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 4/2014

01-04-2014 | Research Article

NOV promoted the growth and migration of pancreatic cancer cells

Authors: Lei Cui, Rong Xie, Shenchun Dang, Qing Zhang, Shengfa Mao, Jixiang Chen, Jianguo Qu, Jianxin Zhang

Published in: Tumor Biology | Issue 4/2014

Login to get access

Abstract

NOV, a member of the CCN (Cyr61, CTGF and NOV) family, is involved in diverse biological processes, such as cell adhesion, proliferation and angiogenesis. However, its function in pancreatic cancer remains poorly understood. Here, we found that the expression of NOV was up-regulated in pancreatic cancer tissues. Moreover, over-expression of NOV in pancreatic cancer cells promoted cell proliferation and migration, while knock down the expression of NOV impaired the tumorigenecity of pancreatic cancer cells in vitro and in vivo. Mechanistically, NOV induced epithelial–mesenchymal transition (EMT) and regulated the expression of multiple EMT marker. Taken together, our study suggested the important role of NOV in pancreatic cancer and NOV might be an important therapeutic target.
Literature
1.
2.
3.
Zucker S, Cao J, Chen WT. Critical appraisal of the use of matrix metalloproteinase inhibitors in cancer treatment. Oncogene. 2000;19:6642–50.PubMedCrossRef
4.
Polyak K, Weinberg RA. Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits. Nat Rev Cancer. 2009;9(4):265–73.PubMedCrossRef
5.
Yang J. Twist, a master regulator of morphogenesis, plays an essential role in tumor metastasis. Cell. 2004;117(7):927–39.PubMedCrossRef
6.
7.
Carver EA, Jiang R, Lan Y, Oram KF, Gridley T. The mouse snail gene encodes a key regulator of the epithelial–mesenchymal transition. Mol Cell Biol. 2001;21(23):8184–8.PubMedCentralPubMedCrossRef
8.
Park SM, Gaur AB, Lengyel E, Peter ME. The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2. Genes Dev. 2008;22(7):894–907.PubMedCentralPubMedCrossRef
9.
Esquela-Kerscher A, Slack FJ. Oncomirs—microRNAs with a role in cancer. Nat Rev Cancer. 2006;6(4):259–69.PubMedCrossRef
10.
11.
Kleer CG, Zhang Y, Pan Q, Merajver SD. WISP3 (CCN6) is a secreted tumorsuppressor protein that modulates IGF signaling in inflammatory breast cancer. Neoplasia. 2004;6:179–85.PubMedCentralPubMedCrossRef
12.
Yu C, Le AT, Yeger H, Perbal B, Alman BA. NOV(CCN3) regulation in the growth plate and CCN family member expression in cartilage neoplasia. J Pathol. 2003;201:609–15.PubMedCrossRef
13.
Maillard M, Cadot B, Ball RY, et al. Differential expression of the ccn3 (nov) proto-oncogene in human prostate cell lines and tissues. Mol Pathol. 2001;54:275–80.PubMedCentralPubMedCrossRef
14.
Albrecht N, Kristopher KF, Tashinga EB, et al. CTGF antagonism with mAb FG-3019 enhances chemotherapy response without increasing drug delivery in murine ductal pancreas cancer. PNAS. 2013;110:12325–30.CrossRef
15.
Inamul H, Archana D, Monami M, et al. The matricellular protein CCN1/Cyr61 is a critical regulator of sonic hedgehog in pancreatic carcinogenesis. J Biol Chem. 2012;287:38569–79.CrossRef
16.
Fidler IJ. The pathogenesis of cancer metastasis: the ‘seed and soil’ hypothesis revisited. Nat Rev Cancer. 2003;3(6):453–8.PubMedCrossRef
Metadata
Title
NOV promoted the growth and migration of pancreatic cancer cells
Authors
Lei Cui
Rong Xie
Shenchun Dang
Qing Zhang
Shengfa Mao
Jixiang Chen
Jianguo Qu
Jianxin Zhang
Publication date
01-04-2014
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 4/2014
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-013-1418-3

Other articles of this Issue 4/2014

Tumor Biology 4/2014 Go to the issue

Research Article

Clinicopathological and prognostic significance of chemokine receptor CXCR4 overexpression in patients with esophageal cancer: a meta-analysis

Research Article

The association between polymorphism of P53 Codon72 Arg/Pro and hepatocellular carcinoma susceptibility: evidence from a meta-analysis of 15 studies with 3,704 cases

Research Article

N-acetyltransferase 2 genetic variants confer the susceptibility to head and neck carcinoma: evidence from 23 case–control studies

Editorial

Letter regarding Wang et al. entitled “Effects of murine double minute 2 polymorphisms on the risk and survival of osteosarcoma: a systemic review and meta-analysis”

Research Article

Tetra-arsenic tetra-sulfide (As4S4) promotes apoptosis in retinoid acid -resistant human acute promyelocytic leukemic NB4-R1 cells through downregulation of SET protein

Research Article

Overexpression of HER-2/neu protein attenuates the oxidative systemic profile in women diagnosed with breast 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