Active multi-focus vortex beam terahertz encoding metasurface based on Dirac semimetals.

An electromagnetic wavefront can be flexibly manipulated by discrete phase coding on the coding unit. In this paper, we designed two coding metasurfaces with 1-bit and 3-bit based on active tuning of Dirac semimetals by controlling the Fermi level (E F) with an external polarization voltage. The size and structure of the metasurface remain unchanged with this strategy. Both designs were found to be dynamically tunable. The 1-bit coding metasurface enables beam conversion, single-focus switching, and switching between single-focus and multi-focus. On the other hand, the 3-bit coding metasurface enables the switching between vortex beams and single-beam mirror reflections. These proposed structures have potential applications in terahertz (THz) communications and terahertz-focused imaging, opening up new possibilities for the dynamic modulation of THz waves.

Parity-time symmetry transition and exceptional points in terahertz metal-graphene hybrid metasurface with switchable transmission and reflection characteristics.

Non-Hermitian metasurfaces provide an excellent platform for the study of parity-time (PT) symmetry transition. The exceptional point (EP) in the transition process exhibits peculiar physical phenomena and enriches the development of metasurfaces. In this study, a terahertz metal-graphene hybrid metasurface that can study PT symmetry transition and EP in transmission and reflection polarization channels is designed by using the phase transition characteristics of VO2. The tunable asymmetric loss and PT symmetry transition can be actively controlled by changing the Fermi energy of the graphene strip. Interestingly, owing to the special chirality of the structure, the original metasurface, and the mirrored metasurface degenerate into a circularly polarized state with opposite rotations at the same Fermi energy. The π-phase mutation at EP is observed following the interaction of circularly polarized waves and the metasurface and is expected to have good application prospects in environmental monitoring and gas sensing.

Bisphenol F induced hyperglycemia via activation of oxidative stress-responsive miR-200 family in the pancreas.

Bisphenol F (BPF), BPS and BPAF are gaining popularity as main substitutes to BPA, but there is no clear evidence that these compounds disrupt glycemic homeostasis in the same way. In this study, four bisphenols were administered to C57BL/6 J mice, and showed that the serum insulin was elevated in the BPA and BPS exposed mice, whereas BPF exposed mice exhibited lower serum insulin and higher blood glucose. BPF decreased oxidized glutathione/reduced glutathione ratio (GSSG/GSH) and N6-methyladenosine (m6A) levels, which was responsible for pancreatic apoptosis in mice. Additionally, the downregulation of Nrf2 and the aberrant regulation of the p53-lncRNA H19 signaling pathway further increased miR-200 family in the BPF-exposed pancreas. The miR-200 family directly suppressed Mettl14 and Xiap by targeting their 3' UTR, leading to islet apoptosis. Antioxidant treatment not only elevated m6A levels and insulin contents but also suppressed the miR-200 family in the pancreas, ultimately improving BPF-induced hyperglycemia. Taken together, miR-200 family could serve as a potential oxidative stress-responsive regulator in the pancreas. And moreover, we demonstrated a novel toxicological mechanism in that BPF disrupted the Keap1-Nrf2 redox system to upregulate miR-141/200b/c which controlled pancreatic insulin production and apoptosis via Mettl14 and Xiap, respectively. As the major surrogates of BPA in various applications, BPF was also diabetogenic, which warrants attention in future research.

MicroRNA as an early diagnostic biomarker for contrast-induced acute kidney injury.

Contrast-induced acute kidney injury (CI-AKI) is a common clinical complication and an important cause of increased mortality, prolonged hospitalization, and increased medical costs. For taking effective interventions in CI-AKI, early diagnosis and active prevention are of key importance. Currently, early CI-AKI detection depends on serum creatinine (Scr) levels, which lags behind the actual time of renal injury and seriously affects early diagnosis and interventions. MicroRNA (miRNA) has been found to be a useful biomarker in early CI-AKI diagnosis. Several studies have reported on tissue and time-specific miRNAs in AKI as effective diagnostic biomarkers and potential therapeutic targets, but there are only a few studies on miRNA in CI-AKI. However, these studies are preliminary exploratory investigations on changes in miRNA expression in CI-AKI, and whether these specific miRNAs can be used as biomarkers for early CI-AKI diagnosis and as clinical therapeutic targets requires systematic and in-depth studies. Therefore, more sensitive and specific miRNAs of CI-AKI could be discovered, providing newer options and development directions for early diagnosis and intervention in clinical CI-AKI practice. This review evaluates the research progress on specific miRNAs in the early diagnosis of CI-AKI with an aim of providing basic data for the clinical application of these molecular markers in CI-AKI.

