摘要：
The prognosis of advanced gastric cancer is poor and understanding the biology and subsequent development of new targeting therapy is still an urgent need. This study was conducted to explore the effect of BR2 (a 17-amino acid peptide)-SOX17 (Human sex determining region Y (SRY)-related high-mobility group (HMG) box protein family member 17) fusion protein on Klotho gene expression in gastric cancer cells. The regulatory effects of SOX17 on Klotho gene in gastric cancer cells were tested using dual-luciferase reporter assay and chromatin immunoprecipitation (ChIP) assay. The therapeutic effects of BR2-SOX17 were evaluated by proliferation, colony formation, invasion assay, and cell apoptosis analysis. Results showed that SOX17 enhanced Klotho gene expression in gastric adenocarcinoma cells through binding to the promoter of Klotho gene. BR2-SOX17 fusion protein was effective in delivering SOX17 into gastric cancer cells and subsequently inhibited the cell proliferation, colony formation, and invasion, increased E-cadherin protein expression, decreased vimentin protein expression, as well as induced apoptosis. Our findings suggested SOX17 can bind to the promoter of Klotho gene to enhance Klotho gene expression in gastric cancer cells. The fused BR2-SOX17 protein is an effective agent for targeting therapy of gastric cancer. This article is protected by copyright. All rights reserved.
期刊：
Translational Cancer Research,2020年9(4):2638-2647 ISSN：2218-676X
通讯作者：
Xie, Biao
作者机构：
[Hu, Fan; Li, Mei; Xie, Biao; Mo, Li; Xu, Chongsi; Wang, Xiaoyan; Xiao, You] Hunan Univ Chinese Med, Dept Anorectal Surg 1, Affiliated Hosp 2, 233 North Cai E Rd, Changsha 410005, Peoples R China.;[Nie, Jing] Hunan Slack King Lab Anim Co Ltd, Changsha 410125, Peoples R China.;[Yang, Lixia] Changsha Med Sch, Dept Canc, Affiliated Hosp 1, Changsha 410219, Peoples R China.
通讯机构：
[Xie, Biao] H;Hunan Univ Chinese Med, Dept Anorectal Surg 1, Affiliated Hosp 2, 233 North Cai E Rd, Changsha 410005, Peoples R China.
关键词：
Colorectal cancer (CRC);linc01615;miR-491-5p;apoptosis;invasion
摘要：
Background: The 5-year survival of colorectal cancer (CRC) has had no obvious improvement during the past decades, although a significant progress in treatments has been established. The molecular mechanisms that drive the progression of CRC are still unclear. This study aims to determine the biological activities of linc01615 and its regulatory microRNAs in CRC cells. Methods: The expression of linc016150 and miR-491-5p was measured in six CRC cell lines and one normal colon mucosal epithelial cell line. Their effects on cell proliferation, apoptosis, invasion, and migration were tested in Caco-2 cells. Results: Linc01615 mRNA expression was upregulated in six colorectal cancer cell lines compared to the normal colon mucosal epithelial cell line, which was negatively regulated by miR-491-5p in Caco-2 cells. Silencing of linc01615 gene expression significantly decreased cell proliferation, increased apoptosis, and inhibited invasion and migration in Caco-2 cells. Overexpression of linc01615 exhibited an opposite effect on silencing of linc01615 expression. Transfection with miR-491-5p mimics downregulated linc01615 expression and inhibited the biological activities of linc01615. In contrast, the inhibitor of mi R-491-5p up-regulated linc01615 expression and subsequently enhanced the biological activities of linco1615. Also, overexpression of linc01615 can block the effects of miR-491-5p mimics in Caco-2 cells. Conclusions: Linc01615 functions as an oncogene while mi R-491-5p functions as a tumor suppressor in colorectal cancer cells through negatively regulating each other; both are involved in cell proliferation, apoptosis, invasion, and migration in colorectal cancer cells.
