Transient receptor potential channel TRPM8 is over-expressed and required for cellular proliferation in pancreatic adenocarcinoma

Nelson S. Yee; Weiqiang Zhou; Minsun Lee

doi:10.1016/j.canlet.2010.04.023

Transient receptor potential channel TRPM8 is over-expressed and required for cellular proliferation in pancreatic adenocarcinoma

Nelson S. Yee
, Weiqiang Zhou
, Minsun Lee

Research output: Contribution to journal › Article › peer-review

95 Scopus citations

Abstract

The roles of transient receptor potential (TRP) cation channels in pancreatic tumorigenesis are essentially unknown. Here, we focus on the TRP melastatin-subfamily (TRPM) members. Expression of the thermally regulated transmembrane Ca²⁺-permeable channel TRPM8 is consistently up-regulated in human pancreatic adenocarcinoma cell lines and tissues. TRPM8-deficient pancreatic cancer cells have reduced ability of proliferation and cell cycle progression with elevated levels of cyclin-dependent kinase inhibitors. These results indicate that TRPM8 is aberrantly over-expressed in pancreatic adenocarcinoma and required for cellular proliferation, and they support further investigation of the potential of TRPM8 as a clinical biomarker and therapeutic target in pancreatic adenocarcinoma.

Original language	English (US)
Pages (from-to)	49-55
Number of pages	7
Journal	Cancer Letters
Volume	297
Issue number	1
DOIs	https://doi.org/10.1016/j.canlet.2010.04.023
State	Published - Nov 2010

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

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10.1016/j.canlet.2010.04.023

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title = "Transient receptor potential channel TRPM8 is over-expressed and required for cellular proliferation in pancreatic adenocarcinoma",

abstract = "The roles of transient receptor potential (TRP) cation channels in pancreatic tumorigenesis are essentially unknown. Here, we focus on the TRP melastatin-subfamily (TRPM) members. Expression of the thermally regulated transmembrane Ca2+-permeable channel TRPM8 is consistently up-regulated in human pancreatic adenocarcinoma cell lines and tissues. TRPM8-deficient pancreatic cancer cells have reduced ability of proliferation and cell cycle progression with elevated levels of cyclin-dependent kinase inhibitors. These results indicate that TRPM8 is aberrantly over-expressed in pancreatic adenocarcinoma and required for cellular proliferation, and they support further investigation of the potential of TRPM8 as a clinical biomarker and therapeutic target in pancreatic adenocarcinoma.",

author = "Yee, \{Nelson S.\} and Weiqiang Zhou and Minsun Lee",

note = "Funding Information: The authors wish to thank Dr. Ming-Sound Tsao at the University of Toronto for generously providing the H6c7 cell line. We wish also to acknowledge the Tissue Procurement Core Facility, Comparative Pathology Laboratory, Central Microscopy Research Facility, DNA Facility, and Flow Cytometry Facility at the University of Iowa for technical and equipment support. This work is supported by the Pilot Grant in Translational Research by the Department of Internal Medicine of the University of Iowa Carver College of Medicine (N.S.Y.), the American Cancer Society Junior Faculty Seed Grant Award (ACS \#IRG-122-0) (N.S.Y.), the Holden Comprehensive Cancer Center Designated Gift Fund for pancreatic cancer research (N.S.Y.), and the Cancer Center Support Grant (P30 CA 086862) by the National Cancer Institute to the Holden Comprehensive Cancer Center at the University of Iowa (N.S.Y.).",

year = "2010",

month = nov,

doi = "10.1016/j.canlet.2010.04.023",

language = "English (US)",

volume = "297",

pages = "49--55",

journal = "Cancer Letters",

issn = "0304-3835",

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T1 - Transient receptor potential channel TRPM8 is over-expressed and required for cellular proliferation in pancreatic adenocarcinoma

AU - Yee, Nelson S.

AU - Zhou, Weiqiang

AU - Lee, Minsun

N1 - Funding Information: The authors wish to thank Dr. Ming-Sound Tsao at the University of Toronto for generously providing the H6c7 cell line. We wish also to acknowledge the Tissue Procurement Core Facility, Comparative Pathology Laboratory, Central Microscopy Research Facility, DNA Facility, and Flow Cytometry Facility at the University of Iowa for technical and equipment support. This work is supported by the Pilot Grant in Translational Research by the Department of Internal Medicine of the University of Iowa Carver College of Medicine (N.S.Y.), the American Cancer Society Junior Faculty Seed Grant Award (ACS #IRG-122-0) (N.S.Y.), the Holden Comprehensive Cancer Center Designated Gift Fund for pancreatic cancer research (N.S.Y.), and the Cancer Center Support Grant (P30 CA 086862) by the National Cancer Institute to the Holden Comprehensive Cancer Center at the University of Iowa (N.S.Y.).

PY - 2010/11

Y1 - 2010/11

N2 - The roles of transient receptor potential (TRP) cation channels in pancreatic tumorigenesis are essentially unknown. Here, we focus on the TRP melastatin-subfamily (TRPM) members. Expression of the thermally regulated transmembrane Ca2+-permeable channel TRPM8 is consistently up-regulated in human pancreatic adenocarcinoma cell lines and tissues. TRPM8-deficient pancreatic cancer cells have reduced ability of proliferation and cell cycle progression with elevated levels of cyclin-dependent kinase inhibitors. These results indicate that TRPM8 is aberrantly over-expressed in pancreatic adenocarcinoma and required for cellular proliferation, and they support further investigation of the potential of TRPM8 as a clinical biomarker and therapeutic target in pancreatic adenocarcinoma.

AB - The roles of transient receptor potential (TRP) cation channels in pancreatic tumorigenesis are essentially unknown. Here, we focus on the TRP melastatin-subfamily (TRPM) members. Expression of the thermally regulated transmembrane Ca2+-permeable channel TRPM8 is consistently up-regulated in human pancreatic adenocarcinoma cell lines and tissues. TRPM8-deficient pancreatic cancer cells have reduced ability of proliferation and cell cycle progression with elevated levels of cyclin-dependent kinase inhibitors. These results indicate that TRPM8 is aberrantly over-expressed in pancreatic adenocarcinoma and required for cellular proliferation, and they support further investigation of the potential of TRPM8 as a clinical biomarker and therapeutic target in pancreatic adenocarcinoma.

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DO - 10.1016/j.canlet.2010.04.023

M3 - Article

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AN - SCOPUS:77956229134

SN - 0304-3835

VL - 297

SP - 49

EP - 55

JO - Cancer Letters

JF - Cancer Letters

IS - 1

ER -

Transient receptor potential channel TRPM8 is over-expressed and required for cellular proliferation in pancreatic adenocarcinoma

Abstract

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