Tumor-associated exosomes promote lung cancer metastasis through multiple mechanisms.

As an important medium of intercellular communication, exosomes play an important role in information transmission between tumor cells and their microenvironment. Tumor metastasis is a serious influencing factor for poor treatment effect and shortened survival. Lung cancer is a major malignant tumor that seriously threatens human health. The study of the underlying mechanisms of exosomes in tumor genesis and development may provide new ideas for early and effective diagnosis and treatment of lung cancer metastasis. Many studies have shown that tumor-derived exosomes promote lung cancer development through a number of processes. By promoting epithelial-mesenchymal transition of tumor cells, they induce angiogenesis, establishment of the pretransfer microenvironment, and immune escape. This understanding enables researchers to better understand the mechanism of lung cancer metastasis and explore new treatments for clinical application. In this article, we systematically review current research progress of tumor-derived exosomes in metastasis of lung cancer. Although positive progress has been made toward understanding the mechanism of exosomes in lung cancer metastasis, systematic basic research and clinical translational research remains lacking and are needed to translate our scientific understanding toward applications in the clinical diagnosis and treatment of lung cancer metastasis in the near future.

Application of CRISPR/Cas9 gene editing technique in the study of cancer treatment.

In recent years, gene editing, especially that using clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9, has made great progress in the field of gene function. Rapid development of gene editing techniques has contributed to their significance in the field of medicine. Because the CRISPR/Cas9 gene editing tool is not only powerful but also has features such as strong specificity and high efficiency, it can accurately and rapidly screen the whole genome, facilitating the administration of gene therapy for specific diseases. In the field of tumor research, CRISPR/Cas9 can be used to edit genomes to explore the mechanisms of tumor occurrence, development, and metastasis. In these years, this system has been increasingly applied in tumor treatment research. CRISPR/Cas9 can be used to treat tumors by repairing mutations or knocking out specific genes. To date, numerous preliminary studies have been conducted on tumor treatment in related fields. CRISPR/Cas9 holds great promise for gene-level tumor treatment. Personalized and targeted therapy based on CRISPR/Cas9 will possibly shape the development of tumor therapy in the future. In this study, we review the findings of CRISPR/Cas9 for tumor treatment research to provide references for related future studies on the pathogenesis and clinical treatment of tumors.

Difficulties and challenges in the development of precision medicine.

The rapid development of precision medicine is introducing a new era of significance in medicine. However, attaining precision medicine is an ambitious goal that is bound to encounter some challenges. Here, we have put forward some difficulties or questions that should be addressed by the progress in this field. The proposed issues include the long road to precision medicine for all types of diseases as the unknown domains of the human genome hinder the development of precision medicine. The challenges in the acquisition and analysis of large amounts of omics data, including difficulties in the establishment of a library of biological samples and large-scale data analysis, as well as the challenges of informed consent and medical ethics in precision medicine, must be overcome to attain the goals of precision medicine. To date, precision medicine programs have accomplished many preliminary achievements and will help to drive a dramatic revolution in clinical practices for the medical community. Through these advances, the diagnosis and treatment of many diseases will achieve many breakthroughs. This project is just beginning and requires a great deal of time and money. Precision medicine also requires extensive collaboration. Ultimately, these difficulties can be overcome. We should realize that precision medicine is good for patients, but there is still a long way to go.

Inhibition of KLF5-Myo9b-RhoA Pathway-Mediated Podosome Formation in Macrophages Ameliorates Abdominal Aortic Aneurysm.