摘要：
Colorectal cancer (CRC) is an aggressive malignancy with a high incidence and mortality rate. Although targeting therapy has been developed, the 5-year survival rate is still very low in CRC patients with distant metastasis. Thus, identification of new targets is still significant for improving CRC treatment. Klotho is a tumor suppressor, and its expression is aberrant in CRC. In this study, the roles of FLI-1 gene in regulating Klotho gene expression and Klotho-associated signaling, as well as the effects of FLI-1 on colony formation, invasion, and apoptosis were investigated in CRC cell lines. The methylation of FLI-1 gene was analyzed using a commercial methylation kit. Results showed that FLI-1 mRNA and protein expression were downregulated in 6 colorectal cancer cell lines when compared with the normal colon mucosal epithelial cell line, which negatively correlated with the level of DNA methylation. Silencing of FLI-1 gene expression decreased Klotho protein expression and phosphorylation of beta-catenin protein at Thr(41) /Ser(45) , but increased Wnt3a and beta-catenin protein expression and IGF-1R phosphorylation in HT29 cells. In contrast to silencing FLI-1, overexpressing FLI-1 significantly increased Klotho protein expression and phosphorylation of beta-catenin protein at Thr(41) /Ser(45) , but decreased Wnt3a and beta-catenin protein expression and IGF-1R phosphorylation in Caco-2 cells. Silencing of FLI-1 gene expression significantly increased colony formation and invasion, but decreased apoptosis in HT29 cells. In contrast, overexpressing of FLI-1 gene significantly decreased colony formation and invasion, but increased apoptosis in Caco-2 cells. These findings suggest that FLI-1 functions as a tumor suppressor in colorectal cancer cells and positively regulates Klotho signaling. Hypermethylation may be one of the causes for the loss of FLI-1 gene expression in colorectal cancer cells. This article is protected by copyright. All rights reserved.
摘要：
BACKGROUND: Clinical or subclinical cardiotoxicity is a concern for cancer patients receiving anthracycline-based chemotherapy. Carvedilol is promising for preventing anthracycline-induced cardiotoxicity (AIC). This review appraised the preventive effects of carvedilol against AIC based on randomized controlled trials (RCTs). METHODS: The Cochrane Collaboration Central Register of Controlled Trials, PubMed, and Embase databases were searched from inception to March 27, 2018. RCTs using carvedilol for the prevention of AIC were selected. Risk of bias and methodological quality were assessed. Meta-analysis was conducted, when applicable, for the trial endpoints; otherwise the data were analyzed descriptively. RESULTS: Nine RCTs comprising 717 patients were selected. The risk of bias was unclear and the methodological quality differed substantially. Data pooling of five eligible studies indicated no decreased mortality in patients receiving carvedilol (risk difference= -0.02, 95% CI: -0.07-0.04, p= 0.57, I(2)= 44%). The impact on the incidence of left ventricular systolic dysfunction (LVSD) was inconsistently reported but meta-analysis was not applicable due to discordant LVSD definitions. Data pooling of eight studies and a subgroup analysis indicated a higher left ventricular ejection fraction (LVEF) with substantial heterogeneity in the carvedilol group (mean difference [MD]= 5.23, 95% CI: 2.20-8.27, p= 0.0007, I(2)= 95%, and MD= 4.65, 95% CI: 0.67-8.64, p= 0.02, I(2)= 90%, respectively). Further analysis of echocardiographic parameters and biomarkers showed weak evidence of improvement in diastolic function and troponin I level by carvedilol administration. CONCLUSION: Preventive use of carvedilol in patients undergoing anthracycline-based chemotherapy may be associated with a reduced incidence of LVSD, higher LVEF value, better diastolic function, and lower troponin I level. RCTs with larger sample size and longer follow-up are needed to verify these findings.
摘要：
Background: Parthenolide (PT), the effective active ingredient of the medicinal plant, feverfew (Tanacetum parthenium), has been used as an anti-inflammatory drug due to its involvement in the inhibition of the NF-kappa B pathway. Moreover, recent studies have demonstrated the anti-tumor effect of PT in several cancers. However, the effect of PT on esophageal carcinoma remains unclear to date. In this study, we examined the inhibitory effects of PT and its underlying mechanism of action in human esophageal squamous cell carcinoma (ESCC) cells - Eca109 and KYSE-510. Methods: The proliferation ability of Eca109 and KYSE-510 treated with PT was detected using the Cell Counting Kit-8 and colony forming assay. The Transwell assay and the wound healing assay were used to analyze the cell invasion and migration ability, respectively. The tube formation assay was used to investigate the effect of PT on tube formation of endothelial cells. The expression level of NF-kappa B, AP-1 and VEGF was analyzed by Western blot. Results: We demonstrated that PT attenuates the proliferation and migration ability of ESCC cells in vitro and also inhibits tumor growth in the mouse xenograft model. In addition, PT exhibited anti-angiogenesis activity by weakening the proliferation, invasion and tube formation of endothelial cells in vitro and reduced microvessel density in the xenograft tumors. Further studies revealed that PT reduced the expression level of NF-kappa B, AP-1 and VEGF in ESCC cells. Conclusion: Collectively, the results of our study demonstrated that PT exerts anti-tumor and anti-angiogenesis effects possibly by inhibiting the NF-kappa B/AP-1/VEGF signaling pathway on esophageal carcinoma and might serve as a promising therapeutic agent for ESCC.
