Aerziguli Tuerxun

Xinjiang Medical University

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Shutao Zheng

First Affiliated Hospital of Xinjiang Medical University

Lifei Yang

Northeast Forestry University

Qiqi Zhang

Shandong Agricultural University

Xiaomei Lu

First Affiliated Hospital of Xinjiang Medical University

Xiujuan Han

Air Force Medical University

Qing Liu

Shandong University

Tao Liu

Northwest A&F University

Xing Wang

Southeast University

Cong-gai Huang

Affiliated Hospital of Southwest Medical University

Renyong Lin

First Affiliated Hospital of Xinjiang Medical University

Cooperative Institutions

Xinjiang Medical University

First Affiliated Hospital of Xinjiang Medical University

Xinjiang Uygur Autonomous Region Disease Prevention and Control Center

Tumor Hospital of Xinjiang Medical University

Sun Yat-sen University

Chinese Academy of Sciences

Medical Research Institute

Central South University

Huazhong University of Science and Technology

Xinjiang Uygur Autonomous Region Education Department

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Plasma‑derived exosomal pyruvate kinase isoenzyme type M2 accelerates the proliferation and motility of oesophageal squamous cell carcinoma cells

Oncology Reports (2021)

Lifei Yang Shutao Zheng Qing Liu Tao Liu Qiqi Zhang

Exosomal pyruvate kinase isoenzyme type M2 (PKM2) has been found to play a key role in the progression of human hepatocarcinoma. However, exosomal PKM2 (especially plasma‑derived exosomal PKM2), in patients with oesophageal squamous cell carcinoma (ESCC) has not been well defined. In the present study, plasma‑derived exosomes were isolated from healthy controls and patients with ESCC, and identified by transmission electronic microscopy, western blotting, nano‑flow cytometry, nanoparticle tracking and phagocytosis analysis; exosomal PKM2 was detected by western blotting and ELISA. In addition, changes in cellular proliferation and motility in recipient cells (Eca109) were assessed using Cell Counting Kit‑8, colony formation, wound‑healing and Transwell assays. The PKM2 content was higher in exosomes from patients with ESCC than in those from healthy donors. Furthermore, exosomes from patients with ESCC enhanced the proliferation and motility of ESCC cells in vitro. Notably, PKM2 was found to be transferred by exosomes, and was able to act by activating STAT3. To verify the association between PKM2 and STAT3, immunohistochemistry was employed to analyse the protein levels of PKM2 and pSTAT3Tyr705. These data revealed that PKM2 and pSTAT3Tyr705 were upregulated and associated with overall survival in patients with ESCC. Therefore, the present study highlights that exosomes from patients with ESCC enhance the migration and invasiveness of ESCC cells by transferring PKM2.

PKM2

Exosome

10.3892/or.2021.8167

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Prognostic significance of pyruvate kinase M2 expression in esophageal squamous cell carcinoma and its meta-analysis

Translational Cancer Research (2021)

Qiqi Zhang Shutao Zheng Qing Liu Tao Liu Aerziguli Tuerxun

Pyruvate kinase 2 (PKM2) is a key enzyme in the glycolysis pathway and has been reported to be associated with the development of esophageal squamous cell carcinoma (ESCC). However, the prognostic value of PKM2 in ESCC remains undetermined.This study aimed to investigate the clinicopathological significance of PKM2 expression in ESCC. A comprehensive and systematic literature search was conducted using the PubMed, Embase, Medline, and Cochrane library databases. The quality of studies and potential for bias were appraised, and meta-analysis was performed to assess the prognostic impact of PKM2 on overall survival (OS).A total of 5 studies with 781 participants were eligible and enrolled. Patients with high PKM2 expression were associated with poor prognosis in ESCC [hazard ratio (HR) =1.72, 95% confidence interval (CI): 1.41-2.09; P<0.01]. Furthermore, upregulated PKM2 was significantly associated with lymph node metastasis [odds ratio (OR) =2.38, 95% CI: 1.68-3.35; P<0.01], clinical stage (OR =3.29, 95% CI: 2.27-4.77; P<0.01), and tumor (T) classification (OR =2.92, 95% CI: 2.05-4.16, P<0.01).High PKM2 expression denotes worse OS in ESCC patients, and correlates with the lymph node metastasis, clinical stage, and T classification. However, further studies are warranted to assess how PKM2 can be implemented as a reliable staging element in clinical practice and whether it could provide a new target for therapeutic intervention.

