Case report: A successful clinical experience of transplantation of liver and kidney from a donor with myelodysplastic syndromes.

With a shortage of organs for transplant, the use of marginal donors can be an effective measure to meet the shortfall. Myelodysplastic syndromes (MDS) are considered an absolute contraindication for organ donation because of the high invasive potential. Currently, organ transplantation from donors with a past history of MDS has not been reported. In this paper, we report the successful clinical experience of one liver transplantation and two kidney transplantations, with organs donated by a 39-year-old patient diagnosed with a past history of MDS following intracranial hemorrhage. Four and a half years after transplantation, the three recipients are all doing well. However, it is still not clear to what extent organs donated by patients with a past history of MDS can be safely transplanted. This report provides support for the careful use of marginal donors. With effective treatment and full peer assessment, livers and kidneys from donors with a past history of MDS may be safely transplanted.

Pretransplant use of immune checkpoint inhibitors for hepatocellular carcinoma: A multicenter, retrospective cohort study.

Immune checkpoint inhibitors (ICIs) as a downstaging or bridging therapy for liver transplantation (LT) in hepatocellular carcinoma patients are rapidly increasing. However, the evidence about the feasibility and safety of pre-LT ICI therapy is limited and controversial. To this end, a multicenter, retrospective cohort study was conducted in 11 Chinese centers. The results showed that 83 recipients received pre-LT ICI therapy during the study period. The median post-LT follow-up was 8.1 (interquartile range 3.3-14.6) months. During the short follow-up, 23 (27.7%) recipients developed allograft rejection, and 7 of them (30.4%) were diagnosed by liver biopsy. Multivariate logistics regression analysis showed that the time interval between the last administration of ICI therapy and LT (TLAT) ≥ 30 days was an independent protective factor for allograft rejection (odds ratio = 0.096, 95% confidence interval 0.026-0.357; P < .001). Multivariate Cox analysis showed that allograft rejection was an independent risk factor for overall survival (hazard ratio = 9.960, 95% confidence interval 1.006-98.610; P = .043). We conclude that patients who receive a pre-LT ICI therapy with a TLAT shorter than 30 days have a much higher risk of allograft rejection than those with a TLAT longer than 30 days. The presence of rejection episodes might be associated with higher post-LT mortality.

Mediating effects of attitude on the relationship between knowledge and willingness to organ donation among nursing students.

Background: The current rate of organ donation in China falls significantly below the global average and the actual demand. Nursing students play a crucial role in supporting and promoting social and public welfare activities. This study primary aims to analyze the levels of knowledge, attitudes, willingness toward organ donation, and attitudes toward death among nursing students, and investigate the mediating role of attitude in the relationship between knowledge and willingness. The secondary aims to identify factors that may influence the willingness. Methods: A convenience sample of nursing students completed online-administered questionnaires measuring the level of knowledge, attitudes, and willingness toward organ donation before and after clinical internship. Spearman correlation and mediation analyses were used for data analyses. Results: Before the clinical internship, there were 435 nursing students who had not yet obtained their degrees and were completing their clinical internships. After the internship, this number decreased to 323. The mean score for knowledge before and after the clinical internship (7.17 before and 7.22 after, with no significant difference), the attitude (4.58 before and 4.36 after, with significant difference), the willingness (12.41% before and 8.67% after, with significant difference), the Death Attitude Profile-Revised (DAP-R) score (94.41 before and 92.56 after, with significant difference). The knowledge indirectly affected nursing students' willingness to organ donation through attitude. Knowledge had a direct and positive impact on attitudes (ß = 1.564). Additionally, nursing students' attitudes positively affected their willingness (ß = 0.023). Attitudes played a mediating role in the relationship between knowledge and willingness (ß = 0.035). Additionally, attitude toward death, fear of death, and acceptance of the concept of escape were found to be correlated with their willingness. Conclusion: Organ donation willingness was found to be low among nursing students. Positive attitudes were identified as a mediating factor between knowledge and willingness. Additionally, DAP-R was a related factor. Therefore, it is recommended to focus on improving knowledge and attitude, as well as providing death education to help nursing students establish a positive attitude toward death. These efforts can contribute to the promotion of organ donation.

NiCo-LDH Hollow Nanocage Oxygen Evolution Reaction Promotes Luminol Electrochemiluminescence.