摘要：
Objective To assess the effect and safety of Hydroxysafflor Yellow A for Injection (HSYAI) in treating patients with acute ischemic stroke (AIS) and blood stasis syndrome (BSS). Methods A multicenter, randomized, double-blind, multiple-dose, active-controlled phase II trial was conducted at 9 centers in China from July 2013 to September 2015. Patients with moderate or severe AIS and BSS were randomly assigned to low-, medium-, high-dose HSYAI groups (25, 50 and 70 mg/d HSYAI by intravenous infusion, respectively), and a control group (Dengzhan Xixin Injection (& x706f;& x76cf;(sic)& x8f9b;(sic)& x5c04;& x6db2;, DZXXI) 30 mL/d by intravenous infusion), for 14 consecutive days. The primary outcome was the Modified Rankin Scale (mRS) score <= 1 at days 90 after treatment. The secondary outcomes included the National Institute of Health Stroke Scale (NIHSS) score <= 1, Barthel Index (BI) score > 95, and BSS score reduced > 30% from baseline at days 14, 30, 60, and 90 after treatment. The safety outcomes included any adverse events during 90 days after treatment. Results Of the 266 patients included in the effectiveness analysis, 66, 67, 65 and 68 cases were in the low-, medium-, and high-dose HSYAI and control groups, respectively. The proportions of patients in the medium- and high-dose HSYAI groups with mRS score <= 1 at days 90 after treatment were significantly larger than the control group (P<0.05). The incidences of favorable outcomes of NIHSS and BI at days 90 after treatment as well as satisfactory improvement of BSS at days 30 and 60 after treatment in the medium- and high-dose HSYAI groups were all significantly higher than the control group (P<0.05). No significant difference was reported among the 4 groups in any specific adverse events (P>0.05). Conclusions HSYAI was safe and well-tolerated at all doses for treating AIS patients with BSS. The medium (50 mg/d) or high dose (75 mg/d) might be the optimal dose for a phase III trial. (Registration No. ChiCTR-2000029608)
作者机构：
[Wu, Juanying; Xiao, Lihua] Univ South China, Affiliated Hosp 2, Dept Clin Lab, Hengyang, Hunan, Peoples R China.;[Tian, Ying; Long, Shiyin; Zhang, Caiping; Xiao, Lihua] Univ South China, Med Coll Hengyang, Dept Biochem & Mol Biol, Hengyang, Hunan, Peoples R China.;[Li, Na] Hunan Univ Chinese Med, Affiliated Hosp 2, Dept Pathol, Changsha, Hunan, Peoples R China.;[Chen, Wuzhe] Yong Zhou Vocat Tech Coll, Dept Biotechnol, Yongzhou, Hunan, Peoples R China.;[Long, Shiyin] Univ South China, Dept Biotechnol, Hengyang, Hunan, Peoples R China.
通讯机构：
[Long, Shiyin] U;Univ South China, Dept Biotechnol, Hengyang, Hunan, Peoples R China.