PKM2

Clinical Significance

10.21037/tcr-21-442

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CXCL6 fuels the growth and metastases of esophageal squamous cell carcinoma cells both in vitro and in vivo through upregulation of PD‐L1 via activation of STAT3 pathway

Journal of Cellular Physiology (2020)

Shutao Zheng Tongxue Shen Qing Liu Tao Liu Aerziguli Tuerxun

Abstract CXCL6, contraction of C‐X‐C motif chemokine ligand 6, whose biological roles have been rarely described in esophageal squamous cell carcinoma (ESCC). To understand the clinicopathological and biological roles played by CXCL6 in the growth and metastasis of ESCC, immunohistochemistry was used to detect the expression of CXCL6 in ESCC tissues, totaling 105 cases; and the correlation was statistically analyzed between CXCL6 expression and clinicopathological parameters. The role mediated in migration and invasion was evaluated using wound‐healing and Transwell assays. MTT and flow cytometry were used to assay the proliferative variation. In vivo, tail vein injection model was established in nude mice xenografted with human ESCC cell lines whose CXCL6 were artificially manipulated. It was found that relative to normal control, CXCL6 was profoundly higher in ESCC; upregulated CXCL6 only significantly correlated with differentiation degree. In vitro, CXCL6 was found to promote the proliferation, migration, and invasion of ESCC cells; which was fully corroborated by nude mice experiment that CXCL6 can promote the growth and metastases of ESCC cells in vivo. Mechanistically, CXCL6 was discovered to be capable of promoting epithelial‐mesenchymal transition and upregulating PD‐L1 expression through activation of the STAT3 pathway. Collectively, all the data we showed here demonstrate that CXCL6 can enhance the growth and metastases of ESCC cells both in vivo and in vitro.

10.1002/jcp.30236

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Effection of short hairpin RNA targeting extracellular signal-regulated kinase 2 on proliferation of Eca109 cells

Zhonghua shiyan waike zazhi (2010)

Qi Huo Shutao Zheng Aerziguli Tuerxun Qing Liu Jun-guo Feng

Objective To study the effect of short hairpin RNA (shRNA) targeting extracellular signal-regulated kinase 2 (ERK2) on proliferation of human esophageal cancer cell line Eca109. Methods The recombinant plasmid (pGeneClipTM-shRNA-ERK2) was constructed and transfected into the human esophageal cancer cell line Eca109 by liposome, and the transfection efficiency was observed by reverse fluorescence microscope. The proliferation ability of esophageal cancer Eca109 cells after transfection was analyzed by methyl thiazolyl tetrazolium (MTF). The expression of ERK2 and inhibitor apoptosis gene Survivin following transfection was detected by Western blotting. Results Sequencing proved that recombinant plasmid was successfully constructed, and the transfection efficiency was about 50%-70% after 72 h following transfection. The Eca109 cell growth at 96 h after transfection was significantly inhibited by 10.45% as compared with negative group and blank group,P ＜0. 05. The protein expression of ERK2 and Survivin was decreased in transfection group as compared with the U0126 group and negative group at 72 h and 96 h ( P ＜ 0. 05 ). Conclusion The recombinant plasmid ( pGeneClipTM-shRNA-ERK2) has been proved not only to be effective for down-regulation of ERK2, but also can affect the expression of Survivin and significantly inhibit the Eca109 cells proliferation. Key words: Esophageal carcinoma; Small interference; Extracellular signal-regulated kinase; Cell proliferation

Survivin

10.3760/cma.j.issn.1001-9030.2010.09.004

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CALM1 Promotes ESCC Progression and Dampens Chemosensitivity to EGFR Inhibitor

Research Square (Research Square) (2020)

