Genetic Diversity and Phylogenetic Analysis of Zygophyllum loczyi in Northwest China's Deserts Based on the Resequencing of the Genome.

In order to study the genetics of local adaptation in all main deserts of northwest China, whole genomes of 169 individuals were resequenced, which covers 20 populations of Zygophyllum loczyi (Zygophyllales: Zygophylaceae). We describe more than 15 million single nucleotide polymorphisms and numerous InDels. The expected heterozygosity and PIC values associated with local adaptation varied significantly across biogeographic regions. Variation in environmental factors contributes largely to the population genetic structure of Z. loczyi. Bayesian analysis performed with STRUCTURE defined four genetic clusters, while the results of principle component analysis were similar. Our results shows that the Qaidam Desert group appears to be diverging into two branches characterized by significant geographic separation and gene flow with two neighboring deserts. Geological data assume that it is possible that the Taklamakan Desert was the original distribution site, and Z. loczyi could have migrated later on and expanded within other desert areas. The above findings provide insights into the processes involved in biogeography, phylogeny, and differentiation within the northwest deserts of China.

Conservation Priorities and Demographic History of Saussurea involucrata in the Tianshan Mountains and Altai Mountains.

Rare and vulnerable endemic plants represent different evolutionary units that occur at different times, and protecting these species is a key issue in biological protection. Understanding the impact of the history of endangered plant populations on their genetic diversity helps to reveal evolutionary history and is crucial for guiding conservation efforts. Saussurea involucrata, a perennial alpine species mainly distributed in the Tianshan Mountains, is famous for its medicinal value but has become endangered due to over-exploitation. In the present study, we employed both nuclear and chloroplast DNA sequences to investigate the genetic distribution pattern and evolutionary history of S. involucrata. A total of 270 individuals covering nine S. involucrata populations were sampled for the amplification and sequencing of nrDNA Internal Transcribed Spacer (ITS) and chloroplast trnL-trnF, matK and ndhF-rpl32 sequences. Via calculation, we identified 7 nuclear and 12 plastid haplotypes. Among the nine populations, GL and BA were characterized by high haplotype diversity, whereas BG revealed the lowest haplotype diversity. Molecular dating estimations suggest that divergence among S. involucrata populations occurred around 0.75 Ma, coinciding with the uplift of Tianshan Mountains. Our results reveal that both isolation-by-distance (IBD) and isolation-by-resistance (IBR) have promoted genetic differentiation among populations of S. involucrata. The results from the ecological niche modeling analyses show a more suitable habitat for S. involucrata in the past than at present, indicating a historical distribution contraction of the species. This study provides new insight into understanding the genetic differentiation of S. involucrata, as well as the theoretical basis for conserving this species.

[Stem and leaf photosynthesis of seven desert woody species and its influencing factors]. / 7ç§è’æ¼ æœ¨æœ¬æ¤ç‰©æžå¹²ä¸Žå¶ç‰‡å ‰åˆç‰¹å¾åŠå ¶å½±å“å› ç´ .

Stem photosynthesis widely presents in desert plants, which increases carbon uptake capacity. In this study, we measured the photosynthetic characteristics of leaves and stems in seven desert woody plants (Populus euphratica, Populus alba var. pyramidalis, Populus pruinose, Haloxylon ammodendron, Calligonum rubicundum, Calligonum caput-medusae, Ammopiptanthus mongolicus) in the same habitat, using a portable Li-6400XT photosynthesis system combined with P-Chamber. We analyzed stem photosynthetic rate and its relationship with leaf photosynthetic rate. We measured the stem functional traits, including water content, stem dry matter content, chlorophyll content, water potential, non-structure carbohydrate (NSC), etc., to find out the main affecting factors of stem photosynthesis. The results showed that stem photosynthetic rate of seven species ranged from 0.72 to 1.71 µmol·m-2·s-1, with the largest of P. pruinose and the smallest of H. ammodendron. Stem photosynthetic rate could offset CO2 of stem respiration by 57%-83%. Leaf photosynthetic rate of the seven sepceis ranged from 12.80 to 22.54 µmol·m-2·s-1, with H. ammodendron and A. mongolicus being lower than those of the other five species. There was a significant positive correlation between leaf photosynthetic rate and stem photosynthetic rate. Stem water use efficiency was 2.2-7.7 times of the leaf. Chlorophyll content, NSC, stem respiration rate, and leaf photosynthetic rate were the main factors affecting stem photosynthesis.

