Peiminine ameliorates Crohn's disease-like colitis by enhancing the function of the intestinal epithelial barrier through Nrf2/HO1 signal.

BACKGROUND AND AIMS: Impaired intestinal barrier function is key in maintaining intestinal inflammation in Crohn's disease (CD). However, no targeted treatment in clinical practice has been developed. Peiminine (Pm) strongly protects the epithelial barrier, the purpose of this study is to investigate whether Pm affects CD-like colitis and potential mechanisms for its action. METHODS: Trinitro-benzene-sulfonic acid (TNBS)-induced mice and Il-10-/- mice were used as CD animal models. Colitis symptoms, histological analysis, and intestinal barrier permeability were used to assess the Pm's therapeutic effect on CD-like colitis. The colon organoids were induced by TNF-α to evaluate the direct role of Pm in inhibiting apoptosis of the intestinal epithelial cells. Western blotting and small molecule inhibitors were used to investigate further the potential mechanism of Pm in inhibiting apoptosis of intestinal epithelial cells. RESULTS: Pm treatment reduced body weight loss, disease activity index (DAI) score, and inflammatory score, demonstrating that colonic inflammation in mice were alleviated. Pm decreased the intestinal epithelial apoptosis, improved the intestinal barrier function, and prevented the loss of tight junction proteins (ZO1 and claudin-1) in the colon of CD mice and TNF-α-induced colonic organoids. Pm activated Nrf2/HO1 signaling, which may protect intestinal barrier function. CONCLUSIONS: Pm inhibits intestinal epithelial apoptosis in CD mice by activating Nrf2/HO1 pathway. This partially explains the potential mechanism of Pm in ameliorating intestinal barrier function in mice and provides a new approach to treating CD.

Plexin domain-containing 1 may be a biomarker of poor prognosis in hepatocellular carcinoma patients, may mediate immune evasion.

BACKGROUND: For the first time, we investigated the oncological role of plexin domain-containing 1 (PLXDC1), also known as tumor endothelial marker 7 (TEM7), in hepatocellular carcinoma (HCC). AIM: To investigate the oncological profile of PLXDC1 in HCC. METHODS: Based on The Cancer Genome Atlas database, we analyzed the expression of PLXDC1 in HCC. Using immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blotting, we validated our results. The prognostic value of PLXDC1 in HCC was analyzed by assessing its correlation with clinicopathological features, such as patient survival, methylation level, tumor immune microenvironment features, and immune cell surface checkpoint expression. Finally, to assess the immune evasion potential of PLXDC1 in HCC, we used the tumor immune dysfunction and exclusion (TIDE) website and immunohistochemical staining assays. RESULTS: Based on immunohistochemistry, qRT-PCR, and Western blot assays, overexpression of PLXDC1 in HCC was associated with poor prognosis. Univariate and multivariate Cox analyses indicated that PLXDC1 might be an independent prognostic factor. In HCC patients with high methylation levels, the prognosis was worse than in patients with low methylation levels. Pathway enrichment analysis of HCC tissues indicated that genes upregulated in the high-PLXDC1 subgroup were enriched in mesenchymal and immune activation signaling, and TIDE assessment showed that the risk of immune evasion was significantly higher in the high-PLXDC1 subgroup compared to the low-PLXDC1 subgroup. The high-risk group had a significantly lower immune evasion rate as well as a poor prognosis, and PLXDC1-related risk scores were also associated with a poor prognosis. CONCLUSION: As a result of this study analyzing PLXDC1 from multiple biological perspectives, it was revealed that it is a biomarker of poor prognosis for HCC patients, and that it plays a role in determining immune evasion status.

Bryostatin-1 attenuates intestinal ischemia/reperfusion-induced intestinal barrier dysfunction, inflammation, and oxidative stress via activation of Nrf2/HO-1 signaling.