Tao Liu Xiujuan Han Shutao Zheng Qing Liu Aerziguli Tuerxun

Abstract Background: Calmodulin1 (CALM1) has been identified as one of the overexpression genes in a variety of cancers and EGFR inhibitor have been widely used in clinical treatment but it is unknown whether CALM1 and epidermal growth factor receptor (EGFR) have a synergistic effect in esophageal squamous cell carcinoma (ESCC). The aim of the present study was to explore the synergistic effects of knock-out CALM1 combined with EGFR inhibitor (Afatinib) and to elucidate the role of CALM1 in sensitizing the resistance to Afatinib in ESCC. Method: Immunohistochemistry (IHC) and qRT-PCR were used to examine the expression of CALM1 and EGFR in ESCC tissues. Kaplan–Meier survival analysis was used to analyze the clinical and prognostic significance of CALM1 and EGFR expression in ESCC. Furthermore, to evaluate the biological function of CALM1 in ESCC, the latest gene editing technique CRISPR/Cas9（Clustered regularly interspaced short palindromic repeats）was applied to knockout CALM1 in ESCC cell lines KYSE150, Eca109 and TE-1. MTT, flow cytometry, Transwell migration, scratch wound-healing and colony formation assays were performed to assay the combined effect of knock-out CALM1 and EGFR inhibitor on ESCC cell proliferation and migration.. In addition, nude mice xenograft model was used to observe the synergistic inhibition of knock-out CALM1 and Afatinib. Results: Both CALM1 and EGFR were found to be significantly over-expressed in ESCC compared with paired normal control. Over- expressed CALM1 and EGFR were significantly associated with clinical stage, T classification and poor overall prognosis, respectively. In vitro, the combined effect of knock-out of CALM1 mediated by the lentivirus and EGFR inhibitor was shown to be capable of inhibiting the proliferation, inducing cell cycle arrest at G1/S stage and increasing apoptosis of KYSE-150 and Eca109 cells; invasion and migration were also suppressed. In vivo, the results of tumor weight and total fluorescence were markedly reduced compared with the sgCtrl-infected group and sgCAML1 group. Conclusion: Our data demonstrated that knock-out of CALM1 could sensitize ESCC cells to EGFR inhibitor, and it may exert oncogenic role via promotion of EMT. Taken together, CALM1 may be a tempting target to overcome Afatinib resistance.

Afatinib

EGFR Inhibitors

10.21203/rs.3.rs-65402/v1

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Effects of propranolol and isoproterenol on infantile hemangioma endothelial cells in vitro

Experimental and Therapeutic Medicine (2014)

Yalin Zhu Aerziguli Tuerxun Hui Yan Paride Abliz

The aim of the present study was to investigate the effects of propranolol and isoproterenol on the growth curve of infantile hemangioma endothelial cells (IHECs) in vitro and determine the functions of the β-adrenergic receptor in the pathogenesis of infantile hemangioma. IHECs were divided into three groups: The control group, the propranolol group (PG) and the isoproterenol group (IG). The PG and IG were administered with high, medium and low concentrations of the corresponding drugs. The cell growth in each group was determined using the MTT assay. A high propranolol concentration resulted in the inhibition of cell growth. By comparison, isoproterenol promoted cell growth. Within a specific time-frame (72-96 h), high drug concentrations (20 μg/ml) elicited strong effects on the cells. At certain concentrations, propranolol inhibited cell growth once the proliferation stage of IHECs had been affected for a specific length of time, whereas isoproterenol yielded opposite results. The β-adrenergic receptor elicits an important effect in the pathogenesis of infantile hemangioma.