Identification of the Efficacy of Ex Situ Conservation of Ammopiptanthus nanus Based on Its ETS-SSR Markers.

Ammopiptanthus possesses ancestral traits and, as a tertiary relict, is one of the surviving remnants of the ancient Mediterranean retreat and climate drought. It is also the only genus of super xerophytic, evergreen, broad-leaved shrubs. Ammopiptanthus nanus, one of the two species in this genus, is predominantly found in extremely arid and frigid environments, and is increasingly threatened with extinction. Study of the species' genetic diversity is thus beneficial for its survival and the efficacy of ex situ conservation efforts. Based on transcriptome data, 15 pairs of effective EST-SSR were screened to evaluate A. nanus genetic diversity. In all, 87 samples from three populations were evaluated, the results of which show that ex situ conservation in the Wuqia region needs to be supplemented. Conservation and breeding of individual A. nanus offspring should be strengthened in the future to ensure their progeny continue to exhibit high genetic diversity and variation.

[Research Progress in the Efficacy and Safety of ALK Inhibitors 
in the Treatment of NSCLC Brain Metastasis].

Lung cancer is one of the most lethal malignancies in the world, with non-small cell lung cancer (NSCLC) accounting for approximately 80%-85% of all pathological types. Approximately 30%-55% of NSCLC patients develop brain metastases. It has been reported that 5%-6% of patients with brain metastases harbor anaplastic lymphoma kinase (ALK) fusion. ALK-positive NSCLC patients have shown significant therapeutic benefits after treatment with ALK inhibitors. Over the past decade, ALK inhibitors have rapidly evolved and now exist in three generations: first-generation drugs such as Crizotinib; second-generation drugs including Alectinib, Brigatinib, Ceritinib, and Ensartinib; and third-generation drugs like Lorlatinib. These drugs have exhibited varying efficacy in treating brain metastases in ALK-positive NSCLC patients. However, the numerous options available for ALK inhibition present a challenge for clinical decision-making. Therefore, this review aims to provide clinical guidance by summarizing the efficacy and safety of ALK inhibitors in treating NSCLC brain metastases.
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Extracorporeal membrane oxygenation combined with minimally invasive surgery for acute respiratory failure and sudden cardiac arrest: A case report.

Acute respiratory failure and sudden cardiac arrest caused by acute intrathoracic infection is a fatal clinical condition with a low resuscitation success rate. The present study describes the case of a patient with acute empyema secondary to an acute lung abscess rupture, complicated by acute respiratory failure and sudden cardiac arrest caused by severe hypoxemia. The patient recovered well through the administration of multiple therapeutic measures, including medication and closed chest drainage, cardiopulmonary resuscitation, extracorporeal membrane oxygenation combined with continuous renal replacement therapy, and minimally invasive surgical resection of the lung lesion with persistent alveolar fistula as the clinical manifestation. To the best of our knowledge, the treatment of such a severe condition combined with thoracoscopic surgery has rarely been reported before, and the present study may provide insight regarding therapeutic schedules for acute respiratory failure by intrathoracic infection, and excision of ruptured lung abscess.

The complete chloroplast genome sequence of Tamarix arceuthoides Bunge and Tamarix ramosissima Ledeb. (Tamaricaceae).

Tamarix L. is of great ecological and economic significance in arid desert ecosystems. This study reports the complete chloroplast (cp) genomic sequences of T. arceuthoides Bunge and T. ramosissima Ledeb., which are currently unknown, by high-throughput sequencing. The cp genomes of T. arceuthoides 1852 and T. ramosissima 1829 were 156,198 and 156,172 bp in length, respectively, and contained a small single-copy region (SSC: 18,247 bp), a large single-copy region (LSC: 84,795 and 84,890 bp, respectively), and a pair of inverted repeat regions (IRs: 26,565 and 26,470 bp, respectively). The two cp genomes possessed 123 genes arranged in the same order, including 79 protein-coding, 36 tRNA, and eight rRNA genes. Of these, 11 protein-coding genes and seven tRNA genes contained at least one intron. The present study found that Tamarix and Myricaria are sister groups with the closest genetic relationship. The obtained knowledge could provide useful information for future phylogenetic, taxonomic, and evolutionary studies on Tamaricaceae.

Influencing factors of care dependence in patients with coronary heart disease after percutaneous coronary intervention-A cross-sectional study.