Conventional luminol co-reactant electrochemiluminescence (ECL) systems suffer from low stability and accuracy due to factors such as the ease of decomposition of hydrogen peroxide and inefficient generation of reactive oxygen species (ROS) from dissolved oxygen. Inspired by the luminol ECL mechanism mediated by oxygen evolution reaction (OER), the nickel-cobalt layered double hydroxide (NiCo-LDH) hollow nanocages with hollow structure and defect state are used as co-reaction promoters to enhance the ECL emission from the luminol-H2 O system. Thanks to the hollow structure and defect state, NiCo-LDH hollow nanocages show excellent OER catalytic activity, which can stabilize and efficiently produce ROS and enhance the ECL emission. Additionally, mechanistic exploration suggests that the ROS involved in the co-reaction of the luminol-H2 O system are derived from the OER reaction process, and there is a positive correlation between ECL intensity and the OER catalytic activity of the co-reaction promoter. The selection of catalysts with excellent OER catalytic activity is a key factor in improving ECL emission. Finally, a dual-mode immunosensor is constructed for the detection and analysis of alpha-fetoprotein (AFP) based on the promoting effect of NiCo-LDH hollow nanocages on the luminol-H2 O ECL system.

A signal amplification electrochemiluminescence biosensor based on Ru(bpy)32+ and ß-cyclodextrin for detection of AFP.

By combining two different materials, metal-organic frameworks (MOF) and ß-cyclodextrins (ß-CD), a signal amplification electrochemical luminescence (ECL) immunosensor was constructed to realize the sensitive detection of AFP. The indium-based metal-organic framework (In-MOF) was used as the carrier of Ru(bpy)32+, and Ru(bpy)32+ was immobilized by In-MOF through suitable pore size and electrostatic interaction. At the same time, using host-guest recognition, ß-CD enriched TPA into the hydrophobic cavity for accelerating the electronic excitation of TPA, then, achieving the purpose of signal amplification. The signal amplification immunosensor structure is constructed among the primary antibody Ab1 connected to the Ru(bpy)32+@In-MOF modified electrode, AFP, BSA and the secondary antibody (Ab2) loaded with TPA-ß-CD. The immunosensor has a good linearity in the range of 10-5 ng/mL-50 ng/mL, and the low limit of detection (LOD) is 1.1 × 10-6 ng/mL. In addition, the electrochemiluminescence immunosensor that we designed has strong stability, good selectivity and repeatability, which provides a choice for the analysis of AFP.

Hypothermic machine perfusion reduces donation after circulatory death liver ischemia-reperfusion injury through the SERPINA3-mediated PI3Kδ/Akt pathway.

Hypothermic machine perfusion (HMP) has been demonstrated to be more effective in mitigating ischemia-reperfusion injury (IRI) of donation after circulatory death (DCD) organs than cold storage (CS), yet the underlying mechanism remains obscure. We aimed to propose a novel therapeutic approach to ameliorate IRI in DCD liver transplantation. Twelve clinical liver samples were randomly assigned to HMP or CS treatment and subsequent transcriptomics analysis was performed. By combining in vivo HMP models, we discovered that HMP attenuated inflammation, oxidative stress, and apoptosis in DCD liver through a SEPRINA3-mediated PI3Kδ/AKT signaling cascade. Moreover, in the hypoxia/reoxygenation (H/R) model of BRL-3A, overexpression of SERPINA3 mitigated H/R-induced apoptosis, while SERPINA3 knockdown exacerbated cell injury. Idelalisib (IDE) treatment also reversed the protective effect of SERPINA3 overexpression. Overall, our research provided new insights into therapeutic strategies and identified potential novel molecular targets for therapeutic intervention against DCD liver.

Hemoperfusion Adsorbents for Removal of Common Toxins in Liver and Kidney Failure: Recent Progress, Challenges, and Prospects.

