Xiujuan Han

Air Force Medical University

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Shaojun Zhu

Air Force Medical University

Yanhong Li

Beijing Children’s Hospital

Shutao Zheng

First Affiliated Hospital of Xinjiang Medical University

Li Gong

Tsinghua University

Xiaomei Lu

First Affiliated Hospital of Xinjiang Medical University

Lan Miao

Xiyuan Hospital

Lifei Yang

Northeast Forestry University

Qiqi Zhang

Shandong Agricultural University

Qing Liu

Shandong University

Aerziguli Tuerxun

Xinjiang Medical University

Cooperative Institutions

Air Force Medical University

Xijing Hospital

Chinese Academy of Medical Sciences & Peking Union Medical College

Huazhong University of Science and Technology

Peking University

Xinjiang Medical University

Sichuan University

Chinese Academy of Sciences

Shanghai Jiao Tong University

Nanjing Medical University

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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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Downregulation of microRNA-1 in esophageal squamous cell carcinoma correlates with an advanced clinical stage and its overexpression inhibits cell migration and invasion

International Journal of Molecular Medicine (2015)

Li Ping Yao Yi Zhang Qiao Zhu Xinyi Li Shaojun Zhu

Esophageal squamous cell carcinoma (ESCC) is one of most common and fatal forms of cancer worldwide. Recent studies have suggested that an aberrant microRNA (miRNA or miR) expression signature exists in ESCC. In the present study, in order to determine the involvement of miRNA in the development and progression of ESCC, the expression profiles of miRNA in 8 paired ESCC tissues and corresponding normal esophageal tissues were analyzed by miRNA microarray. A total of 43 differentially expressed miRNAs, including 27 downregulated and 16 upregulated miRNAs were found in the ESCC tissue samples. Among these miRNAs, we found that miR-1 was significantly downregulated. Subsequently, the expression of miR-1 was validated in 64 pairs of primary ESCC samples by RT-qPCR. The expression level of miR-1 was found to be frequently decreased, and significantly correlated with tumor invasion and an advanced clinical stage (P=0.022 and P=0.028, respectively). In addition, functional assays revealed that miR-1 inhibited cell proliferation, clonogenicity, cell invasion and migration. Bioinformatics analyses identified the major biological processes that were targeted by miR-1. These results suggest that miR-1 has a tumor-suppressive effect on the development and progression of ESCC. The findings of this study may contribute to the further understanding of the functions of miR-1 in ESCC.

10.3892/ijmm.2015.2094

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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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Clonal status and clinicopathological feature of Erdheim-Chester disease

Pathology - Research and Practice (2009)

Li Gong Xianli He Yanhong Li Kaixi Ren Li Zhang

Erdheim–Chester disease

CD68

Birbeck granules

10.1016/j.prp.2009.02.004

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Citations (31)

Clinical efficacy of infrared polarized light in the treatment of frozen shoulder

Xiujuan Han

Objective To evaluate the clinical effect of infrared polarized light irradiation in the treatment of frozen shoulder. Methods A total of 150 patients with frozen shoulder who were treated in the rehabilitation department of Tianjin People's Hospital from October 2015 to December 2018 were randomly divided into a control group (75 cases) and a treatment group (75 cases) using a random number table. Finally, 120 patients who underwent the complete treatment were enrolled including 67 in the treatment group and 53 in the control group. The patients in the treatment group was treated with infrared polarized light irradiation combined with shoulder joint mobilization, and in the control group was treated with shoulder mobilization alone. The whole course is 2 months, and the treatment was 5 times a week. In each treatment, the duration of infrared polarized light irradiation is 10 min and the duration of joint mobilization is 15 to 20 min. Rehabilitation assessment of pain (visual analogue scale, VAS), range of motion (ROM), muscle strength and self-rating anxiety scale (SAS) were performed before the first treatment and after 2 weeks of treatment. Results Before the treatment, there were no statistically significant differences in VAS, ROM, muscle strength and SAS scores between the two groups (all P>0.05). Compared with that before treatment, VAS and SAS scores were significantly decreased, ROM and muscle strength scores were significantly increased in the two groups after 2 weeks treatment (all P 0.05). The improvements of the indicators in the treatment group was greater than that of the control group. Conclusions Infrared polarized light irradiation can significantly improve the treatment effect of frozen shoulder. Key words: Frozen shoulder; Infrared polarized light; Rehabilitation assessment

Frozen shoulder

Joint mobilization

10.3760/cma.j.issn.1673-4181.2019.06.010

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Primary lung seminoma in a 76-year-old man: a case report.

