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Pancreatic Neoplasms: HELP
Articles by Qiao-Ming Zhi
Based on 9 articles published since 2009
(Why 9 articles?)
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Between 2009 and 2019, Qiaoming Zhi wrote the following 9 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Genomic characteristics of pancreatic squamous cell carcinoma, an investigation by using high throughput sequencing after in-solution hybrid capture. 2017

Xu, Meng-Dan / Liu, Shu-Ling / Feng, Yi-Zhong / Liu, Qiang / Shen, Meng / Zhi, Qiaoming / Liu, Zeyi / Gu, Dong-Mei / Yu, Jie / Shou, Liu-Mei / Gong, Fei-Ran / Zhu, Qi / Duan, Weiming / Chen, Kai / Zhang, Junning / Wu, Meng-Yao / Tao, Min / Li, Wei. ·Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Radiation Oncology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Pathology, The Second Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Pathology, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200000, China. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Pathology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Oncology, The First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou 310006, China. · Department of Hematology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Xi'an Tianlong Science and Technology Co., Ltd., Xi'an 710018, China. · PREMED Key Laboratory for Precision Medicine, Soochow University, Suzhou 215021, China. · Jiangsu Institute of Clinical Immunology, Suzhou 215006, China. · Institute of Medical Biotechnology, Soochow University, Suzhou 215021, China. ·Oncotarget · Pubmed #28099906.

ABSTRACT: Squamous cell carcinoma (SCC) of pancreas is a rare histotype of pancreatic ductal carcinoma which is distinct from pancreatic adenocarcinoma (AC). Although there are standard treatments for pancreatic AC, no precise therapies exist for pancreatic SCC. Here, we screened 1033 cases of pancreatic cancer and identified 2 cases of pure SCC, which were pathologically diagnosed on the basis of finding definite intercellular bridges and/or focal keratin peal formation in the tumor cells. Immunohistochemistry assay confirmed the positive expression of CK5/6 and p63 in pancreatic SCC. To verify the genomic characteristics of pancreatic SCC, we employed in-solution hybrid capture targeting 137 cancer-related genes accompanied by high throughput sequencing (HTS) to compare the different genetic variants in SCC and AC of pancreas. We compared the genetic alterations of known biomarkers of pancreatic adenocarcinoma in different pancreatic cancer tissues, and identified nine mutated genes in SCC of pancreas: C7orf70, DNHD1, KPRP, MDM4, MUC6, OR51Q1, PTPRD, TCF4, TET2, and nine genes (ABCB1, CSF1R, CYP2C18, FBXW7, ITPA, KIAA0748, SOD2, SULT1A2, ZNF142) that are mutated in pancreatic AC. This study may have taken one step forward on the discovery of potential biomarkers for the targeted treatment of SCC of the pancreas.

2 Article Long non-coding RNA UCA1 promotes the tumorigenesis in pancreatic cancer. 2016

Chen, Ping / Wan, Daiwei / Zheng, Dingcheng / Zheng, Qi / Wu, Feng / Zhi, Qiaoming. ·Department of General Surgery, Ningbo No. 2 Hospital, Ningbo 315000, China. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. · Department of General Surgery, Ningbo No. 2 Hospital, Ningbo 315000, China. Electronic address: gastroclinical@sina.com. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. Electronic address: strexboy@163.com. ·Biomed Pharmacother · Pubmed #27562722.

ABSTRACT: The contribution of long non-coding RNAs (lncRNAs) to tumorigenesis and metastasis of pancreatic cancer (PC) remains largely unknown. Urothelial cancer-associated 1 (UCA1), which is an originally identified lncRNA in bladder cancer, has be proved to play a pivotal role in bladder cancer progression and embryonic development. In this study, we detected the mRNA expression of UCA1 in 128 PC patients by qRT-PCR, and found that UCA1 expression was significantly, up-regulated in tumor tissues than that in matched adjacent non-tumor tissues (p<0.05). Clinicopathological analysis demonstrated that UCA1 expression in PC significantly correlated with malignant potential factors such as tumor size (p=0.021), depth of invasion (p=0.033), CA19-9 level (p=0.034) and tumor stage (p=0.013). Cox proportional hazards regression analysis also confirmed that high UCA1 expression was an independent prognostic biomarker of PC (p=0.046), which led to an obviously shorter 5-year overall survival (OS) compared to those patients with low UCA1 expressions (p=0.018). Furthermore, we effectively down-regulated UCA1 mRNA expression by transfecting RNA interfere fragments into SW-1990 cells, and our results in vitro indicated that down-regulation of UCA1 could effectively inhibit the cell proliferative activities, induce apoptotic rate and cause cell cycle arrest in PC cells (p<0.05). Meanwhile, UCA1 expression negative-correlated with p27 in PC tissues (r