RATIONALE: Abdominal aortic aneurysms (AAAs) are characterized by pathological remodeling of the aortic wall. Although both increased Krüppel-like factor 5 (KLF5) expression and macrophage infiltration have been implicated in vascular remodeling, the role of KLF5 in macrophage infiltration and AAA formation remains unclear. OBJECTIVE: To determine the role of KLF5 in AAA formation and macrophage infiltration into AAAs. METHODS AND RESULTS: KLF5 expression was significantly increased in human AAA tissues and in 2 mouse models of experimental AAA. Moreover, in myeloid-specific Klf5 knockout mice (myeKlf5-/- mice), macrophage infiltration, medial smooth muscle cell loss, elastin degradation, and AAA formation were markedly decreased. In cell migration and time-lapse imaging analyses, the migration of murine myeKlf5-/- macrophages was impaired, and in luciferase reporter assays, KLF5 activated Myo9b (myosin IXB) transcription by direct binding to the Myo9b promoter. In subsequent coimmunostaining studies, Myo9b was colocalized with filamentous actin, cortactin, vinculin, and Tks5 in the podosomes of phorbol 12,13-dibutyrate-treated macrophages, indicating that Myo9b participates in podosome formation. Gain- and loss-of-function experiments showed that KLF5 promoted podosome formation in macrophages by upregulating Myo9b expression. Furthermore, RhoA-GTP levels increased after KLF5 knockdown in macrophages, suggesting that KLF5 lies upstream of RhoA signaling. Finally, Myo9b expression was increased in human AAA tissues, located in macrophages, and positively correlated with AAA size. CONCLUSIONS: These data are the first to indicate that KLF5-dependent regulation of Myo9b/RhoA is required for podosome formation and macrophage migration during AAA formation, warranting consideration of the KLF5-Myo9b-RhoA pathway as a therapeutic target for AAA treatment.

Hypermethylation of IFN-γ in oral cancer tissues.

OBJECTIVES: The study aimed to evaluate the methylation pattern of the interferon-gamma (IFN-γ) gene in oral cancer tissues compared with normal and benign oral disease tissues. MATERIALS AND METHODS: The oral tissues were gained from the patients of 85 cases of oral squamous cell carcinoma (OSCC), 47 cases of oral dysplastic lesions, and 53 normal biopsies. IFN -γ methylation in oral tissues was verified through methylation-specific polymerase chain reaction (PCR) and DNA sequencing analyses, and the expression levels of IFN-γ messenger RNA (mRNA) and protein were detected using real-time reverse transcription (RT)-PCR and enzyme-linked immunosorbent assays, respectively. IFN-γ was localized in macrophages from oral tissues and detected via immunostaining. RESULTS: IFN-γ mRNA and protein expression levels were evidently decreased in oral cancer tissues, whereas the IFN-γ methylation rate was significantly higher in malignant tumors than in benign and normal tissues (normal, 22.6%; benign, 38.3%; and cancer, 55.3%; P < 0.05). Furthermore, the expression of IFN-γ mRNA was significantly downregulated in oral tumors with methylation compared with tumors without methylation, as determined by real-time RT-PCR (4.76-fold difference; P < 0.05). Likewise, mRNA expression was downregulated by 6.79-fold in oral epithelial dysplasia tissues with methylation compared with those without methylation (P < 0.01). Co-immunostaining to detect MAC2 and IFN-γ demonstrated that macrophages comprised the main source of IFN-γ in oral tissues. IFN-γ methylation demonstrated a significant association with the clinical stage, histopathology grade, and primary tumor. CONCLUSIONS: Aberrant IFN-γ promoter methylation may be involved in the process of tumorigenesis of oral cancer. CLINICAL RELEVANCE: IFN-γ hypermethylation during the process of oral carcinogenesis could be useful for the clinical diagnosis and treatment for OSCC.

Long non-coding RNAs: potential new biomarkers for predicting tumor invasion and metastasis.

Long non-coding RNAs (lncRNAs) play important roles in malignant neoplasia. Indeed, many hallmarks of cancer define that the malignant phenotype of tumor cells are controlled by lncRNAs. Despite a growing number of studies highlighting their importance in cancer, there has been no systematic review of metastasis-associated lncRNAs in various cancer types. Accordingly, we focus on the key metastasis-related lncRNAs and outline their expression status in cancer tissues by reviewing the previous stuides, in order to summarize the nowadays research achivements for lncRNAs related to cancer metastasis. Medline, EMBASE, as well as PubMed databases were applied to study lncRNAs which were tightly associated with tumor invasion and metastasis. Up to now, a substantial number of lncRNAs have been found to have important biological functions. In this review, according to their various features in cancer, lncRNAs were roughly divided into three categories: promoting tumor invasion and metastasis, negative regulation of tumor metastasis and with dual regulatory roles. The present studies may establish the foundation for both further research on the mechanisms of cancer progression and future lncRNA-based clinical applications.

Early Predictors of Acute Kidney Injury: A Narrative Review.