AIM: Care dependence has been scarcely investigated in coronary heart disease patients after percutaneous coronary intervention. This study aimed to investigate the association between frailty, self-efficacy, combined effects of frailty and self-efficacy, mental health, and care dependence in coronary heart disease patients after percutaneous coronary intervention. DESIGN: Cross-sectional study. METHODS: Data from 400 patients after percutaneous coronary intervention were collected from 2017-2020. Logistic regression model and mediating analysis were used to identify the association between frailty, self-efficacy, combined effects of frailty and self-efficacy, and care dependence. RESULTS: Patients with frailty and self-efficacy tended to have severe care dependence symptoms. There was no correlation between frailty symptoms, self-efficacy, and care dependence in patients without symptoms of anxiety or depression. But in patients with anxiety or depression symptoms, there is a strong correlation between frailty symptoms, lower self-efficacy, and care dependence. Mental health played an inhibitory effect on frailty and care dependence.

Leukocyte CH25H is a potential diagnostic and prognostic marker for lung adenocarcinoma.

Metastasis, a major challenge during the treatment of lung cancer, causes deterioration in patient health outcomes. Thus, to address this problem, this study aimed to explore the role and contribution of Cholesterol 25-Hydroxylase (CH25H) as a potential diagnostic and prognostic marker in lung cancer. Online public databases were used to analyze the expression level, prognostic value, gene-pathway enrichment, and immune infiltration of CH25H in lung cancer patients. The Real-Time Quantitative Reverse Transcription PCR (qRT-PCR) was used to analyze and detect the CH25H expression levels in leukocytes from lung cancer patients. The expression level of CH25H was significantly reduced in lung adenocarcinoma (LUAD), which is associated with a higher disease stage, but not in lung squamous cell carcinoma (LUSC). Kaplan-Meier survival analysis indicated that LUAD patients with low CH25H expression had a worse prognosis. Mechanistically, our results showed that in LUAD, CH25H may be a regulatory factor affecting the immune cell infiltration level, and the resultant tumor development. Experimental data showed that low expression of CH25H in leukocytes was significantly associated with LUAD metastasis (P < 0.01). Our study suggests that CH25H may function as a prognostic and risk stratification biomarker for LUAD.

Mechanisms of Casing Deformation during Hydraulic Fracturing in the Horizontal Wells of the Weirong Shale Field.

Casing deformation is frequent during hydraulic fracturing in the Weirong shale gas field, which impedes shale gas production. We investigated the effect of shale elastic modulus on casing deformation based on shale swelling in this work. According to field data, the silicon content in the Weirong shale gas field has a considerable impact on casing deformation during hydraulic fracturing. Furthermore, the results of the experiment show that the silicon content is positively related to the elastic modulus of shale. We conducted numerical simulations to analyze the casing deformation based on shale swelling. We observed that the shale elastic modulus was negatively correlated with the casing stress without shale swelling; however, the shale elastic modulus was positively correlated to casing stress with shale swelling. Furthermore, when the elastic modulus remained constant, casing stress was positively correlated with shale swelling. The numerical simulation results were validated using field data from the WY23-5 shale well. Moreover, factors such as injection pressure, formation pressure, and cement sheath elastic modulus can increase the impact of the shale elastic modulus on casing deformation with shale swelling. Casing deformation is greatly influenced by the distribution of the stimulated reservoir volume (SRV) area. Different SRV area behaviors result in different types of casing deformation. The symmetric distribution of the SRV area causes casing extrusion deformation, whereas the asymmetric distribution of the SRV area causes casing bending deformation. Moreover, casing stress is positively correlated with the length of the SRV area.

Chlorin e6-Induced Photodynamic Effect Polarizes the Macrophage Into an M1 Phenotype Through Oxidative DNA Damage and Activation of STING.