3 Article FH535, a β-catenin pathway inhibitor, represses pancreatic cancer xenograft growth and angiogenesis. 2016

Liu, Lu / Zhi, Qiaoming / Shen, Meng / Gong, Fei-Ran / Zhou, Binhua P / Lian, Lian / Shen, Bairong / Chen, Kai / Duan, Weiming / Wu, Meng-Yao / Tao, Min / Li, Wei. ·Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou, China. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China. · Department of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, China. · Markey Cancer Center, University of Kentucky, Lexington, KY, USA. · Departments of Molecular and Cellular Biochemistry, University of Kentucky College of Medicine, Lexington, KY, USA. · Department of Oncology, Suzhou Xiangcheng People's Hospital, Suzhou, China. · Department of Pathology, Suzhou Xiangcheng People's Hospital, Suzhou, China. · Center for Systems Biology, Soochow University, Suzhou, China. · PREMED Key Laboratory for Precision Medicine, Soochow University, Suzhou, China. · Jiangsu Institute of Clinical Immunology, Suzhou, China. · Institute of Medical Biotechnology, Soochow University, Suzhou, China. ·Oncotarget · Pubmed #27323403.

ABSTRACT: The WNT/β-catenin pathway plays an important role in pancreatic cancer carcinogenesis. We evaluated the correlation between aberrant β-catenin pathway activation and the prognosis pancreatic cancer, and the potential of applying the β-catenin pathway inhibitor FH535 to pancreatic cancer treatment. Meta-analysis and immunohistochemistry showed that abnormal β-catenin pathway activation was associated with unfavorable outcome. FH535 repressed pancreatic cancer xenograft growth in vivo. Gene Ontology (GO) analysis of microarray data indicated that target genes responding to FH535 participated in stemness maintenance. Real-time PCR and flow cytometry confirmed that FH535 downregulated CD24 and CD44, pancreatic cancer stem cell (CSC) markers, suggesting FH535 impairs pancreatic CSC stemness. GO analysis of β-catenin chromatin immunoprecipitation sequencing data identified angiogenesis-related gene regulation. Immunohistochemistry showed that higher microvessel density correlated with elevated nuclear β-catenin expression and unfavorable outcome. FH535 repressed the secretion of the proangiogenic cytokines vascular endothelial growth factor (VEGF), interleukin (IL)-6, IL-8, and tumor necrosis factor-α, and also inhibited angiogenesis in vitro and in vivo. Protein and mRNA microarrays revealed that FH535 downregulated the proangiogenic genes ANGPT2, VEGFR3, IFN-γ, PLAUR, THPO, TIMP1, and VEGF. FH535 not only represses pancreatic CSC stemness in vitro, but also remodels the tumor microenvironment by repressing angiogenesis, warranting further clinical investigation.

4 Article Epidermal growth factor-like domain 7 promotes cell invasion and angiogenesis in pancreatic carcinoma. 2016

Shen, Xiaochun / Han, Ye / Xue, Xiaofeng / Li, Wei / Guo, Xiaobo / Li, Pu / Wang, Yunliang / Li, Dechun / Zhou, Jin / Zhi, Qiaoming. ·Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Gastrointestinal Surgery, Provincial Hospital Affiliated to Shandong University, Jinan 250021, China. · Shanghai Key Laboratory of Gastric Neoplasms, Shanghai Institute of Digestive Surgery, Department of Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. Electronic address: 13913506369@163.com. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, China. Electronic address: strexboy@163.com. ·Biomed Pharmacother · Pubmed #26796281.

ABSTRACT: Epidermal growth factor-like domain 7 (EGFL7), also known as vascular endothelial stain, was firstly identified as a modulator of smooth muscle cell migration. Though the expression of EGFL7 was reported to be up-regulated during tumorigenesis, the clinical and biological functions of EGFL7 in pancreatic carcinoma (PC) were still not fully elucidated. In this study, we found that the serum EGFL7 level in PC tissues was statistically higher than that in normal subjects (p<0.001), and its level in non-resectable patients was also higher than that in resectable ones (p=0.013). Among these resectable PC patients, the postoperative EGFL7 expression was significantly down-regulated when tumors were resected (p=0.018). Using the immunohistochemistry method, our results demonstrated that the positive expression of EGFL7 was significantly associated with the TNM stage (p=0.024), lymph node metastasis (p=0.003) and local invasion (p=0.022), and the EGFL7 expression closely correlated to the micro-vessel density (MVD) in PC tissues by Spearman analysis (r=0.941, p=0.000). In vitro, EGFL7 was silenced by the small interference RNA in PC cells, and our data indicated that down-regulation of EGFL7 did not influence the cycle progression, proliferation, colony formation and apoptosis of PC cells (p>0.05), whereas inhibition of EGFL7 expression could decrease PaCa-2 cell invasion (p<0.05). More interestingly, by tubular formation, Chick embryo chorioallantoic membrane (CAM) and ELISA assays, our results revealed that silencing EGFL7 expression represented a strong inhibiting effect on tubular formation of micro-vessels through down-regulating the protein levels of VEGF and Ang-2 (p<0.05). Our results raised the possibility of using EGFL7as a potential prognostic biomarker and therapy target of PC, and down-regulation of EGFL7 might be considered to be a potentially important molecular treatment strategy for patients with PC.