Accompanied with the broad application of interventional therapy, the incidence of acute kidney injury (AKI) has been recently increasing in clinical renal medicine. The pathogenesis of AKI is diverse and complex. In the context of the requirements for the diagnosis and treatment of a renal disorder, a large number of studies have explored biological markers and their usefulness to the early diagnosis and treatment of AKI, including glomerular injury, renal tubular injury, and others. These biomarkers provide an important basis for early monitoring of AKI, but are still not quite sufficient. More ideal biomarkers are needed to be identified. Therefore, future studies are necessary to explore more effective biomarkers for AKI clinical practice, which would play an important role in the early diagnosis and intervention treatment of AKI. This review summarizes the important biomarkers identified by previous studies and aims to highlight the advancements that might provide new methods for early clinical diagnosis and effective therapeutic options, along with prediction of response to treatment for AKI.

Oxidative injury induced by cadmium sulfide nanoparticles in A549 cells and rat lungs.

BACKGROUND: Rod-shaped cadmium sulfide nanoparticles (CdS NPs) are becoming increasingly important in many industrial fields, but their potential hazards remain unknown. OBJECTIVES: This study aimed to explore the patterns and mechanisms of lung injury induced by CdS NPs. METHODS: A549 cells and rats were exposed to two types of CdS NPs with a same diameter of 20-30 nm but different lengths, CdS1 (80-100 nm) and CdS2 (110-130 nm). The using doses were included 10 µg/ml and 20 µg/ml two types of CdS NPs for cellular experiments and five times dose of 20 mg/kg body weight for rats' exposure. Methylthiazolyldiphenyl-tetrazolium bromide (MTT) and trypan blue staining were used to detect the A549 cell mortality percentage. The levels of reactive oxygen species (ROS) were determined in A549 cell. The vigor of superoxide dismutase (SOD) and the contents of catalase (CAT) and malondialdehyde (MDA) were detected both in A549 cells and in rats' serum and lung tissues. The cellular morphological changes were observed under transmission electron microscopy (TEM) and the pathological changes were observed in rats' lung tissue. RESULTS: CdS NPs significantly increased A549 cell mortality percentage. The CdS NPs also increased the levels of ROS and MDA content, whereas they decreased SOD and CAT activities. In parallel, similar changes of the contents of MDA, SOD and CAT were also observed in the sera and lung tissues of CdS NP-treated rats. The cellular TEM detection revealed that two types of CdS nanorods appeared as orderly arranged rounded fat droplets separately and leading to nucleus condensation (CdS1). These cellular and rats' tissues changes in the group treated with CdS1 were more significant than the CdS2 groups. Furthermore, CdS NPs induced many pathological changes, including emphysematous changes in rat lung tissue. Especially visible lung consolidation can be observed in the CdS1 group. CONCLUSIONS: CdS NPs induce oxidative injury in the respiratory system, and their toxic effects may be related to grain length.

Local anesthetic thoracoscopy for the diagnosis of metastatic pleural melanoma originated from oral malignant melanoma: case report and comments.

BACKGROUND: Oral malignant melanoma (OMM) is an aggressive tumor with very low survival rate and easy to metastasize. Pleural metastatic melanoma via primary OMM is rare. CASE PRESENTATION: In this report, we presented a case of metastatic malignant melanoma of the pleura originated from OMM. A 54-year-old man without primary skin lesion was diagnosed multiple nodular shadows, pleural invasion, and pleural effusion by chest computed tomography (CT). One cyst-form tumor on the tongue base was observed by bronchoscopy, which was diagnosed as OMM by pathological examination and then was resected. After getting the tumor tissues from the pleura by pleural biopsy surgery, the diagnosis of pathological examination was pleural metastatic melanoma. Furthermore, tumor cells displayed a positive immunoreaction for melanocytic markers S100 and HMB-45 combining with positive vimentin and cytokeratin AE1/AE3. The patient was therefore diagnosed with metastatic melanoma of the left pleura and the primary melanoma was OMM. CONCLUSIONS: According to this case, we could draw the conclusion that pleural metastasis from OMM was very rare and thoracoscopy preceded under local anesthesia is an important method for its accurate diagnosis.

Cure and prevention strategy for postoperative gastrointestinal fistula after esophageal and gastric cardiac cancer surgery.

