C1orf106 (INAVA) Is a SMAD3-Dependent TGF-β Target Gene That Promotes Clonogenicity and Correlates with Poor Prognosis in Breast Cancer

Lauren E. Strathearn; Lindsay Spender; Christina Schoenherr; Susan Mason; Ruaridh Edwards; Karen Blyth; Gareth J Inman

doi:10.3390/cells13181530

C1orf106 (INAVA) Is a SMAD3-Dependent TGF-β Target Gene That Promotes Clonogenicity and Correlates with Poor Prognosis in Breast Cancer

Lauren E. Strathearn
, Lindsay Spender
, Christina Schoenherr
, Susan Mason
, Ruaridh Edwards
, Karen Blyth
, Gareth J Inman (Lead / Corresponding author)

Cancer Research

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

1 Citation (Scopus)

121 Downloads (Pure)

Abstract

Transforming Growth Factor-β (TGF-β) can have both tumour-promoting and tumour-suppressing activity in breast cancer. Elucidating the key downstream mediators of pro-tumorigenic TGF-β signalling in this context could potentially give rise to new therapeutic opportunities and/or identify biomarkers for anti-TGF-β directed therapy. Here, we identify C1orf106 (also known as innate immunity activator INAVA) as a novel TGF-β target gene which is induced in a SMAD3-dependent but SMAD2/SMAD4-independent manner in human and murine cell lines. C1orf106 expression positively correlates with tumourigenic or metastatic potential in human and murine breast cancer cell line models, respectively, and is required for enhanced migration and invasion in response to TGF-β stimulation. C1orf106 promoted self-renewal and colony formation in vitro and may promote tumour-initiating frequency in vivo. High C1orf106 mRNA expression correlates with markers of aggressiveness and poor prognosis in human breast cancer. Taken together, our findings indicate that C1orf106 may act as a tumour promoter in breast cancer.

Original language	English
Article number	1530
Number of pages	17
Journal	Cells
Volume	13
Issue number	18
DOIs	https://doi.org/10.3390/cells13181530
Publication status	Published - 12 Sept 2024

UN SDGs

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

SDG 3 Good Health and Well-being

Keywords

C1orf106
INAVA
TGF-β
breast carcinoma

ASJC Scopus subject areas

General Biochemistry,Genetics and Molecular Biology

Access to Document

10.3390/cells13181530Licence: CC BY

Final Published VersionFinal published version, 3.65 MBLicence: CC BY

Cite this

@article{100160b32e774967a9fb07d036de3dc6,

title = "C1orf106 (INAVA) Is a SMAD3-Dependent TGF-β Target Gene That Promotes Clonogenicity and Correlates with Poor Prognosis in Breast Cancer",

abstract = "Transforming Growth Factor-β (TGF-β) can have both tumour-promoting and tumour-suppressing activity in breast cancer. Elucidating the key downstream mediators of pro-tumorigenic TGF-β signalling in this context could potentially give rise to new therapeutic opportunities and/or identify biomarkers for anti-TGF-β directed therapy. Here, we identify C1orf106 (also known as innate immunity activator INAVA) as a novel TGF-β target gene which is induced in a SMAD3-dependent but SMAD2/SMAD4-independent manner in human and murine cell lines. C1orf106 expression positively correlates with tumourigenic or metastatic potential in human and murine breast cancer cell line models, respectively, and is required for enhanced migration and invasion in response to TGF-β stimulation. C1orf106 promoted self-renewal and colony formation in vitro and may promote tumour-initiating frequency in vivo. High C1orf106 mRNA expression correlates with markers of aggressiveness and poor prognosis in human breast cancer. Taken together, our findings indicate that C1orf106 may act as a tumour promoter in breast cancer.",

keywords = "C1orf106, INAVA, TGF-β, breast carcinoma",

author = "Strathearn, \{Lauren E.\} and Lindsay Spender and Christina Schoenherr and Susan Mason and Ruaridh Edwards and Karen Blyth and Inman, \{Gareth J\}",

note = "Publisher Copyright: {\textcopyright} 2024 by the authors.",

year = "2024",

month = sep,

day = "12",

doi = "10.3390/cells13181530",

language = "English",

volume = "13",

journal = "Cells",

issn = "2073-4409",

publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",

number = "18",

}

TY - JOUR

T1 - C1orf106 (INAVA) Is a SMAD3-Dependent TGF-β Target Gene That Promotes Clonogenicity and Correlates with Poor Prognosis in Breast Cancer

AU - Strathearn, Lauren E.

AU - Spender, Lindsay

AU - Schoenherr, Christina

AU - Mason, Susan

AU - Edwards, Ruaridh

AU - Blyth, Karen

AU - Inman, Gareth J

PY - 2024/9/12

Y1 - 2024/9/12

N2 - Transforming Growth Factor-β (TGF-β) can have both tumour-promoting and tumour-suppressing activity in breast cancer. Elucidating the key downstream mediators of pro-tumorigenic TGF-β signalling in this context could potentially give rise to new therapeutic opportunities and/or identify biomarkers for anti-TGF-β directed therapy. Here, we identify C1orf106 (also known as innate immunity activator INAVA) as a novel TGF-β target gene which is induced in a SMAD3-dependent but SMAD2/SMAD4-independent manner in human and murine cell lines. C1orf106 expression positively correlates with tumourigenic or metastatic potential in human and murine breast cancer cell line models, respectively, and is required for enhanced migration and invasion in response to TGF-β stimulation. C1orf106 promoted self-renewal and colony formation in vitro and may promote tumour-initiating frequency in vivo. High C1orf106 mRNA expression correlates with markers of aggressiveness and poor prognosis in human breast cancer. Taken together, our findings indicate that C1orf106 may act as a tumour promoter in breast cancer.

AB - Transforming Growth Factor-β (TGF-β) can have both tumour-promoting and tumour-suppressing activity in breast cancer. Elucidating the key downstream mediators of pro-tumorigenic TGF-β signalling in this context could potentially give rise to new therapeutic opportunities and/or identify biomarkers for anti-TGF-β directed therapy. Here, we identify C1orf106 (also known as innate immunity activator INAVA) as a novel TGF-β target gene which is induced in a SMAD3-dependent but SMAD2/SMAD4-independent manner in human and murine cell lines. C1orf106 expression positively correlates with tumourigenic or metastatic potential in human and murine breast cancer cell line models, respectively, and is required for enhanced migration and invasion in response to TGF-β stimulation. C1orf106 promoted self-renewal and colony formation in vitro and may promote tumour-initiating frequency in vivo. High C1orf106 mRNA expression correlates with markers of aggressiveness and poor prognosis in human breast cancer. Taken together, our findings indicate that C1orf106 may act as a tumour promoter in breast cancer.

KW - C1orf106

KW - INAVA

KW - TGF-β

KW - breast carcinoma

UR - https://www.scopus.com/pages/publications/85205109013

U2 - 10.3390/cells13181530

DO - 10.3390/cells13181530

M3 - Article

C2 - 39329715

SN - 2073-4409

VL - 13

JO - Cells

JF - Cells

IS - 18

M1 - 1530

ER -

C1orf106 (INAVA) Is a SMAD3-Dependent TGF-β Target Gene That Promotes Clonogenicity and Correlates with Poor Prognosis in Breast Cancer

Abstract

UN SDGs

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this