Liver and kidney failure can lead to extensive accumulation of toxic metabolites in the blood and tissues, such as bilirubin, blood ammonia, endotoxins, cytokines, creatinine, uric acid, and urea, which aggravate the progression of the disease. Hemoperfusion can effectively adsorb and remove toxins from the blood and treat liver and kidney failure. However, the adsorption efficiency and safety of traditional hemoperfusion adsorbents are not ideal. Thus, it is urgent to develop adsorbents with good blood compatibility, as well as high adsorption and strong selective capacities, to fulfill the clinical needs. In recent years, new hemoperfusion adsorbents with improved adsorption performance and good blood compatibility have been developed. This review classifies and summarizes the recent research progress in hemoperfusion adsorbents for common blood toxins (bilirubin, blood ammonia, endotoxins, cytokines, creatinine, uric acid, and urea) produced by liver and kidney failure. The composition and structure of various toxin adsorbents, toxin adsorption performance, biocompatibility, blood safety, and the adsorption mechanisms of toxins are discussed. Based on a summary of recent studies, feasible strategies have been explored for designing and preparing hemoperfusion adsorbents to fulfill future development requirements. The trends and clinical application prospects of various toxin adsorbents are also discussed.

[Retracted] PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the tumor images shown in Fig. 4G and H were strikingly similar to tumor images (albeit oriented differently) which had previously appeared in Fig. 8A in another article published in the journal International Journal of Oncology [Tang B, Li Y, Yuan S, Tomlinson S and He S: Upregulation of the δ opioid receptor in liver cancer promotes liver cancer progression both in vitro and in vivo. Int J Oncol 43: 1281­1290, 2013], indicating that results which were purported to have been obtained under different experimental conditions had been derived from the same original source. In view of the fact that these data had already appeared in another publication prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 41: 43­56, 2019; DOI: 10.3892/or.2018.6825].

An electrochemiluminescence resonance energy transfer biosensor based on Luminol-LDH and CuS@Pt for detection of alpha-fetoprotein.

Alpha-fetoprotein (AFP) is the best diagnostic marker for hepatocellular carcinoma (HCC) and plays an important role in the general surveillance of the population. Therefore, the establishment of an ultra-sensitive AFP assay is essential for the early screening and clinical diagnosis of HCC. In this work, we designed a signal-off biosensor for ultra-sensitive detection of AFP based on an electrochemiluminescent resonance energy transfer (ECL-RET) strategy using luminol intercalated layered bimetallic hydroxide (Luminol-LDH) as an ECL donor and Pt nanoparticles-grown on copper sulfide nanospheres (CuS@Pt) as ECL acceptor. The (Au NPs/Luminol-LDH)n multilayer nanomembrane synthesized by our intercalation and layer-by-layer electrostatic assembly process not only effectively immobilizes luminol but also significantly enhances the ECL signal. The CuS@Pt composite has well visible light absorption ability and can burst the light emitted from luminol by ECL-RET. The biosensor showed good linearity in the range from 10-5 ng mL-1 to 100 ng mL-1 and a minimum detection limit of 2.6 fg mL-1. Therefore, the biosensor provides a novel and efficient strategy for the detection of AFP, which is important for the early screening and clinical diagnosis of HCC.

Current Strategies for Modulating Tumor-Associated Macrophages with Biomaterials in Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related deaths in the world. However, there are currently few clinical diagnosis and treatment options available, and there is an urgent need for novel effective approaches. More research is being undertaken on immune-associated cells in the microenvironment because they play a critical role in the initiation and development of HCC. Macrophages are specialized phagocytes and antigen-presenting cells (APCs) that not only directly phagocytose and eliminate tumor cells, but also present tumor-specific antigens to T cells and initiate anticancer adaptive immunity. However, the more abundant M2-phenotype tumor-associated macrophages (TAMs) at tumor sites promote tumor evasion of immune surveillance, accelerate tumor progression, and suppress tumor-specific T-cell immune responses. Despite the great success in modulating macrophages, there are still many challenges and obstacles. Biomaterials not only target macrophages, but also modulate macrophages to enhance tumor treatment. This review systematically summarizes the regulation of tumor-associated macrophages by biomaterials, which has implications for the immunotherapy of HCC.

Circulating tumour cell combined with DNA methylation for early detection of hepatocellular carcinoma.