The tumor-associated macrophage (TAM) serves as an immunosuppressive agent in the malignant tumor microenvironment, facilitating the development and metastasis of lung cancer. The photodynamic effect destabilizes cellular homeostasis owing to the generation of reactive oxygen species (ROS), resulting in the enhanced pro-inflammatory function of immunocytes. In our previous study, the Ce6-mediated photodynamic effect was found to have kept the viability of macrophages and to remodel them into the M1 phenotype. However, the mechanism remains unrevealed. The present study now explores the mechanism of photodynamic therapy (PDT)-mediated reprogramming of macrophages. As expected, Ce6-mediated PDT was capable of generating reactive oxygen species, which was continuously degraded, causing "low intensity" damage to DNA and thereby triggering subsequent DNA damage response in macrophages. The autophagy was thus observed in Ce6-treated macrophages and was shown to protect cells from being photodynamically apoptotic. More importantly, Ce6 PDT could activate the stimulator of interferon genes (STING) molecule, a sensor of DNA damage, which could activate the downstream nuclear factor kappa-B (NF-κB) upon activation, mediating the polarization of macrophages towards the M1 phenotype thereupon. In addition, inhibition of ROS induced by PDT attenuated the DNA damage, STING activation, and M1-phenotype reprogramming. Furthermore, the silence of the STING weakened Ce6 treatment-mediated M1 remodeling of macrophages as well. Altogether, these findings indicate the Ce6-induced photodynamic effect polarizes macrophages into an M1 phenotype through oxidative DNA damage and subsequent activation of the STING. This work reveals the crucial mechanism by which photodynamic therapy regulates the macrophage phenotype and also provides a novel intervenable signaling target for remodeling macrophages into the M1 phenotype.

Expression Level and Clinical Significance of AK021443 in Non-Small-Cell Lung Carcinoma.

To explore the prognostic potential of AK021443 in non-small-cell lung carcinoma (NSCLC), AK021443 levels in NSCLC specimens were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The correlation between the AK021443 level and pathological factors in NSCLC patients was analyzed. Kaplan-Meier curves were plotted for assessing the prognostic value of AK021443 in NSCLC patients. Potential factors influencing NSCLC prognosis were analyzed by multivariable Cox regression test. AK021443 was upregulated in NSCLC specimens than normal ones. Its level was correlated to histological type, tumor differentiation, TNM staging, and lymphatic metastasis in NSCLC patients. AK021443 was the independent risk factor for the overall survival of NSCLC. AK021443 is highly expressed in NSCLC specimens, which is correlated to histological type, tumor differentiation, TNM staging, and lymphatic metastasis in NSCLC patients. It is the independent prognostic factor for NSCLC.

Ferroptosis triggered by dihydroartemisinin facilitates chlorin e6 induced photodynamic therapy against lung cancerthrough inhibiting GPX4 and enhancing ROS.

Photodynamic therapy (PDT) is noninvasive, low toxicity, and photo-selective, but may be resisted by malignant cells. A previous study found chlorin e6 (Ce6) mediated PDT showed drug resistance in lung cancer cells (LLC), which may be associated with PDT-induced DNA damage response (DDR). DDR may up-regulate glutathione peroxidase 4 (GPX4), which in turn degrade ROS induced by PDT. However, dihydroartemisinin (DHA) was found to down-regulate GPX4. Accordingly, the DHA was hypothesized to improve the resistance to PDT. The present work explores the mechanism of Ce6 mediated drug resistance and reveals whether DHA can enhance the efficacy of PDT by suppressing GPX4. The in vitro experiments found Ce6 treatment did not inhibit the viability of LLC within 6 h without inducing significant apoptosis, suggesting LLC were resistant to PDT. Further investigation demonstrated PDT could damage DNA and up-regulate GPX4, thus degrading the generated ROS. DHA effectively inhibited the viability of LLC and induced apoptosis. Importantly, DHA displayed a prominent inhibitory effect on the GPX4 expression and thereby triggered ferroptosis. Combining DHA with Ce6 for treatment of LLC resulted in the suppressed GPX4 and elevated ROS. Finally, the findings showed DHA combined with Ce6 exhibited superb anti-lung cancer efficacy. In summary, Ce6 PDT damages DNA, up-regulates GPX4 to degrade ROS, thereby inducing drug resistance. Down-regulation of GPX4 by DHA-triggered ferroptosis significantly enhances the efficacy of PDT. This study provides an outstanding theoretical basis for the regulation of the intratumoral redox system and improving PDT efficacy against lung cancer by herbal monomer DHA.

Efficacy of Remdesivir for COVID-19.

Remdesivir is a broad-spectrum antiviral agent. With the rapid spread of Coronavirus disease 2019 (COVID-19) globally, remdesivir is taking the spotlight for COVID-19 treatment. Despite the promising signs of anti-CoV activity in several preclinical and clinical studies, more data of remdesivir in the treatment of COVID-19 is still needed for evaluating its efficacy.

Integrated Analysis of Genomic and Immunological Features in Lung Adenocarcinoma With Micropapillary Component.

