Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

At a glance: The STEP trials

A round-up of the STEP phase 3 clinical trials evaluating semaglutide for weight loss in people with overweight or obesity.
ADVANCED SEARCH
Log in
Top
Tumor Biology
Published in: Tumor Biology 2/2016

01-02-2016 | Original Article

TRIM37 promoted the growth and migration of the pancreatic cancer cells

Authors: Jianxin Jiang, She Tian, Chao Yu, Meiyuan Chen, Chengyi Sun

Published in: Tumor Biology | Issue 2/2016

Login to get access

Abstract

Increasing evidence indicated that tripartite motif containing 37 (TRIM37) was involved in the tumorigenesis of several cancer types. However, its expression pattern and biological functions in pancreatic ductal adenocarcinoma (PDAC) remained unknown. In this study, real-time PCR, Western blot and immunohistochemistry was performed to examine the expression of TRIM37 in the pancreatic cancerous tissues. Colony formation assay and cell migration assay were performed to study the functions of TRIM37 in pancreatic cancer cells. Dual-luciferase assay was performed to study the regulation of TRIM37 on beta-catenin/TCF signaling. It was found that the expression level of TRIM37 was significantly higher in pancreatic cancerous tissues compared with the adjacent normal tissues. Function analysis indicated that overexpression of TRIM37 promoted the growth and migration of the pancreatic cancer cells, while knocking down the expression of TRIM37 inhibited the growth and migration of the pancreatic cancer cells. The molecular mechanism study suggested that TRIM37 interacted with beta-catenin and activated the transcriptional activity of beta-catenin/TCF complex as well as the expression of its downstream target genes. Taken together, our study showed the oncogenic roles of TRIM37 in pancreatic cancer, and TRIM37 might be a promising target for pancreatic cancer treatment.
Appendix
Available only for authorised users
Literature
1.
2.
Liang C, Wang Z, Li YY, Yu BH, Zhang F, Li HY. Mir-33a suppresses the nuclear translocation of beta-catenin to enhance gemcitabine sensitivity in human pancreatic cancer cells. Tumour Biol. (ahead of print). 2015.
3.
Jiang S, Zhu L, Tang H, et al. Ape1 regulates wnt/beta-catenin signaling through its redox functional domain in pancreatic cancer cells. Int J Oncol. (ahead of print). 2015.
4.
Chen X, Liu X, Lang H, Zhang S, Luo Y, Zhang J. S100 calcium-binding protein a6 promotes epithelial-mesenchymal transition through beta-catenin in pancreatic cancer cell line. PLoS One. 2015;10:e0121319.CrossRefPubMedPubMedCentral
5.
Kumaran S, Samantha KS, Halagowder D. Does beta-catenin cross-regulate NFkappaB signalling in pancreatic cancer and chronic pancreatitis? Pathobiology. 2015;82:28–35.CrossRefPubMed
6.
Xu W, Wang Z, Zhang W, et al. Mutated k-ras activates cdk8 to stimulate the epithelial-to-mesenchymal transition in pancreatic cancer in part via the wnt/beta-catenin signaling pathway. Cancer Lett. 2015;356:613–27.CrossRefPubMed
7.
8.
9.
10.
Kallijarvi J, Lahtinen U, Hamalainen R, Lipsanen-Nyman M, Palvimo JJ, Lehesjoki AE. Trim37 defective in mulibrey nanism is a novel ring finger ubiquitin e3 ligase. Exp Cell Res. 2005;308:146–55.CrossRefPubMed
11.
Bhatnagar S, Gazin C, Chamberlain L, et al. Trim37 is a new histone h2a ubiquitin ligase and breast cancer oncoprotein. Nature. 2015;516:116–20.
12.
Dimova I, Orsetti B, Negre V, et al. Genomic markers for ovarian cancer at chromosomes 1, 8 and 17 revealed by array cgh analysis. Tumori. 2009;95:357–66.PubMed
13.
Karlberg S, Lipsanen-Nyman M, Lassus H, Kallijarvi J, Lehesjoki AE, Butzow R. Gynecological tumors in mulibrey nanism and role for ring finger protein trim37 in the pathogenesis of ovarian fibrothecomas. Mod Pathol. 2009;22:570–8.CrossRefPubMed
14.
Brodtkorb M, Lingjaerde OC, Huse K, Troen G, et al. Whole-genome integrative analysis reveals expression signatures predicting transformation in follicular lymphoma. Blood. 2014;123:1051–4.CrossRefPubMed
15.
Balestra FR, Strnad P, Fluckiger I, Gonczy P. Discovering regulators of centriole biogenesis through siRNA-based functional genomics in human cells. Dev Cell. 2013;25:555–71.CrossRefPubMed
16.
Tuna M, Smid M, Martens JW, Foekens JA. Prognostic value of acquired uniparental disomy (aupd) in primary breast cancer. Breast Cancer Res Treat. 2012;132:189–96.CrossRefPubMed
17.
Hamalainen RH, Mowat D, Gabbett MT, O’Brien TA, Kallijarvi J, Lehesjoki AE. Wilms’ tumor and novel trim37 mutations in an Australian patient with mulibrey nanism. Clin Genet. 2006;70:473–9.CrossRefPubMed
Metadata
Title
TRIM37 promoted the growth and migration of the pancreatic cancer cells
Authors
Jianxin Jiang
She Tian
Chao Yu
Meiyuan Chen
Chengyi Sun
Publication date
01-02-2016
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 2/2016
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-4078-7

Other articles of this Issue 2/2016

Tumor Biology 2/2016 Go to the issue

Original Article

Cancer-associated fibroblasts promote angiogenesis in gastric cancer through galectin-1 expression

Original Article

Identification of a shared protective genetic susceptibility locus for colorectal cancer and gastric cancer

Review

Hepatic metastatic niche: from normal to pre-metastatic and metastatic niche

Original Article

Clinical value and impact on prognosis of peri-operative CA 19-9 serum levels in stage I and II adenocarcinoma of the pancreas

Original Article

A suggested guiding panel of seromarkers for efficient discrimination between primary and secondary human hepatocarcinoma

Review

The immunobiology of myeloid-derived suppressor cells in cancer
Webinar | 19-02-2024 | 17:30 (CET)

Keynote webinar | Spotlight on antibody–drug conjugates in cancer

Watch now

Antibody–drug conjugates (ADCs) are novel agents that have shown promise across multiple tumor types. Explore the current landscape of ADCs in breast and lung cancer with our experts, and gain insights into the mechanism of action, key clinical trials data, existing challenges, and future directions.

Dr. Véronique Diéras
Prof. Fabrice Barlesi
Developed by: Springer Medicine
Image Credits