Background: The inadequate early detection strategies makes hepatocellular carcinoma (HCC) patients with poor prognisis. Therefore, more effective detection methods are urgently needed for early detection and early intervention of HCC. Methods: 17 cases of suspected HCC patients and 11 cases of HBV-related decompensated cirrhosis (HBV-DeCi) patients were enrolled. For each patient, 5 ml blood sample was separated into circulating tumor cells (CTCs) and plasma, CTCs were stained with Diff staining for counting. Plasma was used for extracting cell free DNA (cfDNA) and then analyzed by qMSP assay. Ct values were recorded for GNB4 and Riplet as target genes and ß-actin as an endogenous reference gene. Finally, clinical efficacy of CTC count combined with GNB4/Riplet methylation detection for early diagnosis of HCC was analyzed. Results: The CTC of HCC patients has pleomorphic characteristics, but it is difficult to distinguish from other blood cells with non-obviously pleomorphic of CTC. Although a small number of CTCs can also be detected in HBV-DeCi patients (control group), the number is significantly lower than that in HCC patients, the sensitivity and specificity of CTC for HCC detection were 70.6% and 90.9% (AUC = 0.81). The Ct values of GNB4 and Riplet methylation were significantly different between HCC patients and control group patients. When CTC combined with two genes, the AUC value was significantly increased to 0.98, the sensitivity was 88.2%, and the specificity was 100%. Conclusion: Our study has developed a novel test that CTC count combined with GNB4/Riplet methylation detection and showed its high performance for early diagnosis of HCC.

M6A-Mediated Upregulation of LINC00106 Promotes Stemness and Metastasis Properties of Hepatocellular Carcinoma via Sponging Let7f.

Background: Hepatocellular carcinoma (HCC) cells exhibit the stemness property, which makes the patient with HCC prone to tumor recurrence and metastasis. Despite the prominent regulatory role of long non-coding RNAs (lncRNAs) in tumor stemness, the roles and molecular mechanisms of LINC00106 in HCC are poorly understood. Methods: LINC00106, let7f and periostin expression levels in tissue specimens and cell lines were assessed through qRT-PCR and immunohistochemistry (IHC). Various in vivo and in vitro assays, namely sphere/colony formation, proportion of side population cells (SP%), invasion, migration, western blot, and murine xenograft model were employed for assessing the stemness and metastatic properties of HCC cells. Luciferase reporter assays, RNA-seq, RNA pull-down, RNA immunoprecipitation (RIP) were conducted to clarificate the target gene and analyze the underlying mechanisms. Results: LINC00106 was prominently upregulated in tissues and cell lines of HCC. Patients having a high LINC00106 level exhibited a poor outcome. Under in vivo and in vitro conditions, the stemness and metastatic properties of HCC cells were augmented by LINC00106. Additionally, LINC00106 was found to sponge let7f to upregulate periostin, which lead to the activation of periostin-associated PI3K-AKT signaling pathway. Moreover, m6A methylation was found to cause LINC00106 upregulation while maintaining LINC00106 RNA transcript stability. Conclusion: m6A methylation triggers the upregulation of LINC00106, which promotes the stemness and metastasis properties in HCC cells by sponging let7f, thereby resulting in periostin activation. The findings indicate the potential of LINC00106 as a diagnostic marker and therapeutic target for HCC.

MMP7 damages the integrity of the renal tubule epithelium by activating MMP2/9 during ischemia-reperfusion injury.

Renal ischemia-reperfusion (IR) injury is a common issue in urological surgery, and the renal tubules, particularly the proximal tubules, are extremely vulnerable to IR injury. In this work, we detected the differently expressed genes (DEGs) between normal rabbit kidneys and IR kidneys by RNA-sequencing, then identified that matrix metalloproteinase-7 (MMP7) played an important role in the progress of IR injury. Indeed, A time-dependent promotion of renal injury was detected in rabbit model, as demonstrated by the increased levels of MMP2/7/9, and the decreased of tight junction protein-1 (TJP1). Furtherly, similar results were confirmed in human renal proximal tubule epithelial (HK-2) cells model. Notably, downregulation of MMP7 affected the activity of MMP2/9 by suppressing expression of cleaved-MMP2/9 not the pro-MMP2/9 protein, which directly alleviated the degradation of TJP1 in HK-2 model. On the contrary, MMP7 had not been affected by inhibiting MMP2/9. In addition, coimmunoprecipitation assay showed that knockdown MMP7 restrained the interaction between MMP2/9 and TJP1. Collectively, this study suggested that MMP7 could serve as early biomarkers for renal tubular injury, and revealed that MMP7 could destroy the integrity of tubular epithelium through degrading TJP1 by activating MMP2/9.