PubMed (2010)

Shaojun Zhu Yanhong Li Guiqiu Liu Xiujuan Han Li Gong

Seminoma is a rare event in old male population. In this report, we present a rare case of primary seminoma in the lung of a 76-years-old man.The patient was a 76-year-old man admitted with respiratory tract symptom and hemoptysis. The Chest Routine Scan and CT showed there was a consolidation area in the basal segments at the lower lobe of left lung. Bronchoscope also exhibited a neoplasm in left lung. During left lower lobectomy, we found that adherence occurred widely in left thoracic wall, and the pleural membrane was shrinkage. No chemotherapy or radiotherapy was given. Patient was died at 140 days after the surgery mainly due to the dyscrasia and secondary seminoma in left 7th to 9th ribs. Placental alkaline phosphatase (PLAP) and CD117 were found to be positive with immunohistochemical studies. Along with other evidences, this case was identified as the manifestations of seminoma.Although primary seminoma of the lung is rare in old male population, the diagnosis should be taken into serious consideration in order to improve the treatment. And in this case, primary lung seminoma is associated with high degree of malignancy and metastasis.

Placental alkaline phosphatase

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The Human Homolog of Drosophila Headcase Acts as a Tumor Suppressor through Its Blocking Effect on the Cell Cycle in Hepatocellular Carcinoma

PLoS ONE (2015)

Jun Wang Li Gong Shaojun Zhu Qiao Zhu Yao Li

The molecular pathogenesis of hepatocellular carcinoma (HCC) is heterogeneous and extremely complex. Thus, for individual molecular targeted therapy, novel molecular markers are needed. The abnormal expression of the human homolog of Drosophila headcase (HECA homo) has been found in pancreatic, colorectal, and oral squamous cell carcinoma. Studies of oral squamous cell carcinoma have also demonstrated that the HECA homo protein can be negatively controlled by the Wnt-pathway and transcription factor 4 (TCF4) and can slow cell division by interacting with cyclins and CDKs. However, the role of HECA in HCC has not been reported elsewhere. Here, immunohistochemical analysis revealed that the downregulation of HECA homo protein occurred in 71.0% (66/93) of HCC cases and was positively correlated with a poorly differentiated grade, high serum AFP level, liver cirrhosis and large tumor size. The expression of HECA homo was detected in five live cell lines. In vitro, the overexpression of HECA homo in HepG2, Huh-7 and MHCC-97H cells could inhibit cell proliferation and colony formation and induce G1 phase arrest. In contrast, the downregulation of HECA homo could promote cell proliferation, colony formation and the cell cycle process. However, neither the overexpression nor downregulation of HECA homo in the three cell lines could affect cell migration or invasion. Collectively, HECA homo is regularly expressed in normal live cells, and the HECA homo protein level is heterogeneously altered in HCC, but the downregulation of HECA homo is more common and positively correlated with several malignant phenotypes. The HECA homo protein can slow cell proliferation to some extent primarily through its blocking effect on the cell cycle. Hence, the HECA homo protein may act as a tumor suppressor in HCC and might be a potential molecular marker for diagnostic classification and targeted therapy in HCC.

HCCS

10.1371/journal.pone.0137579

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Clonality analysis of Sclerosing Angiomatoid Nodular Transformation in Spleen

Research Square (Research Square) (2022)

Xiujuan Han Li Ma Lin Chen Li Xue

Abstract Aims: Use clonality study to detect sclerosing angiomatoid nodular transformation (SANT) of the spleen and to explore the essence and pathogenesis of SANT. Methods: All SANT cases was performed by clonality analysis and in situ hybridization for the presence of EBV encoded small RNAs (EBER). Immunohistochemisty were used to classify the character of SANT, hemangioma. Results: The results of histological and immunohistochemical detection show the obstruction of arterioles and the passive congestion of venules in red pulp might participate in the formation of SANT. The results of clonality analysis show polyclonality was demonstrated in SANT nodules and the surrounding spleen parenchyma. Conclusion: SANT is a benign proliferative lesion. Combined with the immunohistochemisty, clonality analysis can be an useful tool for differential diagnosis of these splenic lesions.

Red pulp

Pathogenesis

Parenchyma

10.21203/rs.3.rs-1700596/v1

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