Bryostatin-1 (Bryo-1) exerts antioxidative stress effects in multiple diseases, and we confirmed that it improves intestinal barrier dysfunction in experimental colitis. Nevertheless, there are few reports on its action on intestinal ischemia/reperfusion (I/R). In this study, we mainly explored the effect of Bryo-1 on intestinal I/R injury and determined the mechanism. C57BL/6J mice underwent temporary superior mesenteric artery (SMA) obturation to induce I/R, on the contrary, Caco-2 cells suffered to oxygen and glucose deprivation/reperfusion (OGD/R) to establish the in vitro model. RAW264.7 cells were stimulated with LPS to induce macrophage inflammation. The drug gradient experiment was used to demonstrate in vivo and in vitro models. Bryo-1 ameliorated the intestinal I/R-induced injury of multiple organs and epithelial cells. It also alleviated intestinal I/R-induced barrier disruption of intestines according to the histology, intestinal permeability, intestinal bacterial translocation rates, and tight junction protein expression results. Bryo-1 significantly inhibited oxidative stress damages and inflammation, which may contribute to the restoration of intestinal barrier function. Further, Bryo-1 significantly activated Nrf2/HO-1 signaling in vivo. However, the deletion of Nrf2 in Caco-2 and RAW264.7 cells attenuated the protective functions of Bryo-1 and significantly abolished the anti-inflammatory effect of Bryo-1 on LPS-induced macrophage inflammation. Bryo-1 protects intestines against I/R-induced injury. It is associated with intestinal barrier protection, as well as inhibition of inflammation and oxidative stress partly through Nrf2/HO-1 signaling.

Hydrogen peroxide treatment mitigates antibiotic resistance gene and mobile genetic element propagation in mariculture sediment.

Mariculture sediments have been exchange and propagation sources of antibiotic resistance genes (ARGs). However, no efficient methods have been generated to remove ARGs from sediments. Here, we explored the impact of hydrogen peroxide (H2O2) and aeration on the efficient removal of ARGs and mobile genetic elements (MGEs) in mariculture sediments. When compared with the aeration group, the ARG abundance was 3.8-32.3% lower in the H2O2 group during the first 14 days. ARG and MGE abundances were also significantly associated with reduced total bacterial population and diversity (P < 0.05). Based on partial squares path modeling, reduction of MGEs had important roles in ARG removal from H2O2 treatments, while in the aeration group, ARG reductions were mainly determined by changes in bacterial community composition. These results suggested that H2O2 treatment represent a promising method for controlling ARG abundance after dosing feed stuff and limit the spread of ARGs in aquaculture environments.

Sotetsuflavone ameliorates Crohn's disease-like colitis by inhibiting M1 macrophage-induced intestinal barrier damage via JNK and MAPK signalling.

OBJECTIVES: Intestinal inflammation and intestinal barrier dysfunction are two important pathological changes in Crohn's disease (CD). Sotetsuflavone (SF) is a natural monomeric herbal compound with anti-inflammatory and cytoprotective effects that is mostly nontoxic. The effect of SF on CD-like spontaneous colitis was investigated in this study. METHODS: Il-10-/- mice were used as a CD model and were administered different doses of SF. Lipopolysaccharide (LPS) plus IFN-γ-induced macrophages (RAW264.7) and a coculture system (RAW264.7 and organoids) were used in vitro. The protective effects of SF against CD-like colitis and macrophage differentiation and the mechanisms were evaluated. RESULTS: SF treatment markedly improved spontaneous colitis in the CD model, as shown by the following evidence: reductions in the DAI, macroscopic scores (3.63 ± 1.30), colonic tissue inflammatory scores (2 ± 0.76) and proinflammatory factor levels and the attenuation of colon shortening (8 ± 0.93 cm) and weight loss (1.75 ± 1.83 g). Decreased intestinal permeability and intestinal bacterial translocation rates provided evidence of the protective effect of SF on intestinal barrier function. We also found that SF suppressed M1 macrophage-induced inflammatory responses. In the coculture system of mouse colonic organoids and RAW264.7 cells, SF significantly ameliorated M1 macrophage-induced intestinal epithelial damage. In addition, SF inhibited JNK and MAPK (p38) signalling in both Il-10-/- mice and LPS plus IFN-γ-induced macrophages (RAW264.7). CONCLUSIONS: The protective effects of SF against CD-like colitis may be achieved partially by inhibiting M1 macrophage-induced intestinal barrier damage via JNK and p38 signalling. SF may have therapeutic potential for treating CD, especially considering its safety.

Models for Predicting Response to Immunotherapy and Prognosis in Patients with Gastric Cancer: DNA Damage Response Genes.