Pathogenesis

Infantile hemangioma

10.3892/etm.2014.1780

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Screening of target genes in esophageal squamous cell cancer in Kazakh by oligonucleotide microarray

Zhōnghuá xiāohuà wàikē zázhì/Zhonghua xiaohua waike zazhi (2008)

Xiaomei Lü Zan Liu Xing Wang Aerziguli Tuerxun Xiaheding Yiliyaer

Objective To screen the differentially expressed genes in esophageal squamous cell cancer (ESCC) and normal tissue of esophageal mucosa in Kazakh. Methods RNA was extracted from the ESCC sections in Kazakh patients, and was amplified to obtain cRNA. The gene expression profiles in ESCC and normal tissue of esophageal mucosa were detected by HG-U133 Plus 2.0 gene chip. The results were analyzed by bioinfor-matics. Results One hundred and seventy differentially expressed genes in ESCC and normal tissue of esophageal mucosa were found, with a difference of more than 10 times in expression levels. Of the 170 genes, 39 were up-regulated (signal log ratio > 3 ) and 131 down-regulated (signal log ratio < - 3). These factors such as cell cycle regulation, apoptosis, cytoskeleton; extracellular matrix, intracellular signal transduction, protein translation and synthesis, and immunological functions were correlated with the genes with abnormal expression. Conclusion The use of oligonucleotide microarray accurately and efficiently screen the 170 target genes in ESCC in Kazakh. It is suggested that these genes may be related to the carcinogenesis and development of ESCC in Kazakh. Key words: Esophageal cancer; Kazakh; Gene expression profile

Kazakh

Tissue microarray

10.3760/cma.j.issn.1673-9752.2008.05.019

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[Corrigendum] Plasma‑derived exosomal pyruvate kinase isoenzyme type M2 accelerates the proliferation and motility of oesophageal squamous cell carcinoma cells

Oncology Reports (2022)

Lifei Yang Shutao Zheng Qing Liu Tao Liu Qiqi Zhang

Subsequently to the publication of the above article, the authors have realized that Fig. 5B on p. 8 was compiled erroneously, in the sense that the two immunohistochemical images selected for Fig 5B did not correspond to each other, meaning they were not derived from the same field under the microscope. This error was inadvertently made during the preparation of the manuscript. A corrected version of Fig. 5, showing the correct data for the expression of PKM2 in NAT in Fig. 5B, is shown on the next page. This inadvertent error did not affect the conclusions reported in this paper, and all the authors agree with this Corrigendum. The authors sincerely thank the Editor of Oncology Reports for presenting them with the opportunity to publish this Corrigendum, and apologize to the readership of the journal for any inconvenience caused. [the original article was published in Oncology Reports 46: Article no. 216, 2021; DOI: 10.3892/or.2021.8167].

Publication

PKM2

10.3892/or.2022.8256

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Proteomic profiling of plasma exosomes reveals CD82 involvement in the development of esophageal squamous cell carcinoma

Journal of Proteomics (2022)

Lifei Yang Adili Salai Sun Xiaohong Qing Liu Tao Liu

10.1016/j.jprot.2022.104662

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Synergic Antitumor and Antitoxicity Effects of the Traditional Uyghur Medicine Abnormal Savda Munziq when Combined with 5-Fluorouracil

Ainiwaer Aikemu Yingying Liu Zhen Gao Lianlian Shan Aerziguli Tuerxun

Objective: A number of traditional Uyghur medicines have been recognized as potent antitumor agents and have been developed and analyzed in vivo.In the present study, the toxic, therapeutic and cytotoxic properties of the Uyghur medicine Abnormal Savda Munziq (ASMq) were investigated.In the presence of certain agents, ASMq results in the fragmentation of plasmid DNA, indicating that it may be a potent antitumor agent in vivo, as it appears to bind to DNA molecules.Thus, the present study investigated the effects of ASMq in combination with 5-fluorouracil (5-FU) in vivo, using an S180 mouse model of cancer.ASMq was observed to enhance the antitumor effect of 5-FU and also attenuated the cytotoxicity of the oxidative stress reactions.Methods: The mice were divided randomly into six groups.Influence of treatment on the activity of mice were observed.The serum levels of SOD, MDA, GSH-Px and pathological change were determined.Results: Compared with the model group, the data turned normal after gavaged 5-FU and ASMq.Conclusion: In summary, a combination of ASMq and 5-FU resulted in a synergistic antitumor effect and attenuated toxicity, suggesting that ASMq may be clinically applicable for the treatment of certain types of cancer.

10.2991/meic-15.2015.256

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