5 Article Inflammatory stimuli promote growth and invasion of pancreatic cancer cells through NF-κB pathway dependent repression of PP2Ac. 2016

Tao, Min / Liu, Lu / Shen, Meng / Zhi, Qiaoming / Gong, Fei-Ran / Zhou, Binhua P / Wu, Yadi / Liu, Haiyan / Chen, Kai / Shen, Bairong / Wu, Meng-Yao / Shou, Liu-Mei / Li, Wei. ·a Department of Oncology , the First Affiliated Hospital of Soochow University , Suzhou , China. · b PREMED Key Laboratory for Precision Medicine, Soochow University , Suzhou , China. · c Jiangsu Institute of Clinical Immunology , Suzhou , China. · d Institute of Medical Biotechnology, Soochow University , Suzhou , China. · e Department of General Surgery , the First Affiliated Hospital of Soochow University , Suzhou , China. · f Department of Hematology , the First Affiliated Hospital of Soochow University , Suzhou , China. · g Markey Cancer Center, University of Kentucky College of Medicine , Lexington , KY , USA. · h Departments of Molecular and Cellular Biochemistry , University of Kentucky College of Medicine , Lexington , KY , USA. · i Molecular and Biomedical Pharmacology, University of Kentucky College of Medicine , Lexington , KY , USA. · j Laboratory of Cellular and Molecular Tumor Immunology, Institute of Biology and Medical Sciences, Soochow University , Suzhou , Jiangsu Province , China. · k Center for Systems Biology, Soochow University , Suzhou , China. · l Department of Oncology , the First Affiliated Hospital of Zhejiang Chinese Medicine University , Hangzhou , China. ·Cell Cycle · Pubmed #26761431.

ABSTRACT: Previous studies have indicated that inflammatory stimulation represses protein phosphatase 2A (PP2A), a well-known tumor suppressor. However, whether PP2A repression participates in pancreatic cancer progression has not been verified. We used lipopolysaccharide (LPS) and macrophage-conditioned medium (MCM) to establish in vitro inflammation models, and investigated whether inflammatory stimuli affect pancreatic cancer cell growth and invasion PP2A catalytic subunit (PP2Ac)-dependently. Via nude mouse models of orthotopic tumor xenografts and dibutyltin dichloride (DBTC)-induced chronic pancreatitis, we evaluated the effect of an inflammatory microenvironment on PP2Ac expression in vivo. We cloned the PP2Acα and PP2Acβ isoform promoters to investigate the PP2Ac transcriptional regulation mechanisms. MCM accelerated pancreatic cancer cell growth; MCM and LPS promoted cell invasion. DBTC promoted xenograft growth and metastasis, induced tumor-associated macrophage infiltration, promoted angiogenesis, activated the nuclear factor-κB (NF-κB) pathway, and repressed PP2Ac expression. In vitro, LPS and MCM downregulated PP2Ac mRNA and protein. PP2Acα overexpression attenuated JNK, ERK, PKC, and IKK phosphorylation, and impaired LPS/MCM-stimulated cell invasion and MCM-promoted cell growth. LPS and MCM activated the NF-κB pathway in vitro. LPS and MCM induced IKK and IκB phosphorylation, leading to p65/RelA nuclear translocation and transcriptional activation. Overexpression of the dominant negative forms of IKKα attenuated LPS and MCM downregulation of PP2Ac, suggesting inflammatory stimuli repress PP2Ac expression NF-κB pathway-dependently. Luciferase reporter gene assay verified that LPS and MCM downregulated PP2Ac transcription through an NF-κB-dependent pathway. Our study presents a new mechanism in inflammation-driven cancer progression through NF-κB pathway-dependent PP2Ac repression.

