectively elevated the yield from 58.1 to 82.4 %. Molecular mechanism analysis indicated that the mutation-induced changes in intermolecular forces resulted in a higher frequency of reactive conformations for (R)-1a in BsBDHAI49L/V266L/G292A compared to BsBDHA.

The role of JNK signaling pathway in organ fibrosis.

BACKGROUND: Fibrosis is a tissue damage repair response caused by multiple pathogenic factors which could occur in almost every apparatus and leading to the tissue structure damage, physiological abnormality, and even organ failure until death. Up to now, there is still no specific drugs or strategies can effectively block or changeover tissue fibrosis. JNKs, a subset of mitogen-activated protein kinases (MAPK), have been reported that participates in various biological processes, such as genetic expression, DNA damage, and cell activation/proliferation/death pathways. Increasing studies indicated that abnormal regulation of JNK signal pathway has strongly associated with tissue fibrosis. AIM OF REVIEW: This review designed to sum up the molecular mechanism progresses in the role of JNK signal pathway in organ fibrosis, hoping to provide a novel therapy strategy to tackle tissue fibrosis. KEY SCIENTIFIC CONCEPTS OF REVIEW: Recent evidence shows that JNK signaling pathway could modulates inflammation, immunoreaction, oxidative stress and Multiple cell biological functions in organ fibrosis. Therefore, targeting the JNK pathway may be a useful strategy in cure fibrosis.

Ependymal cells: roles in central nervous system infections and therapeutic application.

Ependymal cells are arranged along the inner surfaces of the ventricles and the central canal of the spinal cord, providing anatomical, physiological and immunological barriers that maintain cerebrospinal fluid (CSF) homeostasis. Based on this, studies have found that alterations in gene expression, cell junctions, cytokine secretion and metabolic disturbances can lead to dysfunction of ependymal cells, thereby participating in the onset and progression of central nervous system (CNS) infections. Additionally, ependymal cells can exhibit proliferative and regenerative potential as well as secretory functions during CNS injury, contributing to neuroprotection and post-injury recovery. Currently, studies on ependymal cell primarily focus on the basic investigations of their morphology, function and gene expression; however, there is a notable lack of clinical translational studies examining the molecular mechanisms by which ependymal cells are involved in disease onset and progression. This limits our understanding of ependymal cells in CNS infections and the development of therapeutic applications. Therefore, this review will discuss the molecular mechanism underlying the involvement of ependymal cells in CNS infections, and explore their potential for application in clinical treatment modalities.

Secondary products and molecular mechanism of calcium oxalate degradation by the strain Azospirillum sp. OX-1.

The oxalate-carbonate pathway (OCP) involves degradation of soil oxalate to carbonate. To exploit and manage this natural mineralization of assimilated atmospheric CO2 into stable carbonates, improved understanding of this complex biotransformation process is needed. A strain of oxalate-degrading bacteria, Azospirillum sp. OX-1, was isolated from soil, and its secondary products of calcium oxalate degradation were analyzed and characterized using SEM, XRD, TG/DTG-DTA and FTIR-spectroscopy. The molecular mechanism of calcium oxalate degradation was also analyzed using proteomics. The results showed, for the first time, that OX-1 could not only degrade calcium oxalate to calcium carbonate, but also that the process was accompanied by synthesis of methane. Proteomic analysis demonstrated that OX-1 has a dual enzyme system for calcium oxalate degradation, using formyl-CoA transferase (FRC) and thiamine pyrophosphate (ThDP)-dependent oxalyl-CoA decarboxylase (OXC) to form calcium carbonate. Up-regulated expression of enzymes related to methane synthesis was also detected during calcium oxalate degradation. Since methane is also a potent greenhouse gas, these new results suggest that the utility of exploiting the OCP to reduce atmospheric CO2 must be re-evaluated and that further studies should be conducted to reveal how widespread the methane producing capacity of strain OX-1 is in other bacteria and soil environments.

SPOCK: Master regulator of malignant tumors (Review).

SPARC/osteonectin, CWCV and Kazal­like domain proteoglycan (SPOCK) is a family of highly conserved multidomain proteins. In total, three such family members, SPOCK1, SPOCK2 and SPOCK3, constitute the majority of extracellular matrix glycoproteins. The SPOCK gene family has been demonstrated to serve key roles in tumor regulation by affecting MMPs, which accelerates the progression of cancer epithelial­mesenchymal transition. In addition, they can regulate the cell cycle via overexpression, inhibit tumor cell proliferation by inactivating PI3K/AKT signaling and have been associated with numerous microRNAs that influence the expression of downstream genes. Therefore, the SPOCK gene family are potential cancer­regulating genes. The present review summarizes the molecular structure, tissue distribution and biological function of the SPOCK family of proteins, in addition to its association with cancer. Furthermore, the present review documents the progress made in investigations into the role of SPOCK, whilst also discussing prospects for the future of SPOCK­targeted therapy, to provide novel ideas for clinical application and treatment.

Biomarkers of lymph node metastasis in esophageal cancer.

Esophageal cancer (EC) is among the most aggressive malignancies, ranking as the seventh most prevalent malignant tumor worldwide. Lymph node metastasis (LNM) indicates localized spread of cancer and often correlates with a poorer prognosis, emphasizing the necessity for neoadjuvant systemic therapy before surgery. However, accurate identification of LNM in EC presents challenges due to the lack of satisfactory diagnostic techniques. Imaging techniques, including ultrasound and computerized tomography scans, have low sensitivity and accuracy in assessing LNM. Additionally, the existing serological detection lacks precise biomarkers. The intricate and not fully understood molecular processes involved in LNM of EC contribute to current detective limitations. Recent research has shown potential in using various molecules, circulating tumor cells (CTCs), and changes in the microbiota to identify LNM in individuals with EC. Through summarizing potential biomarkers associated with LNM in EC and organizing the underlying mechanisms involved, this review aims to provide insights that facilitate biomarker development, enhance our understanding of the underlying mechanisms, and ultimately address the diagnostic challenges of LNM in clinical practice.