关键词：
metabolic syndrome;HbA1c;HDL subclasses
摘要：
Background: Metabolic syndrome (MS) is characterized by a constellation of metabolic disorders. Hyperglycemia and dyslipidemia are the major risk factors of MS. Here we performed a study to explore the association between glycated hemoglobin A1c (HbA1c) and high-density lipoprotein (HDL) subclasses in patients with MS. Methods: We included 101 MS patients and 77 healthy subjects in this study. Blood tests were executed to assess the blood glucose and lipid indicators, including HbAlc, fasting plasma glucose (FPG), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apo- lipoprotein D-100 (aPoB(100)), pre beta(1)-HDL, HDL3b, aaPoB(100)/AI, apolipoprotein AI (apoAI), HDL2b and HDL2a. Multi- variate linear regression was used to explore potential relationship between HDL subclasses and HbA1c. Results: Compared with control group, the levels of HbA1c, FPG, TG, TC, LDL-C, apoB(100), pre beta(1)-HDL, HDL3b, apoB(100)/AI and LDL-C/HDL-C were significantly increased in MS subjects (p < 0.01), while plasma concentrations of HDL-C, apoAI, HDL2b and HDL2a were significantly decreased in MS subjects (p < 0.01). With the increase of whole blood HbA1c levels in MS subjects, pre beta(1)-HDL was elevated gradually, while HDL2a was decreased gradually. Conclusions: Blood HbA1c level is associated with the changes in HDL subclass distribution in patients with MS.
通讯机构：
[Peng, Youhua] H;Hunan Univ Chinese Med, Affiliated Hosp 2, Dept Dermatol, Changsha 410005, Hunan, Peoples R China.
关键词：
GATA3;IL37;TNF-α;miR-155;psoriasis
摘要：
Psoriasis is a recrudescent chronic immune-mediated inflammatory dermatosis; the production and release of proinflammatory cytokines/chemokines such as TNF-alpha has been regarded as critical issues during psoriasis pathogenesis. Based on online microarray profiles, the expression of the transcription factor GATA3 was downregulated in psoriasis lesion tissues. In the present study, we searched for miRNAs that might be related to TNF-alpha and GATA3 to investigate an in-depth understanding of psoriasis pathogenesis. Herein, higher TNF-alpha and GATA3 protein levels were observed in psoriasis lesion tissues and that GATA3 overexpression significantly reverses TNF-alpha-induced increases within the production of IL-6 and CXCL8 in keratinocytes. TNF-alpha stimulation increases miR-155 expression dose-independently, and the miR-155 inhibitor significantly reverses TNF-alpha-induced suppression of GATA3 protein levels and increases IL-6 and CXCL8 production. miR-155 could suppress the expression of GATA3 by targeting its 3 ' UTR, while GATA3 could activate the transcription of IL37 by targeting its promoter region. miR-155 overexpression reduces IL37 protein and increases CXCL8 production; GATA3 overexpression might significantly attenuate the effects of miR-155 overexpression. In contrast to GATA3, miR-155 expression is significantly upregulated in psoriasis lesion tissue and is negatively correlated with GATA3 and IL37. In summary, the miR-155/GATA3/IL37 axis modulates the production of IL-6 and CXCL8 upon TNF-alpha stimulation to affect psoriasis development. Thus, miR-155/GATA3/IL37 may be potent targets for psoriasis treatment, which needs further in vivo and clinical investigation.
期刊：
Journal of International Medical Research,2020年48(9) ISSN：0300-0605
通讯作者：
Wang, Yuhong
作者机构：
[Cai, Xiong; Ling, Chengli; Lei, Chang; Wang, Yuhong; Zou, Manshu; Xiang, Yun; Huang, Dan] Hunan Univ Chinese Med, Inst Innovat & Appl Res Chinese Med, Training Base Prov Minist Joint State Key Lab Chi, 300 Xueshi Rd, Changsha 410208, Hunan, Peoples R China.;[Xie, Yu] Hunan Univ Chinese Med, Affiliated Hosp 2, Changsha, Hunan, Peoples R China.;[Li, Xuran] Hunan Univ Chinese Med, Sch Pharm, Changsha, Hunan, Peoples R China.
通讯机构：
[Wang, Yuhong] H;Hunan Univ Chinese Med, Inst Innovat & Appl Res Chinese Med, Training Base Prov Minist Joint State Key Lab Chi, 300 Xueshi Rd, Changsha 410208, Hunan, Peoples R China.