Objective: DNA damage response (DDR) is a complex system that maintains genetic integrity and the stable replication and transmission of genetic material. m6A modifies DDR-related gene expression and affects the balance of DNA damage response in tumor cells. In this study, a risk model based on m6A-modified DDR-related gene was established to evaluate its role in patients with gastric cancer. Methods: We downloaded 639 DNA damage response genes from the Gene Set Enrichment Analysis (GSEA) database and constructed risk score models using typed differential genes. We used Kaplan-Meier curves and risk curves to verify the clinical relevance of the model, which was then validated with the univariate and multifactorial Cox analysis, ROC, C-index, and nomogram, and finally this model was used to evaluate the correlation of the risk score model with immune microenvironment, microsatellite instability (MSI), tumor mutational burden (TMB), and immune checkpoints. Results: In this study, 337 samples in The Cancer Genome Atlas (TCGA) database were used as training set to construct a DDR-related gene model, and GSE84437 was used as external data set for verification. We found that the prognosis and immunotherapy effect of gastric cancer patients in the low-risk group were significantly better than those in the high-risk group. Conclusion: We screened eight DDR-related genes (ZBTB7A, POLQ, CHEK1, NPDC1, RAMP1, AXIN2, SFRP2, and APOD) to establish a risk model, which can predict the prognosis of gastric cancer patients and guide the clinical implementation of immunotherapy.

m7G-Related DNA Damage Repair Genes are Potential Biomarkers for Predicting Prognosis and Immunotherapy Effectiveness in Colon Cancer Patients.

Objective: m7G is a post-transcriptional modification modality, however, limited research has been conducted on its role in colon cancer. DNA damage repair (DDR) is an important factor that contributes to colon cancer development, growth and chemoresistance. This study aimed to explore whether m7G-related DNA damage repair genes may be used as biomarkers to predict the prognosis of colon cancer patients. Methods: We use non-negative matrix factorization (NMF) to type CRC patients into. Risk models were constructed using different expression genes in two clusters. We assessed the reliability of risk models with DCA curves, and a Nomogram. Meanwhile, The receiver operating characteristic and C-index curves were used to compare the predictive significance of the constructed risk models with other studies. In additional, we examined the significance of risk models on patients' immunity microenvironment and response to immune therapy. Finally, we used a series of cellular experiments to validate the effect of model genes on the malignant progression of CRC cells. Results: Twenty-eight m7G genes were obtained from the GSEA database. Multivariate Cox and LASSO Cox regression analysis was performed and eleven m7G-related DDR genes were identified for constructing the risk model. Survival and stage of CRC patients were worser in the high-risk group than in the low-risk group for both the training and test sets. Additionally, the different immune microenvironment status of patients in the high- and low-risk groups, suggesting that patients in the low-risk group may be more sensitive to immunotherapy, particularly immune checkpoint inhibitors. Finally, we found that depletion of ATP2A1, one of the risk genes in our model, influence the biologic behaviour of CRC cells significantly. Conclusion: The m7G-related DDR genes can be used as important markers for predicting patient prognosis and immunotherapy response. Our data suggest that ATP2A1 may promote the proliferation of colon cancer cells. These findings may provide new therapeutic targets for the treatment of colon cancer.

ANKFN1 plays both protumorigenic and metastatic roles in hepatocellular carcinoma.

Ankyrin repeat and fibronectin type III domain containing 1 (ANKFN1) is reported to be involved in human height and developmental abnormalities, but the expression profile and molecular function of ANKFN1 in hepatocellular carcinoma (HCC) remain unknown. This study aimed to evaluate the clinical significance and biological function of ANKFN1 in HCC and investigate whether ANKFN1 can be used for differential diagnosis in HCC. Here, we showed that ANKFN1 was upregulated in 126 tumor tissues compared with adjacent nontumorous tissues in HCC patients. The upregulation of ANKFN1 in HCC was associated with cirrhosis, alpha-fetoprotein (AFP) levels and poor prognosis. Moreover, silencing ANKFN1 expression suppressed HCC cell proliferation, migration, invasion, and metastasis in vitro and subcutaneous tumorigenesis in vivo. However, ANKFN1 overexpression promoted HCC proliferation and metastasis in an orthotopic liver transplantation model and attenuated the above biological effects in HCC cells. ANKFN1 significantly affected HCC cell proliferation by inducing G1/S transition and cell apoptosis. Mechanistically, we demonstrated that ANKFN1 promoted cell proliferation, migration, and invasion via activation of the cyclin D1/Cdk4/Cdk6 pathway by stimulating the MEK1/2-ERK1/2 pathway. Moreover, ANKFN1-induced cell proliferation, migration, and invasion were partially reversed by ERK1/2 inhibitors. Taken together, our results indicate that ANKFN1 promotes HCC cell proliferation and metastasis by activating the MEK1/2-ERK1/2 signaling pathway. Our work also suggests that ANKFN1 is a potential therapeutic target for HCC.

