Literature DB >> 32770395

Transportome Malfunctions and the Hallmarks of Pancreatic Cancer.

Qi Ling1, Holger Kalthoff2.   

Abstract

Ion channels and transporters (ICT) play important roles in almost all basic cellular processes. During last decades, abundant evidences have been provided that ICT (e.g., Ca2+ and K+ channels) are notable for regulating physiological pancreatic duct cellular function and deregulation of ICT is closely associated with the widely accepted hallmarks of pancreatic ductal adenocarcinoma (PDAC) such as proliferation, apoptosis resistance, invasion, and metastasis. Hence this review focuses on the role of ICT malfunctions in context with the hallmarks of PDAC. After briefly introducing epidemiology and history of molecular oncology of PDAC and summarizing the recent studies on molecular classification systems, we focus then on the exocrine pancreas as a very active secretory gland which considerably impacts the changes in the ion transport system (the transportome) upon malignant transformation. We highlight multiplicity of ICT members (H+ transporters, Ca2+, K+, Na+ and Cl- channels) and their functional impact in PDAC. We also present some selective therapeutic options to interfere with transportome functions and thereby with key mechanisms of malignant progression. This will hopefully contribute to a better clinical outcome based on improved therapeutic strategies for this still extremely deadly disease.
© 2020. Springer Nature Switzerland AG.

Entities:  

Keywords:  Invasion; Ion channels and transporters; Metastasis; Pancreatic ductal adenocarcinoma; Proliferation

Mesh:

Substances:

Year:  2021        PMID: 32770395     DOI: 10.1007/112_2020_20

Source DB:  PubMed          Journal:  Rev Physiol Biochem Pharmacol        ISSN: 0303-4240            Impact factor:   5.545


  97 in total

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Journal:  Cancer Genomics Proteomics       Date:  2016 May-Jun       Impact factor: 4.069

4.  Comprehensive characterisation of compartment-specific long non-coding RNAs associated with pancreatic ductal adenocarcinoma.

Authors:  Luis Arnes; Zhaoqi Liu; Jiguang Wang; Carlo Maurer; Irina Sagalovskiy; Marta Sanchez-Martin; Nikhil Bommakanti; Diana C Garofalo; Dina A Balderes; Lori Sussel; Kenneth P Olive; Raul Rabadan
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Journal:  Hum Pathol       Date:  2011-02-04       Impact factor: 3.466

6.  Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse.

Authors:  Nabeel Bardeesy; Andrew J Aguirre; Gerald C Chu; Kuang-Hung Cheng; Lyle V Lopez; Aram F Hezel; Bin Feng; Cameron Brennan; Ralph Weissleder; Umar Mahmood; Douglas Hanahan; Mark S Redston; Lynda Chin; Ronald A Depinho
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7.  KCa3.1 (IK) modulates pancreatic cancer cell migration, invasion and proliferation: anomalous effects on TRAM-34.

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Journal:  Pflugers Arch       Date:  2016-10-17       Impact factor: 3.657

8.  Physiological roles of the intermediate conductance, Ca2+-activated potassium channel Kcnn4.

Authors:  Ted Begenisich; Tesuji Nakamoto; Catherine E Ovitt; Keith Nehrke; Carlo Brugnara; Seth L Alper; James E Melvin
Journal:  J Biol Chem       Date:  2004-09-03       Impact factor: 5.157

9.  Most human carcinomas of the exocrine pancreas contain mutant c-K-ras genes.

Authors:  C Almoguera; D Shibata; K Forrester; J Martin; N Arnheim; M Perucho
Journal:  Cell       Date:  1988-05-20       Impact factor: 41.582

10.  The NAD+-dependent histone deacetylase SIRT6 promotes cytokine production and migration in pancreatic cancer cells by regulating Ca2+ responses.

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