Mechanistic insights of epithelial protein lost in neoplasm in prostate cancer metastasis

Ross J. Collins; Liam D. Morgan; Sioned Owen; Fiona Ruge; Wen G. Jiang; Andrew J. Sanders

doi:10.1002/ijc.31786

Mechanistic insights of epithelial protein lost in neoplasm in prostate cancer metastasis

Ross J. Collins, Liam D. Morgan, Sioned Owen, Fiona Ruge, Wen G. Jiang, Andrew J. Sanders^*

^*Corresponding author for this work

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

Abstract

EPLIN is frequently downregulated or lost in various cancers. The purpose of this study was to evaluate the importance of EPLIN in prostate cancer progression, with particular focus on the mechanistic implications to elucidate EPLIN's tumor suppressive function in cancer. EPLIN expression was evaluated in prostate cancer cell lines and tissues. PC-3 and LNCaP EPLIN alpha overexpression models were generated through transfection with EPLIN alpha sequence and EPLIN knockdown was achieved using shRNA in CA-HPV-10 cells. Functional assays were performed to evaluate cellular characteristics and potential mechanisms were evaluated using a protein microarray, and validated using western blot analysis. EPLIN expression was reduced in clinical prostate cancer sections, including hyperplasia (p

Original language	English
Pages (from-to)	2537-2550
Number of pages	14
Journal	International Journal of Cancer
Volume	143
Issue number	10
DOIs	https://doi.org/10.1002/ijc.31786
Publication status	Published - 15 Nov 2018
Externally published	Yes

Keywords

EPLIN
prostate cancer
metastasis
Src
FAK
FOCAL-ADHESION KINASE
REGULATES ACTIN ORGANIZATION
TYROSINE PHOSPHORYLATION
CELL-MIGRATION
MESENCHYMAL TRANSITION
BREAST-CANCER
CROSS-LINKING
SRC
PAXILLIN

UN SDGs

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

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10.1002/ijc.31786Licence: CC BY-NC-ND

Cite this

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title = "Mechanistic insights of epithelial protein lost in neoplasm in prostate cancer metastasis",

abstract = "EPLIN is frequently downregulated or lost in various cancers. The purpose of this study was to evaluate the importance of EPLIN in prostate cancer progression, with particular focus on the mechanistic implications to elucidate EPLIN's tumor suppressive function in cancer. EPLIN expression was evaluated in prostate cancer cell lines and tissues. PC-3 and LNCaP EPLIN alpha overexpression models were generated through transfection with EPLIN alpha sequence and EPLIN knockdown was achieved using shRNA in CA-HPV-10 cells. Functional assays were performed to evaluate cellular characteristics and potential mechanisms were evaluated using a protein microarray, and validated using western blot analysis. EPLIN expression was reduced in clinical prostate cancer sections, including hyperplasia (p",

keywords = "EPLIN, prostate cancer, metastasis, Src, FAK, FOCAL-ADHESION KINASE, REGULATES ACTIN ORGANIZATION, TYROSINE PHOSPHORYLATION, CELL-MIGRATION, MESENCHYMAL TRANSITION, BREAST-CANCER, CROSS-LINKING, SRC, PAXILLIN",

author = "Collins, {Ross J.} and Morgan, {Liam D.} and Sioned Owen and Fiona Ruge and Jiang, {Wen G.} and Sanders, {Andrew J.}",

year = "2018",

month = nov,

day = "15",

doi = "10.1002/ijc.31786",

language = "English",

volume = "143",

pages = "2537--2550",

journal = "International Journal of Cancer",

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T1 - Mechanistic insights of epithelial protein lost in neoplasm in prostate cancer metastasis

AU - Collins, Ross J.

AU - Morgan, Liam D.

AU - Owen, Sioned

AU - Ruge, Fiona

AU - Jiang, Wen G.

AU - Sanders, Andrew J.

PY - 2018/11/15

Y1 - 2018/11/15

N2 - EPLIN is frequently downregulated or lost in various cancers. The purpose of this study was to evaluate the importance of EPLIN in prostate cancer progression, with particular focus on the mechanistic implications to elucidate EPLIN's tumor suppressive function in cancer. EPLIN expression was evaluated in prostate cancer cell lines and tissues. PC-3 and LNCaP EPLIN alpha overexpression models were generated through transfection with EPLIN alpha sequence and EPLIN knockdown was achieved using shRNA in CA-HPV-10 cells. Functional assays were performed to evaluate cellular characteristics and potential mechanisms were evaluated using a protein microarray, and validated using western blot analysis. EPLIN expression was reduced in clinical prostate cancer sections, including hyperplasia (p

AB - EPLIN is frequently downregulated or lost in various cancers. The purpose of this study was to evaluate the importance of EPLIN in prostate cancer progression, with particular focus on the mechanistic implications to elucidate EPLIN's tumor suppressive function in cancer. EPLIN expression was evaluated in prostate cancer cell lines and tissues. PC-3 and LNCaP EPLIN alpha overexpression models were generated through transfection with EPLIN alpha sequence and EPLIN knockdown was achieved using shRNA in CA-HPV-10 cells. Functional assays were performed to evaluate cellular characteristics and potential mechanisms were evaluated using a protein microarray, and validated using western blot analysis. EPLIN expression was reduced in clinical prostate cancer sections, including hyperplasia (p

KW - EPLIN

KW - prostate cancer

KW - metastasis

KW - Src

KW - FAK

KW - FOCAL-ADHESION KINASE

KW - REGULATES ACTIN ORGANIZATION

KW - TYROSINE PHOSPHORYLATION

KW - CELL-MIGRATION

KW - MESENCHYMAL TRANSITION

KW - BREAST-CANCER

KW - CROSS-LINKING

KW - SRC

KW - PAXILLIN

U2 - 10.1002/ijc.31786

DO - 10.1002/ijc.31786

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SN - 0020-7136

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EP - 2550

JO - International Journal of Cancer

JF - International Journal of Cancer

IS - 10

ER -

Mechanistic insights of epithelial protein lost in neoplasm in prostate cancer metastasis

Abstract

Keywords

UN SDGs

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