Ruscogenins Improve CD-Like Enteritis by Inhibiting Apoptosis of Intestinal Epithelial Cells and Activating Nrf2/NQO1 Pathway.

Interaction of intestinal barrier dysfunction and intestinal inflammation promotes the progression of Crohn's disease (CD). A more recent study has suggested that ruscogenins (RUS) can exert anti-inflammatory effects through activation of the Nrf2/NQO1 pathway. The current study is aimed at determining the functionalization of RUS on CD-like colitis. Wild-type (WT) mice induced with trinitrobenzene sulfonic acid (TNBS) exhibit a significant inflammation in their colon and are hence widely used for CD models. In the current study, the mice were treated with the Nrf-2 antagonist (ML385) or ruscogenin (RUS) whereas normal WT mice were kept as the negative control. Comparative analysis was then performed on the inflammation and barrier function of the colons. In vitro analysis of mouse colonic organoid systems revealed the influence of RUS on LPS-induced apoptosis, cytokine, and chemokine expressions in the intestinal epithelium. It was found that RUS ameliorates murine colitis through activation of the Nrf2/NQO1 pathway which was presented as a decrease in inflammation score and downregulated levels of cytokine and chemokine synthesis, as well as increased intestinal permeability. Further, it was noted that RUS alleviated LPS-induced apoptosis in the intestinal epithelium cells through upregulation of the Nrf2/NQO1 signaling pathway in the mouse colonic organoids. In addition, ruscogenin (RUS) attenuated the levels of Bax and C-caspase-3 through activation of the Nrf2/HO1 signaling pathway both in vivo and in vitro. Therefore, it was evident that RUS can be applied as a potential alternative therapeutic agent in CD based on its protective effects on the barrier function and anti-inflammatory activity.

Epac-2 ameliorates spontaneous colitis in Il-10-/- mice by protecting the intestinal barrier and suppressing NF-κB/MAPK signalling.

Intestinal barrier dysfunction and intestinal inflammation interact in the progression of Crohn's disease (CD). A recent study indicated that Epac-2 protected the intestinal barrier and had anti-inflammatory effects. The present study examined the function of Epac-2 in CD-like colitis. Interleukin-10 gene knockout (Il-10-/- ) mice exhibit significant spontaneous enteritis and were used as the CD model. These mice were treated with Epac-2 agonists (Me-cAMP) or Epac-2 antagonists (HJC-0350) or were fed normally (control), and colitis and intestinal barrier structure and function were compared. A Caco-2 and RAW 264.7 cell co-culture system were used to analyse the effects of Epac-2 on the cross-talk between intestinal epithelial cells and inflammatory cells. Epac-2 activation significantly ameliorated colitis in mice, which was indicated by reductions in the colitis inflammation score, the expression of inflammatory factors and intestinal permeability. Epac-2 activation also decreased Caco-2 cell permeability in an LPS-induced cell co-culture system. Epac-2 activation significantly suppressed nuclear factor (NF)-κB/mitogen-activated protein kinase (MAPK) signalling in vivo and in vitro. Epac-2 may be a therapeutic target for CD based on its anti-inflammatory functions and protective effects on the intestinal barrier.

Expression and Clinical Significance of the NCAPH, AGGF1, and FOXC2 Proteins in Serous Ovarian Cancer.

PURPOSE: Recurrence and metastasis are the most common causes of high mortality rates in patients with serous ovarian cancer (SOC). Non-structural maintenance of chromosomes (non-SMC) condensin I complex subunit H (NCAPH) is a newly identified essential oncoprotein whose function in SOC pathogenesis has not been reported yet. Angiogenic factor with G patch and FHA domains 1 (AGGF1) is an effective promoter of angiogenesis in humans, leading to cancer cell infiltration and progression. Forkhead box C2 (FOXC2) plays a pivotal role in epithelial-to-mesenchymal transition (EMT). The present study analyzed the correlations among the expressions of these three proteins and their relationships with the clinicopathological characteristics and survival of patients with SOC. PATIENTS AND METHODS: The expressions of NCAPH, AGGF1, and FOXC2 were detected by the immunohistochemical examination of 153 SOC tissue samples and 30 serous ovarian cystadenoma tissue samples. Clinicopathologic and follow-up data of the patients were collected. RESULTS: The expressions of NCAPH, AGGF1, and FOXC2 were remarkably higher in the SOC tissue samples than in the serous ovarian cystadenoma tissue samples. The protein expressions were positively correlated with the histological tumor grade, the International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and intraperitoneal implantation, but were negatively correlated with the overall survival (OS). Moreover, multivariate analysis showed that the NCAPH, AGGF1, and FOXC2 expressions, FIGO stage, and histological tumor grade were independent adverse prognostic factors for OS in patients with SOC. CONCLUSION: The results of this study show that the expressions of NCAPH, AGGF1, and FOXC2 are promising biomarkers and possible therapeutic targets in patients with SOC.