BACKGROUND: Micropapillary adenocarcinoma is one of the most aggressive histologic subtypes of lung adenocarcinoma (LADC), and even a minor proportion of micropapillary component (MPC) within the LADC could contribute to poor prognosis. Comprehensive analysis of genetic and immunological features of LADC with different percentages of MPC would help better understand cancer biology of this LADC subtype and direct future treatments. METHODS: We performed next-generation sequencing (NGS) for a discovery cohort of 43 LADC patients whose tumors were micro-dissected to separate MPC and non-MPC lesions and a reference cohort of 113 LADC patients. MPC-enriched genetic alterations that were detected in the discovery cohort were then confirmed using a validation cohort of 183 LADC patients. Immunological staining was also conducted on the MPC-containing samples in the discovery cohort. RESULTS: Tumors with a higher percentage of MPC tended to harbor more tumor mutation burdens (TMBs) and chromosome instability (CIN). Some rare genetic events may serve as the genetic landscape to drive micropapillary tumor progression. Specifically, alterations in transcription termination factor 1 (TTF1), brain-specific angiogenesis inhibitor 3 (BAI3), mammalian target of rapamycin (MTOR), and cyclin-dependent kinase inhibitor 2A (CDKN2A) were cross-validated to be enriched in MPC-contained LADC. Additionally, tumors with a higher percentage of MPC were associated with a higher percentage of CD4+, CD8+, and PD-L1+ staining, and some genetic changes that were enriched in MPC, including MET amplification and MTOR mutation, were correlated with increased PD-L1 expression. CONCLUSION: We identified multiple novel MPC-enriched genetic changes that could help us understand the nature of this aggressive cancer subtype. High MPC tumors tended to have elevated levels of TMBs, T cell infiltration, and immunosuppression than low MPC tumors, implying the potential link between MPC content and sensitivity to immunotherapy.

miR-335-5p Regulates Cell Cycle and Metastasis in Lung Adenocarcinoma by Targeting CCNB2.

BACKGROUND: Lots of studies have shown that cyclin disorders can promote tumor development. This study aims to investigate the biological function and molecular mechanism of CCNB2 in lung adenocarcinoma (LUAD). METHODS: LUAD data were downloaded from GEO database and TCGA-LUAD database. Differential analysis was conducted to find the differentially expressed miRNAs and mRNAs, while targeted prediction was done for the access of potential target mRNAs. Gene expression level was detected by qRT-PCR and Western blot in human LUAD cell lines A-427, A549, Calu-3, PC-9 and human bronchial epithelial cell line BEAS-2B. MTT, colony formation, Transwell and flow cytometry assays were used to detect cell proliferation, metastasis, and cell cycle changes of PC-9 cell line. The dual-luciferase reporter gene was used to detect the targeted binding relationship of the target miRNA and mRNA. RESULTS: CCNB2 was highly expressed and served as a biomarker indicating poor prognosis in LUAD patients. Cell function experiments confirmed the inhibitory effects of silencing CCNB2 on the proliferation, migration and invasion of LUAD cells and cell cycle was blocked in the G0/G1 phase. In addition, with regard to the regulatory mechanism, we demonstrated that miR-335-5p had binding sites with 3'-UTR of CCNB2, indicating that miR-335-5p could target the regulation expression of CCNB2. In subsequent cell function tests, overexpression of miR-335-5p inhibited the proliferation and metastasis of cancer cells, and the rescue experiments also verified that miR-335-5p could reverse the promotion of CCNB2 overexpression on the progress of cancer cells. CONCLUSION: In summary, our results revealed that miR-335-5p could target the down-regulation of CCNB2 to inhibit the occurrence and development of LUAD.

Lobaplatin-Induced Apoptosis Requires p53-Mediated p38MAPK Activation Through ROS Generation in Non-Small-Cell Lung Cancer.

Platinum-based chemotherapy is recommended as the first-line treatment regimen for patients with advanced non-small-cell lung cancer (NSCLC). Lobaplatin (LBP), a third-generation platinum anti-neoplastic agent, has shown an improved efficacy. This study is aimed to investigate the mechanisms of LBP-induced apoptosis in the A549 p53 wild-type cell line. The Cell Counting Kit-8 assay (CCK-8), flow cytometry (FCM), Western blot, xenograft tumor models, terminal deoxynucleotide transferase dUTP nick end labeling (TUNEL), and RNA interference were used in this study. Our results showed that the proliferation of A549 cells could be inhibited by LBP. At lower concentrations, LBP triggered cell cycle arrest at the G1 phase in A549 cells. LBP could also induce apoptosis of A549 cells. LBP also increased the expression of PARP and Bax and the cleavage of caspase-3, caspase-8, and caspase-9 and reduced Bcl-2 expression. In vivo experiment confirmed that LBP could inhibit tumor growth in the A549 xenograft models and induce apoptosis. Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells. Our data demonstrate that LBP could be a promising candidate for the treatment of NSCLC with wild-type p53.