关键词：
Cerebral ischemia;reperfusion;neuropharmacology;apigenin;flavonoids;PC12 cell model;oxidative stress;mitochondria;middle cerebral artery occlusion rat model
摘要：
Objective The therapeutic efficacy of apigenin in PC12 cells and rats remains uncertain. The aim of this study was to investigate the neuroprotective effects of apigenin against cerebral ischemia/reperfusion injury, both in vitro and in vivo. Methods We first treated PC12 cells with cobalt chloride (CoCl2) to create a model of oxidative stress injury. Cell viability was then determined using a multifunctional microplate reader. In addition, reactive oxygen species (ROS) levels, apoptosis, and mitochondrial membrane potentials (MMPs) were examined using high-content cytometer analysis. The efficacy of apigenin treatment was also analyzed in a rat middle cerebral artery occlusion (MCAO) model using TTC staining and neurological deficit scores. Results The half-inhibitory concentration of CoCl2 was 1.2 mM. Pretreatment with 10 µg ⋅ mL−1 apigenin significantly enhanced cell viability, reduced ROS levels, alleviated apoptosis, and improved MMP in PC12 cells with CoCl2-induced injury in vitro. In addition, apigenin treatment in vivo significantly improved neurological deficit scores and reduced infarct areas in MCAO rats. These results suggest that the neuroprotective mechanisms of apigenin may be related to mitochondrial activation. Conclusions Apigenin had excellent neuroprotective effects for the treatment of cerebral ischemia/reperfusion injury in vitro and in vivo.
期刊：
Boletin de Malariologia y Salud Ambiental,2020年60(1):83-87 ISSN：1690-4648
通讯作者：
He, Yongheng
作者机构：
[Yang, Fang] Hunan Univ Chinese Med, Changsha, Peoples R China.;[Lan, Zhihua] Univ South China, Dept Pathol, Affiliated Hosp 1, Hengyang, Peoples R China.;[Zeng, Yuheng] Xiamen Hosp Tradit Chinese Med, Dept Anorectal Surg, Xiamen, Peoples R China.;[Song, Yan; He, Yongheng] Hunan Univ Chinese Med, Dept Anorectal Surg 1, Affiliated Hosp 2, Changsha, Peoples R China.
通讯机构：
[He, Yongheng] H;Hunan Univ Chinese Med, Dept Anorectal Surg 1, Affiliated Hosp 2, Changsha, Peoples R China.
关键词：
Clearing away heat and dampness;Anorectal surgery;Wound healing;Drug role
摘要：
This paper analyze the effect of Qingre Lishi Recipe on wound healing in patients after anorectal surgery. Results shos that the clinical efficacy of the two groups was compared. The results showed that the total effective rate was 93.18% in the study group and 70.45% in the control group. The difference between the groups was statistically significant (P<0.05). Comparing the wounds of the two groups, the results showed that the wound area, wound healing time and wound healing rate of the study group were significantly better than those of the control group. The difference between the groups was statistically significant (P<0.05). In the course of this study, the results showed that there was no significant difference in granulation color, wound exudate and wound pain score between the two groups before treatment. After treatment, the granulation color, wound exudate and wound pain level of the wound in the study group The score was significantly better than the control group, and the difference between the groups was statistically significant (P<0.05). Qingre Lishi Decoction is beneficial to the wound healing of patients after anorectal surgery, which can effectively accelerate the wound healing time and reduce the pain of patients' wounds. It is worthy of popularization.
期刊：
Bioscience, Biotechnology, and Biochemistry,2020年84(7):1436-1443 ISSN：0916-8451
通讯作者：
Yang, Zhibo
作者机构：
[Li, Kai; Huang, Pan; Zeng, Bijun; Wang, Chang; Wang, Haizhen; Yang, Zhibo; Pan, Yi] Hunan Univ Chinese Med, Domest First Class Discipline Construct Project C, Dept Dermatol, Affiliated Hosp 2, Changsha, Hunan, Peoples R China.
通讯机构：
[Yang, Zhibo] H;Hunan Univ Chinese Med, Domest First Class Discipline Construct Project C, Dept Dermatol, Affiliated Hosp 2, Changsha, Hunan, Peoples R China.
