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SNAIL2 contributes to tumorigenicity and chemotherapy resistance in pancreatic cancer by regulating IGFBP2

Masuo, Kenji ; Chen, Ru ; Yogo, Akitada ; Sugiyama, Aiko ; Fukuda, Akihisa ; Masui, Toshihiko ; Uemoto, Shinji ; Seno, Hiroshi ; Takaishi, Shigeo

Cancer science, 2021-12, Vol.112 (12), p.4987-4999 [Periódico revisado por pares]

England: John Wiley & Sons, Inc

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Título:
SNAIL2 contributes to tumorigenicity and chemotherapy resistance in pancreatic cancer by regulating IGFBP2
Autor: Masuo, Kenji ; Chen, Ru ; Yogo, Akitada ; Sugiyama, Aiko ; Fukuda, Akihisa ; Masui, Toshihiko ; Uemoto, Shinji ; Seno, Hiroshi ; Takaishi, Shigeo
Assuntos: Animals ; Antineoplastic Agents - therapeutic use ; Breast cancer ; cancer stem cells ; Carcinogenesis - genetics ; Carcinogenesis - metabolism ; CD44 antigen ; Cell culture ; Cell Line ; Cell Line, Tumor ; Chemoresistance ; Chemotherapy ; Cloning ; Committees ; DNA microarrays ; Drug Resistance, Neoplasm - genetics ; Epithelial-Mesenchymal Transition - genetics ; epithelial‐mesenchymal transition ; Gemcitabine ; Gene expression ; Gene Expression Profiling - methods ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Infections ; Insulin ; Insulin-Like Growth Factor Binding Protein 2 - genetics ; Insulin-Like Growth Factor Binding Protein 2 - metabolism ; Insulin-like growth factor-binding protein 2 ; Insulin-like growth factors ; Kinases ; Medical prognosis ; Mesenchyme ; Metastasis ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplastic Stem Cells - metabolism ; Original ; Pancreatic cancer ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Plasmids ; Prognosis ; Proteins ; RNA Interference ; RNA-mediated interference ; Snail Family Transcription Factors - genetics ; Snail Family Transcription Factors - metabolism ; SNAIL2 ; Solid tumors ; Spheroids ; Stem cells ; Transcription factors ; Tumor cell lines ; tumor spheroid ; Tumorigenicity ; Tumors ; Xenograft Model Antitumor Assays - methods ; Xenografts ; Zinc finger proteins
É parte de: Cancer science, 2021-12, Vol.112 (12), p.4987-4999
Notas: Funding information
This work was supported by a Grants‐in‐Aid KAKENHI (17K09460), a research program from the Ministry of Education, Culture, Sports, Science, and Technology, and research funding for the DSK Project was provided by Sumitomo Dainippon Pharma, Inc
Descrição: Pancreatic cancer has an extremely poor prognosis because of its resistance to conventional therapies. Cancer stem cell (CSC)‐targeted therapy is considered a promising approach for this disease. Epithelial‐mesenchymal transition‐inducing transcription factors (EMT‐TFs) contribute to CSC properties in some solid tumors; however, this mechanism has not been fully elucidated in pancreatic cancer. Zinc finger protein, SNAIL2 (also known as SLUG), is a member of the SNAIL superfamily of EMT‐TFs and is commonly overexpressed in pancreatic cancer. Patients exhibiting high SNAIL2 expression have a poor prognosis. In this study, we showed that the suppression of SNAIL2 expression using RNA interference decreased tumorigenicity in vitro (sphere formation assay) and in vivo (xenograft assay) in 2 pancreatic cancer cell lines, KLM1 and KMP5. In addition, SNAIL2 suppression resulted in increased sensitivity to gemcitabine and reduced the expression of CD44, a pancreatic CSC marker. Moreover, experiments on tumor spheroids established from surgically resected pancreatic cancer tissues yielded similar results. A microarray analysis revealed that the mechanism was mediated by insulin‐like growth factor (IGF) binding protein 2. These results indicate that IGFBP2 regulated by SNAIL2 may represent an effective therapeutic target for pancreatic cancer. SNAIL2 knockdown reduces tumorigenicity and resistance to gemcitabine in tumor spheroid established from resected tissue of human pancreatic cancer as well as human pancreatic cancer cell lines.
Editor: England: John Wiley & Sons, Inc
Idioma: Inglês

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SNAIL2 contributes to tumorigenicity and chemotherapy resistance in pancreatic cancer by regulating IGFBP2

Masuo, Kenji ; Chen, Ru ; Yogo, Akitada ; Sugiyama, Aiko ; Fukuda, Akihisa ; Masui, Toshihiko ; Uemoto, Shinji ; Seno, Hiroshi ; Takaishi, Shigeo

England: John Wiley & Sons, Inc

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