Gastrointestinal fistula is the most serious complication of esophageal and gastric cardiac cancer surgery. According to occurrence of organ, gastrointestinal fistula can be divided into anastomotic fistula, gastric fistula; According to occurrence site, fistula can be divided into cervical fistula, thoracic fistula; According to time of occurrence, can be divided into early, middle and late fistula. There are special types of fistula including 'thoracic cavity'-stomach-bronchial fistula, 'thoracic cavity'-stomach-aortic fistula. Early diagnosis needs familiarity with various types of clinical gastrointestinal fistulas. However, Prevention of gastrointestinal fistula is better than cure, including perioperative nutritional support, respiratory tract management, and acid suppression, positive treatment of complications, antibiotic prophylaxis, and gastrointestinal decompression and eating timing. Prevention can effectively reduce the incidence of postoperative gastrointestinal fistula. Collectively, early diagnosis and treatment, nutritional supports are key to reducing mortality of gastrointestinal fistula.

Kidney Bean Protein Prevents High-Fat and High-Fructose Diet-Induced Obesity, Cognitive Impairment, and Disruption of Gut Microbiota Composition.

A long-term intake of a high-fat and high-fructose diet (HFFD), even a high-fat, high-fructose but low-protein diet (HFFD + LP), could cause obesity associated with cognitive impairments. In the present study, rats were subjected to a normal diet (ND), an HFFD diet, an HFFD + LP diet, and an HFFD with kidney bean protein (KP) diet for 8 weeks to evaluate the effect of KP on HFFD- or HFFD + LP-induced obesity and cognitive impairment. The results demonstrated that compared with the HFFD diet, KP administration significantly decreased the body weight by 7.7% and the serum Angiotensin-Converting Enzyme 2 (ACE-2) and Insulin-like Growth Factor 1 (IGF-1) levels by 14.4% and 46.8%, respectively (p < 0.05). In addition, KP suppressed HFFD-induced cognitive impairment, which was evidenced by 8.7% less time required to pass the water maze test. The 16s RNA analysis of the colonic contents showed that the relative abundance of Bifidobacterium, Butyricimonas, and Alloprevotella was increased by KP by 5.9, 44.2, and 79.2 times. Additionally, KP supplementation primarily affected the choline metabolic pathway in the liver, and the synthesis and functional pathway of neurotransmitters in the brain, thereby improving obesity and cognitive function in rats.

Fluoride-elicited developmental testicular toxicity in rats: roles of endoplasmic reticulum stress and inflammatory response.

Long-term excessive fluoride intake is known to be toxic and can damage a variety of organs and tissues in the human body. However, the molecular mechanisms underlying fluoride-induced male reproductive toxicity are not well understood. In this study, we used a rat model to simulate the situations of human exposure and aimed to evaluate the roles of endoplasmic reticulum (ER) stress and inflammatory response in fluoride-induced testicular injury. Sprague-Dawley rats were administered with sodium fluoride (NaF) at 25, 50 and 100mg/L via drinking water from pre-pregnancy to gestation, birth and finally to post-puberty. And then the testes of male offspring were studied at 8weeks of age. Our results demonstrated that fluoride treatment increased MDA accumulation, decreased SOD activity, and enhanced germ cell apoptosis. In addition, fluoride elevated mRNA and protein levels of glucose-regulated protein 78 (GRP78), inositol requiring ER-to-nucleus signal kinase 1 (IRE1), and C/EBP homologous protein (CHOP), indicating activation of ER stress signaling. Furthermore, fluoride also induced testicular inflammation, as manifested by gene up-regulation of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in a nuclear factor-κB (NF-κB)-dependent manner. These were associated with marked histopathological lesions including injury of spermatogonia, decrease of spermatocytes and absence of elongated spermatids, as well as severe ultrastructural abnormalities in testes. Taken together, our results provide compelling evidence that ER stress and inflammation would be novel and significant mechanisms responsible for fluoride-induced disturbance of spermatogenesis and germ cell loss in addition to oxidative stress.

The complete chloroplast genome sequence of the medicinal plant Crotalaria albida.

Crotalaria albida (C. albida) is a traditional Chinese medicinal plant that belongs to Fabaceae family. In this study, the complete chloroplast genome sequence of C. albida was sequenced. The genome is 152,743 bp in length and includes two inverted repeat regions of 25,535 bp. It was predicted to contain 127 genes in the chloroplast genome, among which 82 were protein-coding genes, 37 were tRNA genes, and 8 were rRNA genes. The maximum likelihood phylogenetic analysis based on 24 complete chloroplast genome sequences showed that C. albida was closely related to Ormosia semicastrata, Ormosia emarginata, and Ormosia xylocarpa.