6 Article miRNA-101 Suppresses Epithelial-to-Mesenchymal Transition by Targeting HMGA2 in Pancreatic Cancer Cells. 2016

Jiang, Wenli / Gu, Wen / Qiu, Ronglin / He, Songbing / Shen, Chenglong / Wu, Yaohao / Zhang, Jie / Zhou, Jiajia / Guo, Yixing / Wan, Daiwei / Li, Zhixi / Deng, Jiemin / Zeng, Lexiang / Tang, Jin / Zhou, Jin / Zhi, Qiaoming / Deng, Xiaogeng. ·Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China, 215006. strexboy@163.com. ·Anticancer Agents Med Chem · Pubmed #25968875.

ABSTRACT: miR-101 is an outstanding tumor suppressor in various cancers, while its role in pancreatic cancer (PC) is still unknown. The aim of this study was to investigate the role of miR-101 in epithelial-to-mesenchymal transition (EMT) and its clinical relevance in PC. Our data showed that the miR-101 expression was significantly decreased in human PC tissues, compared to non-tumor counterparts (p<0.05), which was reversely correlated to clinical characteristics, including lymph node metastasis, more venous infiltration, higher expression of CA19-9 and TNM stage (p<0.05). Low miR-101 expression was also confirmed to be associated with a poorer overall survival rate in PC patients (p<0.05). We identified high-mobility group AT-hook 2 (HMGA2) gene as a putative target of miR-101 in PC by bioinformatics analysis, dual luciferase activity and western blot assay, and found that miR-101 could specifically target the HMGA2 3'-untranslated region (3'-UTR) (p<0.05). Knockdown of HMGA2 reversed EMT resembling that of miR-101 over-expression. An inverse correlation between miR-101 and HMGA2 was observed in patients with PC (p<0.05). Taken together, our findings speculated that miR-101 might act as an inhibiting factor in EMT process in PC and up-regulation of miR-101 might be considered as a potentially key molecular treatment strategy for PC patients.

7 Article Cantharidin and norcantharidin impair stemness of pancreatic cancer cells by repressing the β-catenin pathway and strengthen the cytotoxicity of gemcitabine and erlotinib. 2015

Wang, Wen-Jie / Wu, Meng-Yao / Shen, Meng / Zhi, Qiaoming / Liu, Ze-Yi / Gong, Fei-Ran / Tao, Min / Li, Wei. ·Department of Oncology, The First Affiliated Hospital of Soochow University, Suzhou 215006, P.R. China. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, P.R. China. · Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou 215006, P.R. China. · Department of Hematology, The First Affiliated Hospital of Soochow University, Suzhou 215006, P.R. China. ·Int J Oncol · Pubmed #26398277.

ABSTRACT: Increasing evidence suggests that tumors are composed of a heterogeneous cell population with a small subset of cancer stem cells (CSCs) that sustain tumor formation and growth, and are hypothesized to account for therapeutic resistance. Based on the expression of the surface markers CD44, CD24, and EPCAM, putative CSCs have also been identified in pancreatic cancers. It has been well established that aberrant activation of β-catenin signaling pathway may contribute to the maintenance of CSCs. Cantharidin is an active constituent of mylabris, a traditional Chinese medicine. In our previous studies, we demonstrated that cantharidin treatment induced phosphorylation of β-catenin, leading to repression on β-catenin pathway. Therefore, in the present study, we investigated whether cantharidin and its derivant, norcantharidin, could repress the stemness of pancreatic cancer cells through repression on β-catenin pathway. By using microarray and flow cytometry, we found that treatment with cantharidin and norcantharidin repressed the expression of CD44, CD24, and EPCAM at both mRNA and protein levels, leading to decreased CD44(+)/CD24(+)/EPCAM(+) proportion, the putative pancreatic CSC subset. Pretreatment with the β-catenin pathway inhibitor FH535, attenuated the cantharidin- and norcantharidin-induced repression on CD44, CD24, and EPCAM, suggesting cantharidin and its derivant repressed stemness of pancreatic cancer cells in β-catenin pathway-dependent manner. Furthermore, cantharidin and norcantharidin strengthened the cytotoxicity of gemcitabine and erlotinib, two well established pharmacotherapeutics against pancreatic cancers, indicating cantharidin and norcantharidin could be promising candidates for reversing drug resistance in pancreatic cancers. In conclusion, we presently propose that cantharidin and norcantharidin hold their promise in pancreatic cancer therapy through repression on stemness and strengthening the cytotoxicity of the present therapeutics.