Clinical characteristics and immunosuppressant management of coronavirus disease 2019 in solid organ transplant recipients.

Over 1 000 000 cases of coronavirus disease 2019 (COVID-19) have been confirmed since the worldwide outbreak began. Not enough data on infected solid organ transplant (SOT) recipients are available, especially data about the management of immunosuppressants. We report two cases of COVID-19 in two transplant recipients, with different treatments and prognoses. The first patient received liver transplantation due to hepatitis B virus-related hepatocellular carcinoma and was confirmed to have COVID-19 9 days later. Following a treatment regimen consisting of discontinued immunosuppressant use and low-dose methylprednisolone-based therapy, the patient developed acute rejection but eventually recovered. The other patient had undergone a renal transplant from a living-related donor 17 years ago, and was admitted to the hospital because of persistent fever. This patient was also diagnosed with COVID-19. His treatment regimen consisted of reduced immunosuppressant use. No signs of rejection were observed during the regimen. In the end, the patient successfully recovered from COVID-19. These effectively treated cases can provide a basis for immunosuppressant management of COVID-19-positive SOT recipients.

Vagus Nerve Stimulation Alleviates Hepatic Ischemia and Reperfusion Injury by Regulating Glutathione Production and Transformation.

Inflammation and oxidative stress are pivotal mechanisms for the pathogenesis of ischemia and reperfusion injury (IRI). Vagus nerve stimulation (VNS) may participate in maintaining oxidative homeostasis and response to external stimulus or injury. We investigated whether the in vivo VNS can protect the liver from IRI. In this study, hepatic IRI were induced by ligating the vessels supplying the left and middle lobes of the liver, which underwent 1 h occlusion followed with 24 h reperfusion. VNS was initiated 15 min after ischemia and continued 30 min. Hepatic function, histology, and apoptosis rates were evaluated after 24 h reperfusion. Compared with the IRI group, VNS significantly improved hepatic function. The protective effect was accompanied by a reduction in histological damage in the ischemic area, and the apoptosis rate of hepatocytes has considerable reduction. To find the underlying mechanism, proteomic analysis was performed and differential expression of glutathione synthetase (GSS) and glutathione S-transferase (GST) was observed. Subsequently, test results indicated that VNS upregulated the expression of mRNA and protein of GSS and GST. Meanwhile, VNS increased the plasma levels of glutathione and glutathione peroxidases. We found that VNS alleviated hepatic IRI by upregulating the antioxidant glutathione via the GSS/glutathione/GST signaling pathway.

Elucidation of molecular pathways responsible for the accelerated wound healing induced by a novel fibrous chitin dressing.

Fibrous chitin dressing (FCD) prepared from a NaOH-urea aqueous solution of chitin via a physical process was used to study its effect on wound healing using a full-thickness cutaneous wound model in rats and mice. It was demonstrated that wounds in rats covered with the FCD showed faster collagen (especially type I collagen) growth and speedier healing than those with Gauze (12 days versus 16 days). The ability of FCD to promote wound healing was also observed on wild-type (WT) mice. For MyD88-knockout mice, however, FCD displayed no beneficial but an adverse effect on wound healing: the healing time for wounds treated with FCD was even longer than those treated with gauze. Importantly, in vivo studies indicated that FCD-treated mice, compared to gauze-treated ones, exhibited markedly higher expressions of MyD88, IKBα, TGF-ß, P-TßR II, TßR II and P-Smad2/3 in wild-type mice. For MyD88 knockout mice, however, the expressions of those molecules were inhibited and lowered in FCD-treated ones than those treated with gauze. In vitro studies confirmed that chitin increased the expression of TGF-ß, P-TßRII and P-Smad2/3 while the expressions of those molecules were significantly inhibited with CD14 antibody (p < 0.05). These results indicated that FCD accelerated wound healing through a MyD88-dependent pathway, followed by a TGF-ß/Smad pathway. This work not only demonstrated the superior wound healing effect of chitin-derived dressing, but also provided for the first time the underlying molecular mechanism, further establishing chitin as an important biomedical material for potential clinical applications.

High expression of ubiquitin carboxyl-terminal hydrolase 22 is associated with poor prognosis in hepatitis B virus-associated liver cancer.