Integrated Bioinformatics Analysis Identifies a New Stemness Index-Related Survival Model for Prognostic Prediction in Lung Adenocarcinoma.

BACKGROUND: Lung adenocarcinoma (LUAD) is one of the most lethal malignancies and is currently lacking in effective biomarkers to assist in diagnosis and therapy. The aim of this study is to investigate hub genes and develop a risk signature for predicting prognosis of LUAD patients. METHODS: RNA-sequencing data and relevant clinical data were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) was performed to identify hub genes associated with mRNA expression-based stemness indices (mRNAsi) in TCGA. We utilized LASSO Cox regression to assemble our predictive model. To validate our predictive model, me applied it to an external cohort. RESULTS: mRNAsi index was significantly associated with the tissue type of LUAD, and high mRNAsi scores may have a protective influence on survival outcomes seen in LUAD patients. WGCNA indicated that the turquoise module was significantly correlated with the mRNAsi. We identified a 9-gene signature (CENPW, MCM2, STIL, RACGAP1, ASPM, KIF14, ANLN, CDCA8, and PLK1) from the turquoise module that could effectively identify a high-risk subset of these patients. Using the Kaplan-Meier survival curve, as well as the time-dependent receiver operating characteristic (tdROC) analysis, we determined that this gene signature had a strong predictive ability (AUC = 0.716). By combining the 9-gene signature with clinicopathological features, we were able to design a predictive nomogram. Finally, we additionally validated the 9-gene signature using two external cohorts from GEO and the model proved to be of high value. CONCLUSION: Our study shows that the 9-gene mRNAsi-related signature can predict the prognosis of LUAD patient and contribute to decisions in the treatment and prevention of LUAD patients.

Development in Detection Methods for the Expression of Surface-Displayed Proteins.

Directed evolution is a widely-used engineering strategy for improving the stabilities or biochemical functions of proteins by repeated rounds of mutation and selection. A protein of interest is selected as the template and expressed on a molecular display platform such as a bacteriophage for engineering. Initially, the surface-displayed protein template needs to be checked against the desired target via ELISA to examine whether the functions of the displayed template remain intact. The ELISA signal is subject to the protein-target binding affinity. A low-affinity results in a weak ELISA signal which makes it difficult to determine whether the weak signal is because of low affinity or because of poor expression of the protein. Using a methyllysine-binding chromodomain protein Cbx1 that weakly binds to the histone H3K9me3 peptide, we developed and compared three different approaches to increase the signal-to-background ratio of ELISA measurements. We observed that the specific peptide-binding signal was enhanced by increasing the Cbx1 phage concentration on the ELISA plate. The introduction of previously known gain-of-function mutations to the Cbx1 protein significantly increased the ELISA signals. Moreover, we demonstrated that the H3K9me3-specific binding signal was enhanced by fusing Cbx1 with a high-affinity phosphotyrosine-binding protein and by coating the ELISA plate with a mixture of H3K9me3 and phosphotyrosine peptides. This approach also worked with binding to a lower affinity momomethyllysine peptide H3K9me1. These approaches may help improve ELISA experiments when dealing with low-affinity ligand-protein interactions.

Extracellular vesicles promotes liver metastasis of lung cancer by ALAHM increasing hepatocellular secretion of HGF.

Tumor-derived extracellular vesicles (EVs) are involved in tumor metastasis. Highly enriched lncRNA-ALAHM was identified from serum EVs of lung adenocarcinoma (LUAD) patients with liver metastasis by high-throughput sequencing. A mouse model of in situ lung cancer was used to determine the effect of ALAHM in LUAD cell EVs on liver metastasis. The effects of ALAHM on hepatocyte paracrine HGF as well as proliferation, invasion, and migration of LUAD cells were observed in vitro. As results, ALAHM expression in LUAD cell EVs was significantly increased. LUAD-cell-derived EVs overexpressing ALAHM significantly promoted lung cancer liver metastasis in model mice. ALAHM of LUAD cell EVs also promotes hepatocyte parasecretion of HGF by binding with AUF1 and increases the proliferation, invasion, and migration of LUAD cells. Thus, LUAD-cell-derived EVs containing ALAHM causes increasing HGF and promoting liver metastasis of LUAD cells.