Oncotarget

Research Papers:

NBPF7 promotes the proliferation of α-catenin-knockdown HaCaT cells via functional interaction with the NF-κB pathway

Hua-Yu Zhu, Wen-Dong Bai, Chao Li, Jun Li and Da-Hai Hu _

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Oncotarget. 2017; 8:65800-65808. https://doi.org/10.18632/oncotarget.19480

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Abstract

Hua-Yu Zhu1,*, Wen-Dong Bai2,*, Chao Li1,3,*, Jun Li1 and Da-Hai Hu1

1Department of Burns and Cutaneous Surgery, Xijing Hospital, Fourth Military Medical University, Xi’an, Shaanxi, P.R. China

2Clinical Laboratory Center, Xinjiang Command General Hospital of Chinese People’s Liberation Army, Urumqi, Xinjiang, P.R. China

3Center of Military Burns and Plastic Surgery, Lanzhou General Hospital of Lanzhou Military Command of Chinese People’s Liberation Army, Lanzhou, Gansu, P.R. China

*These authors have contributed equally to this work

Correspondence to:

Da-Hai Hu, email: [email protected]

Jun Li, email: [email protected]

Keywords: α-catenin, NBPF7, NF-κB, HaCaT, proliferation

Received: April 18, 2017    Accepted: June 29, 2017    Published: July 22, 2017

ABSTRACT

Loss of key components that form cell-cell adherens junctions, such as α-catenin, triggers severe epidermal hyperproliferation. However, the underlying molecular mechanisms remain largely unknown. We report here that neuroblastoma breakpoint family (NBPF) genes are upregulated and that NBPF7 specifically promotes cellular proliferation of α-catenin-silenced HaCaT cells through functional linkage with the NF-κB pathway. Genome-wide profiling of HaCaT cells shows that NBPF genes are upregulated following α-catenin knockdown. Data from western blot analyses are consistent with the activation of the NF-κB pathway as well as increased expression of NBPF7 by α-catenin knockdown. Co-immunoprecipitation assays indicate that NBPF7 could be detected in endogenous activated NF-κB immunoprecipitates. Immunoflurence analyses demonstrate that NBPF7 co-localizes with activated NF-κB in the nucleus after α-catenin silencing. Moreover, inhibition of NBPF7 decreases the proliferation of HaCaT cells and abolishes the enhanced proliferation associated with α-catenin knockdown in HaCaT cells. These results indicate that NBPF7 plays a key role in the α-catenin signaling pathway that regulates cell proliferation of keratinocytes. Our findings suggest that the classical NF-κB pathway plays a critical role in cellular proliferation and that NBPF7 is a functional mediator for α-catenin in the regulation of keratinocyte growth.


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