Deubiquitinating enzymes regulate protein activity and cell homeostasis by removing ubiquitin moieties from various substrates. Ubiquitin carboxyl-terminal hydrolase 22 (USP22) is a member of the deubiquitinating protease family and is associated with the development of several tumor types. A previous study demonstrated that USP22 is highly expressed in liver cancer, and its high expression is associated with resistance to chemotherapy. However, the role of USP22 in hepatitis B virus (HBV)-associated liver cancer has not yet been elucidated. The current study demonstrated that USP22 was highly expressed in the tissues of patients with HBV-associated liver cancer, and its high expression was associated with clinicopathological characteristics, including tumor size, clinical stage and prognosis. Further results indicated that USP22 may regulate the proliferative and apoptotic abilities of HepG2.2.15 cells. Additionally, investigation into the underlying mechanism, using small interfering RNA, revealed that the downregulation of USP22 inhibited proliferation and promoted apoptosis though the phosphoinositide 3-kinase/protein kinase B signaling pathway. Therefore, USP22 has the potential to be used as an independent predictor of patient prognosis, as well as a therapeutic target for the treatment of HBV-associated liver cancer.

Hypothermic Oxygenated Machine Perfusion Alleviates Donation After Circulatory Death Liver Injury Through Regulating P-selectin-dependent and -independent Pathways in Mice.

BACKGROUND: Hypothermic oxygenated machine perfusion (HOPE) has been shown to improve the quality of liver donation after circulatory death (DCD) compared to cold storage (CS). However, the mechanism by which HOPE works is unclear. In this study, a mouse liver HOPE system was developed to characterize the role of P-selectin in the protective effect of HOPE on DCD livers. METHODS: A warm ischemia model of the liver and an isolated perfused liver system were established to determine a suitable flow rate for HOPE. Perfusate and tissue samples from wild-type and P-selectin knockout (KO) mice were used to determine liver function, apoptosis and necrosis rates, deoxyribonucleic acid injury and oxidative stress levels, leukocyte and endothelial cell activation, and inflammatory reactions. RESULTS: A mouse liver HOPE system was successfully established. HOPE at flow rates between 0.1 and 0.5 mL/min · g were shown to have a protective effect on the DCD liver. P-selectin KO improved the quality of the DCD liver in the CS group, and reduction of P-selectin expression in the wild-type HOPE group had similar protective effects. Moreover, there was a reduction in the degree of oxidative stress and deoxyribonucleic acid injury in the P-selectin KO HOPE group compared with the P-selectin KO CS group. CONCLUSIONS: We established a mouse HOPE system and determined its suitable flow. We also proved that P-selectin deficiency alleviated DCD liver injury. HOPE protected the DCD liver through regulating P-selectin-dependent and -independent pathways.

PEA15 promotes liver metastasis of colorectal cancer by upregulating the ERK/MAPK signaling pathway.

Liver metastasis is one of the major causes of death in patients with colorectal cancer, and although treatment has improved recently, the long­term survival rate of patients has not improved significantly. In the present study, we used immunohistochemistry to determine that phosphoprotein enriched in astrocytes­15 kDa (PEA15) was highly expressed in colorectal cancer tissues and liver metastatic cancer tissues. It was also highly expressed in metastatic colorectal cancer patients compared to non­metastatic patients. Through clinicopathological data of patients with liver metastasis of colorectal cancer, we found that high expression of PEA15 was positively correlated with TNM staging, liver metastasis and poor prognosis of colorectal cancer patients. Using confocal immunofluorescence microscopy, western blotting and cell proliferation, migration and invasion assays, we also determined that PEA15 could promote cancer cell proliferation in vitro and in vivo, epithelial mesenchymal transition (EMT) and the characteristics of cancer stem cells in vitro, thus promoting the abilities of invasion and migration. In addition, we revealed that PEA15 promoted the liver metastasis of colorectal cancer cells in a xenograft tumor metastasis model. In addition, concerning the mechanism, we used gene chip analysis to determine that PEA15 upregulated the ERK/MAPK signaling pathway in colorectal cancer cells. Therefore, we concluded that PEA15 may be a potential biomarker for liver metastasis of colorectal cancer therapy. Collectively, PEA15 promoted the development of liver metastasis of colorectal cancer through the ERK/MAPK signaling pathway.