The role of multiple metabolic genes in predicting the overall survival of colorectal cancer: A study based on TCGA and GEO databases.

The recent advances in gene chip technology have led to the identification of multiple metabolism-related genes that are closely associated with colorectal cancer (CRC). Nevertheless, none of these genes could accurately diagnose or predict CRC. The prognosis of CRC has been made by previous prognostic models constructed by using multiple genes, however, the predictive function of multi-gene prognostic models using metabolic genes for the CRC prognosis remains unexplored. In this study, we used the TCGA-CRC cohort as the test dataset and the GSE39582 cohort as the experimental dataset. Firstly, we constructed a prognostic model using metabolic genes from the TCGA-CRC cohort, which were also associated with CRC prognosis. We analyzed the advantages of the prognostic model in the prognosis of CRC and its regulatory mechanism of the genes associated with the model. Secondly, the outcome of the TCGA-CRC cohort analysis was validated using the GSE39582 cohort. We found that the prognostic model can be employed as an independent prognostic risk factor for estimating the CRC survival rate. Besides, compared with traditional clinical pathology, it can precisely predict CRC prognosis as well. The high-risk group of the prognostic model showed a substantially lower survival rate as compared to the low-risk group. In addition, gene enrichment analysis of metabolic genes showed that genes in the prognostic model are enriched in metabolism and cancer-related pathways, which may explain its underlying mechanism. Our study identified a novel metabolic profile containing 11 genes for prognostic prediction of CRC. The prognostic model may unravel the imbalanced metabolic microenvironment, and it might promote the development of biomarkers for predicting treatment response and streamlining metabolic therapy in CRC.

miR-107 regulates the effect of MCM7 on the proliferation and apoptosis of colorectal cancer via the PAK2 pathway.

Microchromosome maintenance protein 7 (MCM7), a DNA replication permitting factor, plays an essential role in initiating DNA replication. MCM7 is reported to be involved in tumor formation and progression, whereas the expression profile and molecular function of MCM7 in colorectal cancer (CRC) remain unknown. In this study, we aimed to evaluate the clinical significance and biological function of MCM7 in CRC and investigated whether MCM7 can be used for a differential diagnosis in CRC and whether it may serve as a more sensitive proliferation marker for CRC evaluation. Moreover, immunohistochemical analysis of MCM7 was performed in a total of 89 specimens, and high MCM7 expression levels were associated with worse overall survival (OS) in CRC patients. Furthermore, the cell functional test suggested that lentivirus-mediated silencing of MCM7 with shRNA in CRC cells significantly inhibited cellular proliferation and promoted apoptosis in vitro and inhibited tumor growth in vivo. Additionally, mechanistic studies further demonstrated that P21-activated protein kinase 2 (PAK2) was regulated by MCM7 via microarray analysis and cell functional recovery tests, and miR-107 played a role in regulating expression MCM7 via miRNA microarray analysis and 3'UTR reporter assays. Taken together, our results suggest that the miR-107/MCM7/PAK2 pathway may participate in cancer progression and that MCM7 may serve as a prognostic biomarker in CRC.

LncRNA-CASC7 inhibits the proliferation and migration of colon cancer by negatively regulating the PI3K/Akt signaling pathway.