Gambogenic acid inhibits the proliferation of small­cell lung cancer cells by arresting the cell cycle and inducing apoptosis.

Gambogenic acid (GNA), which is an important active compound present in gamboge, exerts anticancer activity in various types of tumor cells. However, the effect of GNA on small­cell lung cancer (SCLC) cell lines and the underlying mechanism involved still remain unclear. In the present study, GNA inhibited the proliferation and cell cycle progression of SCLC cells. GNA also promoted the apoptosis of SCLC cells in a dose­dependent manner, which is associated with modulating the levels of proteins involved in apoptosis pathways in NCI­H446 and NCI­H1688 cells. The results demonstrated that GNA increased the level of cleaved caspase­3, ­8 and ­9, and Bax but decreased the expression of anti­apoptotic protein, Bcl­2. Furthermore, similar results were obtained in a mouse tumor xenograft model. Additionally, GNA exhibit low toxicity in tissues when administered to mice in the SCLC xenograft models. Collectively, our findings demonstrated that GNA significantly inhibited the proliferation of SCLC cells and promoted cell apoptosis via cell cycle arrest and induction of apoptosis.

Progress in research on the role of circular RNAs in lung cancer.

BACKGROUND: Circular RNA (circRNA), as a covalently closed circular RNA molecule, is widely present, which is recognized as a competing endogenous RNA. A large number of differentially expressed circRNAs have been identified and are recognized as potential biomarkers for the diagnosis of tumors. MAIN BODY: CircRNAs play an important role in the regulation of cell signaling pathways. The main biological functions of circRNAs include acting as miRNA sponges, regulating the transcription of the parental genes, and acting as adapters to regulate the interactions between proteins and encoding proteins. Compared with normal tissues, there are differentially expressed circRNAs in lung cancer tissue, and the expression levels of circRNAs are correlated with clinicopathological features of lung cancer. Their roles in pathway regulation are described, and the diagnostic and prognostic values are further evaluated. CONCLUSION: In lung cancer, circRNAs participate in the proliferation, migration, and invasion, acting as a competitive endogenous RNA. Differentially expressed circRNAs may serve as non-invasive diagnostic markers for lung cancers. Further investigation of the roles of circRNAs in the pathogenesis and regulatory pathways is conducive to the development of novel approaches for the diagnosis and accurate treatment of lung cancers.

Overexpression of PEAK1 contributes to epithelial-mesenchymal transition and tumor metastasis in lung cancer through modulating ERK1/2 and JAK2 signaling.

Pseudopodium-enriched atypical kinase 1 (PEAK1), a novel non-receptor tyrosine kinase, has been demonstrated to act as an oncogenic regulator in breast and pancreatic cancers. However, the role of PEAK1 in the progression and metastasis of lung cancer is still unknown. Here, we observed that ectopic PEAK1 expression promoted lung cancer cell migration and invasion, while PEAK1 knockout resulted in suppressed cell migration and invasion. Interestingly, cell proliferation did not significantly increase or decrease in either the PEAK1 overexpression or knockout groups compared with the corresponding control cells. In addition, PEAK1 overexpression could induce epithelial-to-mesenchymal transition (EMT) and the expression of matrix metalloproteinase-2 (MMP2) and MMP9 both in vitro and in vivo, whereas PEAK1 knockout had the opposite effects. Then, we had confirmed that PEAK1 was significantly upregulated in lung cancer tissues, and correlated with a higher tumor node metastasis stage. Moreover, PEAK1 upregulation markedly enhanced the activation of extracellular signal-regulated kinase-1/2 (ERK1/2) and Janus kinase-2 (JAK2) signaling in lung cancer cells. Further work demonstrated that the combination of PD98059 with AZD1480 could reverse the effects of PEAK1-induced EMT, cell migration and invasion. Our findings highlight a newer mechanism for PEAK1 in regulating EMT and metastasis in lung cancer, which might serve as a therapeutic target for lung cancer patients.