关键词：
Cathepsin B (CSTB);Cathepsin D (CSTD);isoimperatorin (ISO);Melanin degradation;miR-3619
摘要：
ABSTRACT Melanin metabolism disorders may cause severe impacts on the psychological and social activities of patients. Different from the other two steps of melanin metabolism, namely synthesis and transport, little has been known about the mechanism of melanin degradation. Isoimperatorin (ISO) suppressed the activity of tyrosinase, an essential enzyme in melanin biosynthesis, hence, we investigated the effects and mechanism of ISO in melanin reduction. ISO stimulation significantly reduces the melanin contents and PMEL 17 protein levels; meanwhile, the activity and the protein levels of two critical lysosomal enzymes, Cathepsin B and Cathepsin D, can be significantly increased by ISO treatment. MiR-3619 inhibited the expression of CSTB and CSTD, therefore affecting ISO-induced degradation of melanin. In summary, ISO reduces the melanin content via miR-3619/CSTB and miR-3619/CSTD axes. ISO could be a potent skin-whitening agent, which needs further in vivo and clinical investigation. Graphical Abstract ISO reduces the melanin content and increase lysosomal enzye activity via miR-3619/CSTB and miR-3619/CSTD axes.
摘要：
INTRODUCTION: Vitiligo is the most common type of depigmented skin disease. Cellular oxidative stress caused by reactive oxygen species (ROS) has been implicated in the pathogenesis of vitiligo. Nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway plays an important role in melanocytes against hydrogen peroxide (H(2)O(2)) induced oxidative stress. In addition, vitexin may protect vitiligo by inhibiting oxidative stress and inflammation. OBJECTIVE: In the present study, we aimed to investigate the antioxidant effect of vitexin-activated mitogen-activated protein kinase (MAPK)-Nrf2/ARE axis in vitiligo. METHODS: MTT assay identified cell viability of human melanocyte PIG1. Cell apoptosis was evaluated by flow cytometry. Gene and protein expression levels were analyzed by quantitative real-time PCR (qPCR) and Western blotting. Enzyme-linked immunosorbent assay (ELISA) was used to detect the expressions of inflammatory factors and ROS production. RESULTS: Vitexin inhibited H(2)O(2)-induced melanocyte apoptosis and promoted cell proliferation. Moreover, vitexin decreased expression of interleukin-1β (IL-1β), IL-17A, and ROS in melanocytes induced by H(2)O(2). Subsequently, activation of MAPK-Nrf2/ARE signaling was readily induced by vitexin treatment, as evidenced by the upregulation of antioxidant genes including heme oxygenase 1 (HO-1) and superoxide dismutase (SOD). Knockdown of Nrf2 reversed the protective effect of vitexin on H(2)O(2)-induced melanocytes. And, knockdown of Nrf2 increased the expression of IL-1β, IL-17A and ROS, and reduced HO-1 and SOD expression. CONCLUSIONS: Vitexin protected melanocytes from oxidative stress by activating MAPK-Nrf2/ARE signaling pathway. Our results suggested that the role of the Nrf2/ARE axis in the antioxidant defense of melanocytes, and the potential therapeutic strategy for vitiligo.
摘要：
Purpose: Accumulating reports have shown the oncogenic properties of PPMD1 (protein phosphatase, Mg2+/Mn2+ dependent 1D) in different cancer types. This study was undertaken to explore the role and therapeutic potential of PPM1D in colon cancer. Methods: HT-29 colon cancer cell line was used in this study. Expression analysis of PPMD1 was performed by qRT-PCR. Cell viability was determined by CCK-8 assay. DAPI, acridin orange/ethidium bromide (AO/EB) and propidium iodide (PI) staining assays were used for apoptosis detection. Cell cycle analysis was performed by flow cytometry. Protein expression was determined by western blot analysis. Results: The results showed that the expression of PPMD1 was significantly upregulated in colon cancer by 3.2 to 4.8 fold. Silencing of PPMD1 caused significant decline in the proliferation rate of the HT-29 colon cancer cells that was due to induction of apoptosis as evidenced by DAPI, AO/EB and PI staining. Annexin V/PI showed a significant increase in the percentage of apoptotic of HT-29 cells upon silencing of PPMD1. The induction of apoptosis was also accompanied by increase in Bax and decrease in Bcl-2 expression. PPMD1 silencing also resulted in arrest of the HT-29 cells in the G2/M phase of the cell cycle which was also associated with upsurge of p21 and p53 and depletion of cyclin B1 expression levels. PPMD1 silencing also caused decrease in the viability of the HT-29 cells which was concomitant with suppression of MMP-2 and MMP-9 expression. Conclusion: These findings suggest that PPMD1 has oncogenic properties in colon cancer and exhibit therapeutic implications in colon cancer treatment.