8 Article Cantharidin represses invasion of pancreatic cancer cells through accelerated degradation of MMP2 mRNA. 2015

Shen, Meng / Wu, Meng-Yao / Chen, Long-Pei / Zhi, Qiaoming / Gong, Fei-Ran / Chen, Kai / Li, Dao-Ming / Wu, Yadi / Tao, Min / Li, Wei. ·Department of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou 215006, China. · Department of Hematology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China. · 1] Department of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China [2] Jiangsu Institute of Clinical Immunology, Suzhou 215006, China [3] Institute of Medical Biotechnology, Soochow University, Suzhou 215021, China [4] PREMED Key Laboratory for Precision Medicine, Soochow University, Suzhou 215021, China. · 1] Department of Oncology, the First Affiliated Hospital of Soochow University, Suzhou 215006, China [2] PREMED Key Laboratory for Precision Medicine, Soochow University, Suzhou 215021, China. ·Sci Rep · Pubmed #26135631.

ABSTRACT: Cantharidin is an active constituent of mylabris, a traditional Chinese medicine, and is a potent and selective inhibitor of protein phosphatase 2A (PP2A) that plays an important role in cell cycle control, apoptosis, and cell-fate determination. In the present study, we found that cantharidin repressed the invasive ability of pancreatic cancer cells and downregulated matrix metalloproteinase 2 (MMP2) expression through multiple pathways, including ERK, JNK, PKC, NF-κB, and β-catenin. Interestingly, transcriptional activity of the MMP2 promoter increased after treatment with PP2A inhibitors, suggesting the involvement of a posttranscriptional mechanism. By using an mRNA stability assay, we found accelerated degradation of MMP2 mRNA after treatment of cantharidin. Microarray analyses revealed that multiple genes involved in the 3' → 5' decay pathway were upregulated, especially genes participating in cytoplasmic deadenylation. The elevation of these genes were further demonstrated to be executed through ERK, JNK, PKC, NF-κB, and β-catenin pathways. Knockdown of PARN, RHAU, and CNOT7, three critical members involved in cytoplasmic deadenylation, attenuated the downregulation of MMP2. Hence, we present the mechanism of repressed invasion by cantharidin and other PP2A inhibitors through increased degradation of MMP2 mRNA by elevated cytoplasmic deadenylation.

9 Article Suppression of the Epidermal Growth Factor-like Domain 7 and Inhibition of Migration and Epithelial-Mesenchymal Transition in Human Pancreatic Cancer PANC-1 Cells. 2015

Wang, Yun-Liang / Dong, Feng-Lin / Yang, Jian / Li, Zhi / Zhi, Qiao-Ming / Zhao, Xin / Yang, Yong / Li, De-Chun / Shen, Xiao-Chun / Zhou, Jin. ·Department of General Surgery, the First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China E-mail : 13913500369@163.com; sxcsmile20008@163.com. ·Asian Pac J Cancer Prev · Pubmed #25987088.

ABSTRACT: BACKGROUND: Epidermal growth factor-like domain multiple 7 (EGFL7), a secreted protein specifically expressed by endothelial cells during embryogenesis, recently was identified as a critical gene in tumor metastasis. Epithelial-mesenchymal transition (EMT) was found to be closely related with tumor progression. Accordingly, it is important to investigate the migration and EMT change after knock-down of EGFL7 gene expression in human pancreatic cancer cells. MATERIALS AND METHODS: EGFL7 expression was firstly testified in 4 pancreatic cancer cell lines by real-time polymerase chain reaction (Real-time PCR) and western blot, and the highest expression of EGFL7 was found in PANC-1 cell line. Then, PANC-1 cells transfected with small interference RNA (siRNA) of EGFL7 using plasmid vector were named si-PANC-1, while transfected with negative control plasmid vector were called NC-PANC-1. Transwell assay was used to analyze the migration of PANC-1 cells. Real-time PCR and western blotting were used to detect the expression change of EGFL7 gene, EMT markers like E-Cadherin, N-Cadherin, Vimentin, Fibronectin and transcription factors like snail, slug in PANC-1, NC- PANC-1, and si-PANC-1 cells, respectively. RESULTS: After successful plasmid transfection, EGFL7 gene were dramatically knock-down by RNA interference in si-PANC-1 group. Meanwhile, migration ability decreased significantly, compared with PANC-1 and NC-PANC-1 group. Meanwhile, the expression of epithelial phenotype marker E-Cadherin increased and that of mesenchymal phenotype markers N-Cadherin, Vimentin, Fibronectin dramatically decreased in si-PANC-1 group, indicating a reversion of EMT. Also, transcription factors snail and slug decreased significantly after RNA interference. CONCLUSIONS: Current study suggested that highly-expressed EGFL7 promotes migration of PANC-1 cells and acts through transcription factors snail and slug to induce EMT, and further study is needed to confirm this issue.