BACKGROUND: This study aims to investigate the effect of LncRNA-CASC7 (cancer susceptibility candidate 7) on the proliferation and migration of colon cancer cells and its possible mechanism. METHODS: In this study, quantitative real-time polymerase chain reaction (qRT-PCR) was employed for the detection of lncRNA-CASC7 expression in 54 colon cancer tissues and 5 colon cancer cell lines. This study aimed to evaluate the significant correlation between the lncRNA-CASC7 expression, the clinical features, and the survival rate of patients. LncRNA-CASC7 was overexpressed by lipofectin transfection. Cell proliferation was detected by the methyl thiazolyl tetrazolium (MTT) assay. Transwell assay was conducted to examine cell migration and invasion. The target gene was verified by dual fluorescein. The expression of proliferation and invasion-related proteins was detected via western blotting (WB). RESULTS: The LncRNA-CASC7 expression in colon cancer was considerably decreased than in nearby healthy tissues (P<0.01). Its expression level was linked to survival rate, lymph node metastasis, and tumor node metastasis (TNM) stage. Similarly, the expression of lncRNA-CASC7 was decreased in 5 colon cancer cell lines. The proliferative, invasive, and migratory potential of cells was considerably decreased by lncRNA-CASC7 overexpression. Overexpression of lncRNA-CASC7 significantly inhibited the expression of proteins Ki-67 and PNCA (associated with proliferation) and proteins N-cadherin, E-cadherin, and vimentin (linked with metastasis). Further studies showed that overexpression of LncRNA-CASC7 could significantly inhibit the PI3K/Akt signaling pathway in colon cancer cells. CONCLUSIONS: The PI3K/Akt signaling cascade is negatively regulated by LncRNA-CASC7, which serves as a tumor suppressor gene by attenuating colon cancer cell proliferation, invasion, and migration, thus affecting the tumor progression and prognosis of colon cancer patients.

Comprehensive analysis of competitive endogenous RNAs network reveals potential prognostic lncRNAs in gastric cancer.

Long non-coding RNAs (lncRNAs) are key regulators of a range of human diseases, including various cancers, with multiple previous studies having explored lncRNA dysregulation in the context of gastric cancer (GC). The present study sought to expand upon these previous results by downloading lncRNA, mRNA, and microRNA (miRNA) expression profiles derived from 180 GC tissues and 24 normal control tissues within the Cancer Genome Atlas (TCGA) database. These datasets were then interrogated to identify GC-related differentially expressed (DE) RNAs (|fold change| ≥ 2, FDR< 0.01), leading to the identification of 1946 DE lncRNAs, 123 DE miRNAs, and 3159 DE mRNAs. These results were then used to generate a putative GC-related competitive endogenous RNA (ceRNA) network composed of 131 lncRNAs, 9 miRNAs, and 78 mRNAs. Subsequent survival analyses based upon this network revealed 17 of these lncRNAs to be significantly associated with GC patient survival (P < 0.05). Further multivariable Cox regression and lasso analyses allowed for the construction of an 8-lncRNA risk score that was able to effectively predict GC patient survival with good discriminative ability. The Kaplan-Meier Plotter database further confirmed that network hub genes that were related to these 8 lncRNAs were associated with GC patient prognosis (P < 0.05). As the ceRNA network in the present study was constructed with a focus on both disease stage and differential gene expression, it represents a key resource that will offer valuable insights into the mechanistic roles of ceRNA pathways in GC development and progression.

Feature Extraction and Reconstruction by Using 2D-VMD Based on Carrier-Free UWB Radar Application in Human Motion Recognition.

As the size of the radar hardware platform becomes smaller and smaller, the cost becomes lower and lower. The application of indoor radar-based human motion recognition has become a reality, which can be realized in a low-cost device with simple architecture. Compared with narrow-band radar (such as continuous wave radar, etc.), the human motion echo signal of the carrier-free ultra-wideband (UWB) radar contains more abundant characteristic information of human motion, which is helpful for identifying different types of human motion. In this paper, a novel feature extraction method by two-dimensional variational mode decomposition (2D-VMD) algorithm is proposed. And it is used for extracting the primary features of human motion. The 2D-VMD algorithm is an adaptive non-recursive multiscale decomposition method for nonlinear and nonstationary signals. Firstly, the original 2D radar echo signals are decomposed by the 2D-VMD algorithm to capture several 2D intrinsic mode function (BIMFs) which represent different groups of central frequency components of a certain type of human motion. Secondly, original echo signals are reconstructed according to the several BIMFs, which not only have a certain inhibitory effect on the clutter in the echo signal, but can also further demonstrate that the BIMFs obtained by the 2D-VMD algorithm can represent the original 2D echo signal well. Finally, based on the measured ten different types of UWB radar human motion 2D echo analysis signals, the characteristics of these different types of human motion are extracted and the original echo signal are reconstructed. Then, the three indicators of the PCC, UQI, and PSNR between the original echo signals and extraction/reconstruction 2D signals are analyzed, which illustrate the effectiveness of 2D-VMD algorithm to extract feature of human motion 2D echo signals of the carrier-free UWB radar. Experimental results show that BIMFs by 2D-VMD algorithm can well represent the echo signal characteristics of this type of human motion, which is a very effective tool for human motion radar echo signal feature extraction.